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Journal articles on the topic 'Cerebellar nuclei'
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1
Yildiz, D., and M. E. Gultiken. "Vascularisation of the cerebellar nuclei in Akkaraman sheep." Acta Veterinaria Hungarica 51, no. 4 (October 1, 2003): 433–37. http://dx.doi.org/10.1556/avet.51.2003.4.1.
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This study reports an anatomical study of the vascular supply in 20 Akkaraman sheep cerebelli from adult subjects of both sexes. The origin and branching pattern of the cerebellar artery vascularising the cerebellar nuclei were studied by gross dissection and vascular injection. Then dissection was performed and vessels nourishing the cerebellar nuclei were documented. Four bilaterally symmetrical cerebellar nuclei were determined as nucleus lateralis cerebelli, nucleus interpositus lateralis cerebelli, and nucleus interpositus medialis cerebelli and nucleus fastigii from lateral to medial side. It has been previously confirmed that vascularisation of the cerebellar nuclei is carried out by intermediary branches of the rostral cerebellar artery and the caudal cerebellar artery. However, this study has confirmed that the caudal cerebellar artery has no contribution in the vascularisation of the cerebellar nuclei.
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Mitoma, Hiroshi, Shinji Kakei, Hirokazu Tanaka, and Mario Manto. "Morphological and Functional Principles Governing the Plasticity Reserve in the Cerebellum: The Cortico-Deep Cerebellar Nuclei Loop Model." Biology 12, no. 11 (November 16, 2023): 1435. http://dx.doi.org/10.3390/biology12111435.
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Cerebellar reserve compensates for and restores functions lost through cerebellar damage. This is a fundamental property of cerebellar circuitry. Clinical studies suggest (1) the involvement of synaptic plasticity in the cerebellar cortex for functional compensation and restoration, and (2) that the integrity of the cerebellar reserve requires the survival and functioning of cerebellar nuclei. On the other hand, recent physiological studies have shown that the internal forward model, embedded within the cerebellum, controls motor accuracy in a predictive fashion, and that maintaining predictive control to achieve accurate motion ultimately promotes learning and compensatory processes. Furthermore, within the proposed framework of the Kalman filter, the current status is transformed into a predictive state in the cerebellar cortex (prediction step), whereas the predictive state and sensory feedback from the periphery are integrated into a filtered state at the cerebellar nuclei (filtering step). Based on the abovementioned clinical and physiological studies, we propose that the cerebellar reserve consists of two elementary mechanisms which are critical for cerebellar functions: the first is involved in updating predictions in the residual or affected cerebellar cortex, while the second acts by adjusting its updated forecasts with the current status in the cerebellar nuclei. Cerebellar cortical lesions would impair predictive behavior, whereas cerebellar nuclear lesions would impact on adjustments of neuronal commands. We postulate that the multiple forms of distributed plasticity at the cerebellar cortex and cerebellar nuclei are the neuronal events which allow the cerebellar reserve to operate in vivo. This cortico-deep cerebellar nuclei loop model attributes two complementary functions as the underpinnings behind cerebellar reserve.
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Petrovic-Minic, Bosiljka, Jelena Mojsilovic-Petrovic, Soren Holm, Jesper Mogensen, and Ivan Divac. "Absence of transsynaptic transport in cerebello-thalamo-cortical path of the rat." Acta Neurobiologiae Experimentalis 54, no. 1 (March 31, 1994): 39–45. http://dx.doi.org/10.55782/ane-1994-1000.
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Attempts to visualize the cerebello-thalamo-cortical path in the rat were made with different approaches. We tried (1) double labelling with somatopetal tracing from the motor cortex and somatofugal from the cerebellar nuclei, (2) transmembrane labelling by depositing biocytin or wheat germ agglutinin (WGA)into the motor cortex or cerebellum. WGA was either iodinated with 125I or conjugated with horseradish peroxidase (HRP). The double labelling technique showed an overlap of the tracers in the same thalamic region but no evidence of transsynaptic transport in either direction was obtained. Our results indicate a difference in the organization of this system in primates and rodents, since transsynaptic labelling in the cerebellar nuclei after injections of WGA-HRP conjugate in the monkey motor cortex has been found.
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Stasi, Kalliope, Adamantia Mitsacos, Lazaros C. Triarhou, and Elias D. Kouvelas. "Cerebellar Grafts Partially Reverse Amino Acid Receptor Changes Observed in the Cerebellum of Mice with Hereditary Ataxia: Quantitative Autoradiographic Studies." Cell Transplantation 6, no. 3 (May 1997): 347–59. http://dx.doi.org/10.1177/096368979700600317.
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We used quantitative autoradiography of [3H]CNQX (200 nM), [3H]muscimol (13 nM), and [3H]flunitrazepam (10 nM) binding to study the distribution of non-NMDA and GABAA receptors in the cerebellum of pcd mutant mice with unilateral cerebellar grafts. Nonspecific binding was determined by incubation with 1 mM Glu, 200 μM GABA, or 1 μM clonazepam, respectively. Saturation parameters were defined in wild-type and mutant cerebella. In mutants, non-NMDA receptors were reduced by 38% in the molecular layer and by 47% in the granule cell layer. The reduction of non-NMDA receptors in the pcd cerebellar cortex supports their localization on Purkinje cells. [3H] CNQX binding sites were visualized at higher density in grafts that had migrated to the cerebellar cortex of the hosts (4.1 and 11.0 pmol/mg protein, respectively, at 23 and 37 days after grafting) than in grafts arrested intraparen-chymally (2.6 and 6.2 pmol/mg protein, respectively, at 23 and 37 days after grafting). The pattern of expression of non-NMDA receptors in cortical vs. parenchymal grafts suggests a possible regulation of their levels by transacting elements from host parallel fibers. GABAA binding levels in the grafts for both ligands used were similar to normal molecular layer. Binding was increased in the deep cerebellar nuclei of pcd mutants: the increase in [3H]muscimol binding over normal was 215% and the increase in [3H]flunitrazepam binding was 89%. Such increases in the pcd deep cerebellar nuclei may reflect a denervation-induced supersensitivity subsequent to the loss of Purkinje axon terminal innervation. In the deep nuclei of pcd mutants with unilateral cerebellar grafts, [3H]muscimol binding was 31% lower in the grafted side than in the contralateral nongrafted side at 37 days after transplantation; [3H]fluni-trazepam binding was also lower in the grafted side by 15% compared to the nongrafted side. Such changes in GABAA receptors suggest a significant, albeit partial, normalizing trend of cerebellar grafts on the state of postsynaptic supersensitive receptors in the host cerebellar nuclei.
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Monaco, Jessica, Lorenzo Rocchi, Francesca Ginatempo, Egidio D'Angelo, and John C. Rothwell. "Cerebellar Theta-Burst Stimulation Impairs Memory Consolidation in Eyeblink Classical Conditioning." Neural Plasticity 2018 (October 9, 2018): 1–8. http://dx.doi.org/10.1155/2018/6856475.
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Associative learning of sensorimotor contingences, as it occurs in eyeblink classical conditioning (EBCC), is known to involve the cerebellum, but its mechanism remains controversial. EBCC involves a sequence of learning processes which are thought to occur in the cerebellar cortex and deep cerebellar nuclei. Recently, the extinction phase of EBCC has been shown to be modulated after one week by cerebellar continuous theta-burst stimulation (cTBS). Here, we asked whether cerebellar cTBS could affect retention and reacquisition of conditioned responses (CRs) tested immediately after conditioning. We also investigated a possible lateralized cerebellar control of EBCC by applying cTBS on both the right and left cerebellar hemispheres. Both right and left cerebellar cTBSs induced a statistically significant impairment in retention and new acquisition of conditioned responses (CRs), the disruption effect being marginally more effective when the left cerebellar hemisphere was stimulated. These data support a model in which cTBS impairs retention and reacquisition of CR in the cerebellum, possibly by interfering with the transfer of memory to the deep cerebellar nuclei.
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Alahmadi, Adnan A. S. "The Cerebellum’s Orchestra: Understanding the Functional Connectivity of Its Lobes and Deep Nuclei in Coordination and Integration of Brain Networks." Tomography 9, no. 2 (April 21, 2023): 883–93. http://dx.doi.org/10.3390/tomography9020072.
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The cerebellum, a crucial brain region, significantly contributes to various brain functions. Although it occupies a small portion of the brain, it houses nearly half of the neurons in the nervous system. Previously thought to be solely involved in motor activities, the cerebellum has since been found to play a role in cognitive, sensory, and associative functions. To further elucidate the intricate neurophysiological characteristics of the cerebellum, we investigated the functional connectivity of cerebellar lobules and deep nuclei with 8 major functional brain networks in 198 healthy subjects. Our findings revealed both similarities and differences in the functional connectivity of key cerebellar lobules and nuclei. Despite robust functional connectivity among these lobules, our results demonstrated that they exhibit heterogeneous functional integration with different functional networks. For instance, lobules 4, 5, 6, and 8 were linked to sensorimotor networks, while lobules 1, 2, and 7 were associated with higher-order, non-motor, and complex functional networks. Notably, our study uncovered a lack of functional connectivity in lobule 3, strong connections between lobules 4 and 5 with the default mode networks, and connections between lobules 6 and 8 with the salience, dorsal attention, and visual networks. Additionally, we found that cerebellar nuclei, particularly the dentate cerebellar nuclei, were connected to sensorimotor, salience, language, and default-mode networks. This study provides valuable insights into the diverse functional roles of the cerebellum in cognitive processing.
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Elnegiry, Ahmed, Hazem Hamoda, and Foad Farrag. "Histomorphological Study on the Cerebellum of the African Ostrich." Alexandria Journal of Veterinary Sciences 73, no. 2 (2022): 1. http://dx.doi.org/10.5455/ajvs.33484.
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In this, we use six male African ostriches aging 10-13 months. Our findings revealed the morphometric and histological structure of the African ostrich cerebellum that controls the balance and locomotion of the largest, heaviest, and fastest flightless bird. The average length, width, perimeter, and surface area of ostrich cerebella were measured. The large-sized cerebellum of the ostrich provides the bird with proper control of locomotion and balance in addition to complex cognitive abilities. Histologically, we describe the histoarchitecture of the ostrich cerebellum with the distinct three layers, molecular layer, Purkinje, and granular layers. Purkinje cell Nissl granules and cell Processes were demonstrated using special stains. The complicated cerebellar circuity and the different information inputs to the cerebellum from the vestibular system, spinocerebellar tracts, and pontine nuclei were discussed. Pontine nuclei of the ventral pons which represent the main input of information to the cerebellum were also demonstrated.
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Draganova, Rossitza, Viktor Pfaffenrot, Katharina M. Steiner, Sophia L. Göricke, Naveen Elangovan, Dagmar Timmann, and Jürgen Konczak. "Neurostructural changes and declining sensorimotor function due to cerebellar cortical degeneration." Journal of Neurophysiology 125, no. 5 (May 1, 2021): 1735–45. http://dx.doi.org/10.1152/jn.00266.2020.
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NEW & NOTEWORTHY: Neurodegeneration of the cerebellum progresses over years and primarily affects cerebellar cortex. It leads to a progressive loss of control and coordination of movement. We here show that the neurodegenerative process not only leads to cells loss in cerebellar cortex but also induces neurostructural changes in the form of increased gray matter in the efferent targets of the cerebellar cortex, namely, the cerebellar output nuclei, the SMA, and premotor cortex.
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Pose-Méndez, Sol, Isabel Rodríguez-Moldes, Eva Candal, Sylvie Mazan, and Ramón Anadón. "A Developmental Study of the Cerebellar Nucleus in the Catshark, a Basal Gnathostome." Brain, Behavior and Evolution 89, no. 1 (2017): 1–14. http://dx.doi.org/10.1159/000453654.
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The output of the cerebellar cortex is mainly released via cerebellar nuclei which vary in number and complexity among gnathostomes, extant vertebrates with a cerebellum. Cartilaginous fishes, a basal gnathostome lineage, show a conspicuous, well-organized cerebellar nucleus, unlike ray-finned fishes. To gain insight into the evolution and development of the cerebellar nucleus, we analyzed in the shark Scyliorhinus canicula (a chondrichthyan model species) the developmental expression of several genes coding for transcription factors (ScLhx5,ScLhx9,ScTbr1, and ScEn2) and the distribution of the protein calbindin, since all appear to be involved in cerebellar nuclei patterning in other gnathostomes. Three regions (subventricular, medial or central, and lateral or superficial) became recognizable in the cerebellar nucleus of this shark during development. Present genoarchitectonic and neurochemical data in embryos provide insight into the origin of the cerebellar nucleus in chondrichthyans and support a tripartite mediolateral organization of the cerebellar nucleus, as previously described in adult sharks. Furthermore, the expression pattern of ScLhx5,ScLhx9, and ScTbr1 in this shark, together with that of markers of proliferation, migration, and early differentiation of neurons, is compatible with the hypothesis that, as in mammals, different subsets of cerebellar nucleus neurons are originated from progenitors of 2 different sources: the ventricular zone of the cerebellar plate and the rhombic lip. We also present suggestive evidence that Lhx9 expression is involved in cerebellar nuclei patterning early on in gnathostome evolution, rather than representing an evolutionary innovation of the dentate nucleus in mammals, as previously hypothesized.
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Kornegay, J. N. "Cerebellar Vermian Hypoplasia in Dogs." Veterinary Pathology 23, no. 4 (July 1986): 374–79. http://dx.doi.org/10.1177/030098588602300405.
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Six dogs with cerebellar dysplasia, in which the cerebellar vermis was hypoplastic, are described. Clinical signs in these dogs were noted around 2 weeks of age and included ataxia, dysmetria, and intention tremors. A variable portion of the caudal cerebellar vermis was absent in each dog; portions of the cerebellar hemispheres and flocculus also were absent in some of them. Neurons in certain brain stem nuclei that project to the cerebellum were either chromatolytic or vacuolated. Cerebellar vermian hypoplasia of dogs is analogous to the Dandy-Walker syndrome of human beings.
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Dumas, Daniël B., Simona V. Gornati, Youri Adolfs, Tomomi Shimogori, R. Jeroen Pasterkamp, and Freek E. Hoebeek. "Anatomical Development of the Cerebellothalamic Tract in Embryonic Mice." Cells 11, no. 23 (November 27, 2022): 3800. http://dx.doi.org/10.3390/cells11233800.
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The main connection from cerebellum to cerebrum is formed by cerebellar nuclei axons that synapse in the thalamus. Apart from its role in coordinating sensorimotor integration in the adult brain, the cerebello-thalamic tract (CbT) has also been implicated in developmental disorders, such as autism spectrum disorders. Although the development of the cerebellum, thalamus and cerebral cortex have been studied, there is no detailed description of the ontogeny of the mammalian CbT. Here we investigated the development of the CbT at embryonic stages using transgenic Ntsr1-Cre/Ai14 mice and in utero electroporation of wild type mice. Wide-field, confocal and 3D light-sheet microscopy of immunohistochemical stainings showed that CbT fibers arrive in the prethalamus between E14.5 and E15.5, but only invade the thalamus after E16.5. We quantified the spread of CbT fibers throughout the various thalamic nuclei and found that at E17.5 and E18.5 the ventrolateral, ventromedial and parafascicular nuclei, but also the mediodorsal and posterior complex, become increasingly innervated. Several CbT fiber varicosities express vesicular glutamate transporter type 2 at E18.5, indicating cerebello-thalamic synapses. Our results provide the first quantitative data on the developing murine CbT, which provides guidance for future investigations of the impact that cerebellum has on thalamo-cortical networks during development.
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Keifer, J. "Effects of red nucleus inactivation on burst discharge in turtle cerebellum in vitro: evidence for positive feedback." Journal of Neurophysiology 76, no. 4 (October 1, 1996): 2200–2210. http://dx.doi.org/10.1152/jn.1996.76.4.2200.
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1. In behaving animals the red nucleus produces sustained action potential discharge during movements of the limbs. These bursts are thought to encode parameters of movement and thereby represent motor commands. Similar bursts can be recorded in the in vitro brain stem-cerebellum from the turtle. In this preparation, sustained discharge of red nucleus neurons was postulated to be generated by N-methyl-D-aspartate-mediated cellular mechanisms acting in combination with positive feedback in a recurrent cerebellorubral network. The present study was designed to test this positive feedback hypothesis. During recording of sustained discharge in the deep cerebellar nuclei and cortex, the red nucleus was reversibly inactivated by microinjection. The positive feedback hypothesis would be supported if activity in the cerebellum was attenuated by inactivation of the red nucleus. A nonrecurrent source of excitation would have to be postulated if cerebellar activity was unaffected. 2. Extracellular single-unit recordings were made from neurons in the deep cerebellar nuclei, cerebellar cortex, and vestibular nuclei. Burst discharges were evoked by brief electrical stimuli applied to the spinal cord that activated sensory structures. During inactivation of the red nucleus, sensory projections to the cerebellum that may evoke burst discharge were unaffected. Pressure microinjections of cobalt, lidocaine, gamma-aminobutyric acid (GABA), or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were used to reversibly inactivate the red nucleus. Saline injections were also tested. 3. Sustained discharge of all neurons recorded in the lateral cerebellar nucleus was greatly attenuated or blocked completely by injection of the pharmacological agents into the red nucleus. These effects were reversible. Of the recordings in the cerebellar cortex, 63% of these were blocked. All four compounds tested were effective blockers of the bursts, although the effects of GABA were less potent than the others. Saline injections into the red nucleus showed no effect. Burst discharges of single units recorded in either the medial cerebellar nucleus or the vestibular complex, which do not receive input from the red nucleus, showed no effect of red nucleus inactivation. 4. The results showed that sustained discharge in the cerebellum was significantly attenuated by inactivation of the red nucleus even though sensory input that may trigger the bursts was intact. These data support the hypothesis that sustained discharge in the cerebellorubral circuit is generated by a distributed neuronal network that uses positive feedback. The results have implications for mechanisms underlying normal brain function and some motor disorders.
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Mehdizadeh, Mehdi, Niloufar Ashtari, Xiaodan Jiao, Maryam Rahimi Balaei, Asghar Marzban, Farshid Qiyami-Hour, Jiming Kong, Saeid Ghavami, and Hassan Marzban. "Alteration of the Dopamine Receptors’ Expression in the Cerebellum of the Lysosomal Acid Phosphatase 2 Mutant (Naked–Ataxia (NAX)) Mouse." International Journal of Molecular Sciences 21, no. 8 (April 21, 2020): 2914. http://dx.doi.org/10.3390/ijms21082914.
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A spontaneous mutation in the lysosomal acid phosphatase (Acp2) enzyme (nax: naked–ataxia) in experimental mice results in delayed hair appearance and severe cytoarchitectural impairments of the cerebellum, such as a Purkinje cell (PC) migration defect. In our previous investigation, our team showed that Acp2 expression plans a significant role in cerebellar development. On the other hand, the dopaminergic system is also a player in central nervous system (CNS) development, including cerebellar structure and function. In the current investigation, we have explored how Acp2 can be involved in the regulation of the dopaminergic pathway in the cerebellum via the regulation of dopamine receptor expression and patterning. We provided evidence about the distribution of different dopamine receptors in the developing cerebellum by comparing the expression of dopamine receptors on postnatal days (P) 5 and 17 between nax mice and wild–type (wt) littermates. To this aim, immunohistochemistry and Western blot analysis were conducted using five antibodies against dopamine receptors (DRD1, –2, –3, –4, and –5) accompanied by RNAseq data. Our results revealed that DRD1, –3, and –4 gene expressions significantly increased in nax cerebella but not in wt, while gene expressions of all 5 receptors were evident in PCs of both wt and nax cerebella. DRD3 was strongly expressed in the PCs’ somata and cerebellar nuclei neurons at P17 in nax mice, which was comparable to the expression levels in the cerebella of wt littermates. In addition, DRD3 was expressed in scattered cells in a granular layer reminiscent of Golgi cells and was observed in the wt cerebella but not in nax mice. DRD4 was expressed in a subset of PCs and appeared to align with the unique parasagittal stripes pattern. This study contributes to our understanding of alterations in the expression pattern of DRDs in the cerebellum of nax mice in comparison to their wt littermates, and it highlights the role of Acp2 in regulating the dopaminergic system.
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Kros, Lieke, Chantal A. Angueyra Aristizábal, and Kamran Khodakhah. "Cerebellar involvement in migraine." Cephalalgia 38, no. 11 (January 22, 2018): 1782–91. http://dx.doi.org/10.1177/0333102417752120.
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Background Although there is a great wealth of knowledge about the neurobiological processes underlying migraine and its accompanying symptoms, the mechanisms by which an attack starts remain elusive, and the disease remains undertreated. Although the vast majority of literature focuses on the involvement of the trigeminovascular systems and higher systems it innervates, such as thalamic and hypothalamic nuclei, several lines of evidence implicate the cerebellum in the pathophysiology of migraine. Aim In this review, we aim to summarize potential cerebellar involvement seen from different perspectives including the results from imaging studies, cerebellar connectivity to migraine-related brain structures, comorbidity with disorders implying cerebellar dysfunction, similarities in triggers precipitating both such disorders, and migraine and cerebellar expression of migraine-related genes and neuropeptides. We aim to inspire an increase in interest for future research on the subject. Conclusion It is hoped that future studies can provide an answer as to how the cerebellum may be involved and whether treatment options specifically targeting the cerebellum could provide alleviation of this disorder.
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Rijkers, Kim, Véronique M. P. Moers-Hornikx, Roelof J. Hemmes, Marlien W. Aalbers, Yasin Temel, Johan S. H. Vles, and Govert Hoogland. "Sustained Reduction of Cerebellar Activity in Experimental Epilepsy." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/718591.
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Clinical and experimental evidence suggests a role for the cerebellum in seizure control, while no data are available on cerebellar activity between seizures. We hypothesized that interictal regional activity of the deep cerebellar nuclei is reduced in epilepsy and tested this in an animal model by using ΔFosB and cytochrome oxidase (COX) (immuno)histochemistry. The expression of these two markers of neuronal activity was analysed in the dentate nucleus (DN), interpositus nucleus (IN), and fastigial nucleus (FN) of the cerebellum of fully amygdala kindled rats that were sacrificed 48 hours after their last seizure. The DN and FN of kindled rats exhibited 25 to 29% less ΔFosB immunopositive cells than their respective counterpart in sham controls (P<0.05). COX expression in the DN and FN of kindled animals was reduced by 32 to 33% compared to respective control values (P<0.05). These results indicate that an epileptogenic state is characterized by decreased activity of deep cerebellar nuclei, especially the DN and FN. Possible consequences may include a decreased activation of the thalamus, contributing to further seizure spread. Restoration of FN activity by low frequency electrical stimulation is suggested as a possible treatment option in chronic epilepsy.
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Cummins, Daniel D., Hyun Joo Park, and Fedor Panov. "Neurosurgical treatment of spasticity: a potential return to the cerebellum." Neurosurgical Focus 56, no. 6 (June 2024): E3. http://dx.doi.org/10.3171/2024.3.focus2446.
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OBJECTIVE Neurosurgical targeting of the cerebellar dentate nucleus via ablative dentatotomy and stimulation of the dentate nucleus was historically used for effective treatment of spasticity. Yet for decades, neurosurgical treatment of spasticity targeting the cerebellum was bypassed in favor of alternative treatments such as intrathecal baclofen pumps and selective dorsal rhizotomies. Cerebellar neuromodulation has recently reemerged as a promising and effective therapy for spasticity and related movement disorders. METHODS In this narrative review, the authors contextualize the historical literature of cerebellar neuromodulation, comparing it with modern approaches and exploring future directions with regard to cerebellar neuromodulation for spasticity. RESULTS Neurosurgical intervention on the cerebellum dates to the use of dentatotomy in the 1960s, which had progressed to electrical stimulation of the cerebellar cortex and dentate nucleus by the 1980s. By 2024, modern neurosurgical approaches such as tractography-based targeting of the dentate nucleus and transcranial magnetic stimulation of cerebellar cortex have demonstrated promise for treating spasticity. CONCLUSIONS Cerebellar neuromodulation of the dentate nucleus and cerebellar cortex are promising therapies for severe cases of spasticity. Open areas for exploration in the field include the following: tractography-based targeting, adaptive cerebellar stimulation, and investigations into the network dynamics between the cerebellar cortex, deep cerebellar nuclei, and the subcortical and cortical structures of the cerebrum.
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Albazron, Fatimah M., Joel Bruss, Robin M. Jones, Torunn I. Yock, Margaret B. Pulsifer, Alexander L. Cohen, Peg C. Nopoulos, Annah N. Abrams, Mariko Sato, and Aaron D. Boes. "Pediatric postoperative cerebellar cognitive affective syndrome follows outflow pathway lesions." Neurology 93, no. 16 (September 16, 2019): e1561-e1571. http://dx.doi.org/10.1212/wnl.0000000000008326.
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ObjectiveTo evaluate lesion location after pediatric cerebellar tumor resection in relation to the development of severe cognitive and affective disturbances, or cerebellar cognitive affective syndrome (CCAS).MethodsThe postsurgical lesion location of 195 pediatric patients with cerebellar tumors was mapped onto a template brain. Individuals with CCAS were matched to 2 participants without CCAS by sex, age, and lesion volume. Lesion analyses included both a hypothesis-driven evaluation of the cerebellar outflow pathway (deep nuclei and superior cerebellar peduncles) and data-driven multivariate lesion symptom mapping. Lesion-associated networks were evaluated by comparing connectivity patterns between the lesion location of cases with and those without CCAS with resting-state functional connectivity MRI data from large normative adult and pediatric cohorts.ResultsCCAS was present in 48 of 195 participants (24.6%) and was strongly associated with cerebellar outflow tract lesions (p < 0.0001). Lesion symptom mapping also highlighted the cerebellar outflow pathway, with peak findings in the fastigial nuclei extending into the inferior vermis. Lesion network mapping revealed that the cerebellar region most associated with CCAS was functionally connected to the thalamic mediodorsal nucleus, among other sites, and that higher connectivity between lesion location and the mediodorsal nucleus predicts CCAS occurrence (p < 0.01). A secondary analysis of 27 participants with mutism revealed similar localization of lesions and lesion-associated networks.ConclusionLesions of the cerebellar outflow pathway and inferior vermis are associated with major cognitive and affective disturbances after pediatric cerebellar tumor resection, and disrupted communication between the cerebellum and the thalamic mediodorsal nucleus may be important.
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Wetmore, Daniel Z., Eran A. Mukamel, and Mark J. Schnitzer. "Lock-and-Key Mechanisms of Cerebellar Memory Recall Based on Rebound Currents." Journal of Neurophysiology 100, no. 4 (October 2008): 2328–47. http://dx.doi.org/10.1152/jn.00344.2007.
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A basic question for theories of learning and memory is whether neuronal plasticity suffices to guide proper memory recall. Alternatively, information processing that is additional to readout of stored memories might occur during recall. We formulate a “lock-and-key” hypothesis regarding cerebellum-dependent motor memory in which successful learning shapes neural activity to match a temporal filter that prevents expression of stored but inappropriate motor responses. Thus, neuronal plasticity by itself is necessary but not sufficient to modify motor behavior. We explored this idea through computational studies of two cerebellar behaviors and examined whether deep cerebellar and vestibular nuclei neurons can filter signals from Purkinje cells that would otherwise drive inappropriate motor responses. In eyeblink conditioning, reflex acquisition requires the conditioned stimulus (CS) to precede the unconditioned stimulus (US) by >100 ms. In our biophysical models of cerebellar nuclei neurons this requirement arises through the phenomenon of postinhibitory rebound depolarization and matches longstanding behavioral data on conditioned reflex timing and reliability. Although CS–US intervals <100 ms may induce Purkinje cell plasticity, cerebellar nuclei neurons drive conditioned responses only if the CS–US training interval was >100 ms. This bound reflects the minimum time for deinactivation of rebound currents such as T-type Ca2+. In vestibulo-ocular reflex adaptation, hyperpolarization-activated currents in vestibular nuclei neurons may underlie analogous dependence of adaptation magnitude on the timing of visual and vestibular stimuli. Thus, the proposed lock-and-key mechanisms link channel kinetics to recall performance and yield specific predictions of how perturbations to rebound depolarization affect motor expression.
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Nah, Sangun, Han Bit Kim, Sangsoo Han, Sungwoo Choi, and Hoon Lim. "Cerebellar Hippocampal and Basal Nuclei Transient Edema with Restricted diffusion (CHANTER) syndrome due to antidepressant." Journal of The Korean Society of Clinical Toxicology 20, no. 1 (June 30, 2022): 31–34. http://dx.doi.org/10.22537/jksct.2022.20.1.31.
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Cerebellar Hippocampal and Basal Nuclei Transient Edema with Restricted diffusion (CHANTER) syndrome is characterized by an altered mental status. The acute MRI lesions show abnormal restricted diffusion imaging bilaterally and symmetrically in the cerebellum, hippocampus, and basal nuclei. This syndrome is an unknown syndrome and is presumed to be mainly an opioidinduced toxidrome. Here, we present a case study wherein we show that it can also be caused by an antidepressant overdose.
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Yamaguchi, Katsuyuki, Noboru Goto, and Toshi Yuki Yamamoto. "Development of Human Cerebellar Nuclei." Cells Tissues Organs 136, no. 1 (1989): 61–68. http://dx.doi.org/10.1159/000146799.
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Hintzen, Andreas, and Marc Tittgemeyer. "P29 Cerebellar nuclei fiber anatomy." Basal Ganglia 1, no. 2 (July 2011): 116. http://dx.doi.org/10.1016/j.baga.2011.06.030.
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Noorafshan, Ali, Reza Asadi-Golshan, Mahboobeh Erfanizadeh, and Saied Karbalay-Doust. "Beneficial Effects of Olive Oil on the Rats’ Cerebellum: Functional and Structural Evidence." Folia Medica 60, no. 3 (September 1, 2018): 454–63. http://dx.doi.org/10.2478/folmed-2018-0022.
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Abstract Background: Olive oil is a food additive and used in many biological studies as a solvent for other chemicals, including drugs. Aim: The present study aimed to investigate the effects of olive oil on rats’ cerebellum structure and motor function. Materials and methods: Male rats were randomly divided into two groups orally receiving distilled water and olive oil (1 ml/kg/day). At the end of week 4, motor function was assessed in the rotarod test. The cerebellum was removed for stereo-logical assessment. Data were analyzed using a two-way repeated measures ANOVA for rotarod test and Kruskal-Wallis and Mann-Whitney U test for quantitative histological parameters. Results: Performance of the olive oil-treated rats in fixed and accelerating speed rotarod was better and their riding time (endurance) was greater compared to the control group (p<0.05). However, no significant difference was found between the two groups regarding the total volume of the cerebellar hemisphere, its cortex, and deep cerebellar nuclei. The total number of the Purkinje, Bergman, and Golgi of the granular layer as well as neurons of the deep cerebellar nuclei was 26 - 36% higher in the olive oil-treated rats than in the distilled water treated group (p<0.03). Conclusion: The study findings suggest that olive oil has neuroprotective effects on the cerebellum and induces better performance of the rats in the rotarod.
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Elliott, Robert, and David H. Harter. "Rhombencephalosynapsis associated with autosomal dominant polycystic kidney disease Type 1." Journal of Neurosurgery: Pediatrics 2, no. 6 (December 2008): 435–37. http://dx.doi.org/10.3171/ped.2008.2.12.435.
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Rhombencephalosynapsis (RES) is a rare congenital malformation of the cerebellum characterized by hypogenesis or agenesis of the vermis and fusion of the cerebellar hemispheres with or without fusion of the dentate nuclei and superior cerebellar peduncles. No genetic or chromosomal abnormalities have been identified for RES. Although the occurrence of RES is presumed to be sporadic, no clear pattern of inheritance has been identified. The authors report on a 17-year-old girl with autosomal dominant polycystic kidney disease Type 1 as well as RES.
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Cirillo, Sara, Maria A. Rocca, Angelo Ghezzi, Paola Valsasina, Lucia Moiola, Pierangelo Veggiotti, Maria P. Amato, Giancarlo Comi, Andrea Falini, and Massimo Filippi. "Abnormal cerebellar functional MRI connectivity in patients with paediatric multiple sclerosis." Multiple Sclerosis Journal 22, no. 3 (July 10, 2015): 292–301. http://dx.doi.org/10.1177/1352458515592191.
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Objectives: We investigated resting state functional connectivity (RSFC) of the cerebellar dentate nuclei in paediatric MS patients and its correlations with clinical, neuropsychological and structural MRI measures. Methods: RSFC analysis was performed using a seed-region correlation approach and SPM8 from 48 paediatric MS patients and 27 matched healthy controls. Results: In both groups, dentate nuclei RSFC was significantly correlated with RSFC of several cerebellar and extra-cerebellar brain regions. Compared with healthy controls, paediatric MS patients had reduced RSFC between the right dentate nuclei and the bilateral caudate nuclei and left thalamus as well as increased RSFC between the right dentate nuclei and the left precentral and postcentral gyri. Cognitively impaired patients showed a reduced RSFC between the dentate nuclei and bilateral regions located in the parietal, frontal and temporal lobes. Decreased RSFC was correlated with longer disease duration and higher T2 lesion volumes, whereas increased RSFC correlated with shorter disease duration, lower T2 lesion volume and a better motor performance. Conclusions: Modifications of cerebellar RSFC occur in paediatric MS and are influenced by the duration of the disease and brain focal lesions. Decreased RSFC may reflect early maladaptive plasticity contributing to cognitive impairment.
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Geminiani, Alice, Claudia Casellato, Alberto Antonietti, Egidio D’Angelo, and Alessandra Pedrocchi. "A Multiple-Plasticity Spiking Neural Network Embedded in a Closed-Loop Control System to Model Cerebellar Pathologies." International Journal of Neural Systems 28, no. 05 (April 19, 2018): 1750017. http://dx.doi.org/10.1142/s0129065717500174.
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The cerebellum plays a crucial role in sensorimotor control and cerebellar disorders compromise adaptation and learning of motor responses. However, the link between alterations at network level and cerebellar dysfunction is still unclear. In principle, this understanding would benefit of the development of an artificial system embedding the salient neuronal and plastic properties of the cerebellum and operating in closed-loop. To this aim, we have exploited a realistic spiking computational model of the cerebellum to analyze the network correlates of cerebellar impairment. The model was modified to reproduce three different damages of the cerebellar cortex: (i) a loss of the main output neurons (Purkinje Cells), (ii) a lesion to the main cerebellar afferents (Mossy Fibers), and (iii) a damage to a major mechanism of synaptic plasticity (Long Term Depression). The modified network models were challenged with an Eye-Blink Classical Conditioning test, a standard learning paradigm used to evaluate cerebellar impairment, in which the outcome was compared to reference results obtained in human or animal experiments. In all cases, the model reproduced the partial and delayed conditioning typical of the pathologies, indicating that an intact cerebellar cortex functionality is required to accelerate learning by transferring acquired information to the cerebellar nuclei. Interestingly, depending on the type of lesion, the redistribution of synaptic plasticity and response timing varied greatly generating specific adaptation patterns. Thus, not only the present work extends the generalization capabilities of the cerebellar spiking model to pathological cases, but also predicts how changes at the neuronal level are distributed across the network, making it usable to infer cerebellar circuit alterations occurring in cerebellar pathologies.
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Mirino, Pierandrea, Anna Pecchinenda, Maddalena Boccia, Adriano Capirchio, Fabrizia D’Antonio, and Cecilia Guariglia. "Cerebellum-Cortical Interaction in Spatial Navigation and Its Alteration in Dementias." Brain Sciences 12, no. 5 (April 20, 2022): 523. http://dx.doi.org/10.3390/brainsci12050523.
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The cerebellum has a homogeneous structure and performs different computational functions such as modulation/coordination of the communication between cerebral regions, and regulation/integration of sensory information. Albeit cerebellar activity is generally associated with motor functions, several recent studies link it to various cognitive functions, including spatial navigation. In addition, cerebellar activity plays a modulatory role in different cognitive domains and brain processes. Depending on the network involved, cerebellar damage results in specific functional alterations, even when no function loss might be detected. In the present review, we discuss evidence of brainstem degeneration and of a substantial reduction of neurons in nuclei connected to the inferior olivary nucleus in the early stages of Alzheimer’s disease. Based on the rich patterns of afferences from the inferior olive nucleus to the cerebellum, we argue that the subtle alterations in spatial navigation described in the early stages of dementia stem from alterations of the neuromodulatory functions of the cerebellum.
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Kalmbach, Brian E., Tobin Davis, Tatsuya Ohyama, Frank Riusech, William L. Nores, and Michael D. Mauk. "Cerebellar Cortex Contributions to the Expression and Timing of Conditioned Eyelid Responses." Journal of Neurophysiology 103, no. 4 (April 2010): 2039–49. http://dx.doi.org/10.1152/jn.00033.2010.
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We used micro-infusions during eyelid conditioning in rabbits to investigate the relative contributions of cerebellar cortex and the underlying deep nuclei (DCN) to the expression of cerebellar learning. These tests were conducted using two forms of cerebellum-dependent eyelid conditioning for which the relative roles of cerebellar cortex and DCN are controversial: delay conditioning, which is largely unaffected by forebrain lesions, and trace conditioning, which involves interactions between forebrain and cerebellum. For rabbits trained with delay conditioning, silencing cerebellar cortex by micro-infusions of the local anesthetic lidocaine unmasked stereotyped short-latency responses. This was also the case after extinction as observed previously with reversible blockade of cerebellar cortex output. Conversely, increasing cerebellar cortex activity by micro-infusions of the GABAA antagonist picrotoxin reversibly abolished conditioned responses. Effective cannula placements were clustered around the primary fissure and deeper in lobules hemispheric lobule IV (HIV) and hemispheric lobule V (HV) of anterior lobe. In well-trained trace conditioned rabbits, silencing this same area of cerebellar cortex or reversibly blocking cerebellar cortex output also unmasked short-latency responses. Because Purkinje cells are the sole output of cerebellar cortex, these results provide evidence that the expression of well-timed conditioned responses requires a well-timed decrease in the activity of Purkinje cells in anterior lobe. The parallels between results from delay and trace conditioning suggest similar contributions of plasticity in cerebellar cortex and DCN in both instances.
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Wang, Jian-Jun, Yury Shimansky, Vlastislav Bracha, and James R. Bloedel. "Effects of Cerebellar Nuclear Inactivation on the Learning of a Complex Forelimb Movement in Cats." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2447–59. http://dx.doi.org/10.1152/jn.1998.79.5.2447.
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Wang, Jian-Jun, Yury Shimansky, Vlastislav Bracha, andJames R. Bloedel. Effects of cerebellar nuclear inactivation on thelearning of a complex forelimb movement in cats. J. Neurophysiol. 79: 2447–2459, 1998. The purpose of this study was to determine the effects of inactivating concurrently the cerebellar interposed and dentate nuclei on the capacity of cats to acquire and retain a complex, goal-directed forelimb movement. To assess the effects on acquisition, cats were required to learn to move a vertical manipulandum bar through a two-segment template with a shape approximating an inverted “L” after the injection of muscimol (saline for the control group) in the interposed and dentate cerebellar nuclei. During training periods, they were exposed progressively to more difficult templates, which were created by decreasing the angle between the two segments of the template. After determining the most difficult template the injected animals could learn within the specified time and performance constraints, the retraining phase of the experiment was initiated in which the cats were required to execute the same sequence of templates in the absence of any injection. This stage of the experiment assessed retention and determined the extent of any relearning required to execute the task at criterion levels. Next, the animals were overtrained without any injection on the most difficult template they could perform. Finally, to determine the effects of nuclear inactivation on retention after extensive retraining, their capacity to perform the same template was determined after muscimol injection in the interposed and dentate nuclei. The findings show that during the inactivation of the dentate and interposed nuclei the animals could learn to execute the more difficult templates. However, when required to execute the most difficult template learned under muscimol on the day after injections were discontinued, the cats had to “relearn” (reacquire) the movement. Finally, when the cerebellar nuclei were inactivated after the animals learned the task in the absence of any injections during the retraining phase, retention was not blocked. The data indicate that the intermediate and lateral cerebellum are not required either for learning this type of complex voluntary movement or for retaining the capacity to perform the task once it is learned. Nevertheless, when the cerebellum becomes available for executing a task learned in the absence of this structure, reacquisition of the behavior usually is necessary. It is hypothesized that the relearning observed after acquisition during muscimol inactivation reflects the tendency of the system to incorporate the cerebellum into the interactions responsible for the learning and performance of a motor sequence that is optimal for executing the task.
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Gorassini, M., A. Prochazka, and J. L. Taylor. "Cerebellar ataxia and muscle spindle sensitivity." Journal of Neurophysiology 70, no. 5 (November 1, 1993): 1853–62. http://dx.doi.org/10.1152/jn.1993.70.5.1853.
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1. The cerebellum has long been known to participate in movement control. One of the enduring theories of cerebellar function is that it "tunes" and coordinates sensorimotor traffic in other parts of the CNS. In particular, it has been implicated in the control of the sensitivity of muscle spindle stretch receptors through the fusimotor system. 2. The stretch sensitivity of spindle primary endings can be varied approximately over a 10-fold range by fusimotor efferent action. For many years it has been believed that cerebellar dysfunction is associated with reduced drive to the fusimotor system and that this in turn causes hypotonia by reducing the reflex excitation of alpha-motoneurons by spindle afferents. 3. The data on which this hypothesis is based were obtained in anesthetized or decerebrate animals. Little direct information is available on animals or humans performing voluntary movements and exhibiting ataxia or other cerebellar symptoms. 4. We tested the hypothesis by recording from nine muscle spindle afferents in behaving cats before and during reversible inactivation of cerebellar interpositus and dentate nuclei. In normal cats fusimotor action varies with motor task, greatly altering spindle stretch sensitivity. We investigated whether this same range of task-related sensitivity manifested itself during ataxia. 5. We found that the full range of spindle sensitivity was still present during ataxia. We therefore conclude that the cerebellar nuclei studied are not primarily responsible for fusimotor control, nor is the ataxia primarily caused by disordered proprioceptive sensitivity.
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Cury, Rubens Gisbert, Carina França, Egberto Reis Barbosa, Manoel Jacobsen Teixeira, and Daniel Ciampi de Andrade. "Little Brain, Big Expectations." Brain Sciences 10, no. 12 (December 7, 2020): 944. http://dx.doi.org/10.3390/brainsci10120944.
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The cerebellum has been implicated in the mechanisms of several movement disorders. With the recent reports of successful modulation of its functioning, this highly connected structure has emerged as a promising way to provide symptomatic relief not yet obtained by usual treatments. Here we review the most relevant papers published to date, the limitations and gaps in literature, discuss why several papers have failed in showing efficacy, and present a new way of stimulating the cerebellum. References for this critique review were identified by searches on PubMed for the terms “Parkinson’s disease”, “ataxia”, “dystonia”, “tremor”, and “dyskinesias” in combination with the type of stimulation and the stimulation site. Studies conducted thus far have shed light on the potential of cerebellar neuromodulation for attenuating symptoms in patients with some forms of isolated and combined dystonia, dyskinesia in Parkinson’s disease, and neurodegenerative ataxia. However, there is still a high heterogeneity of results and uncertainty about the possibility of maintaining long-term benefits. Because of the complicated architecture of the cerebellum, the modulation techniques employed may have to focus on targeting the activity of the cerebellar nuclei rather than the cerebellar cortex. Measures of cerebellar activity may reduce the variability in outcomes.
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Thier, Peter, and Akshay Markanday. "Role of the Vermal Cerebellum in Visually Guided Eye Movements and Visual Motion Perception." Annual Review of Vision Science 5, no. 1 (September 15, 2019): 247–68. http://dx.doi.org/10.1146/annurev-vision-091718-015000.
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The cerebellar cortex is a crystal-like structure consisting of an almost endless repetition of a canonical microcircuit that applies the same computational principle to different inputs. The output of this transformation is broadcasted to extracerebellar structures by way of the deep cerebellar nuclei. Visually guided eye movements are accommodated by different parts of the cerebellum. This review primarily discusses the role of the oculomotor part of the vermal cerebellum [the oculomotor vermis (OMV)] in the control of visually guided saccades and smooth-pursuit eye movements. Both types of eye movements require the mapping of retinal information onto motor vectors, a transformation that is optimized by the OMV, considering information on past performance. Unlike the role of the OMV in the guidance of eye movements, the contribution of the adjoining vermal cortex to visual motion perception is nonmotor and involves a cerebellar influence on information processing in the cerebral cortex.
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Antonietti, Alberto, Jessica Monaco, Egidio D'Angelo, Alessandra Pedrocchi, and Claudia Casellato. "Dynamic Redistribution of Plasticity in a Cerebellar Spiking Neural Network Reproducing an Associative Learning Task Perturbed by TMS." International Journal of Neural Systems 28, no. 09 (September 26, 2018): 1850020. http://dx.doi.org/10.1142/s012906571850020x.
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During natural learning, synaptic plasticity is thought to evolve dynamically and redistribute within and among subcircuits. This process should emerge in plastic neural networks evolving under behavioral feedback and should involve changes distributed across multiple synaptic sites. In eyeblink classical conditioning (EBCC), the cerebellum learns to predict the precise timing between two stimuli, hence EBCC represents an elementary yet meaningful paradigm to investigate the cerebellar network functioning. We have simulated EBCC mechanisms by reconstructing a realistic cerebellar microcircuit model and embedding multiple plasticity rules imitating those revealed experimentally. The model was tuned to fit experimental EBCC human data, estimating the underlying learning time-constants. Learning started rapidly with plastic changes in the cerebellar cortex followed by slower changes in the deep cerebellar nuclei. This process was characterized by differential development of long-term potentiation and depression at individual synapses, with a progressive accumulation of plasticity distributed over the whole network. The experimental data included two EBCC sessions interleaved by a trans-cranial magnetic stimulation (TMS). The experimental and the model response data were not significantly different in each learning phase, and the model goodness-of-fit was [Formula: see text] for all the experimental conditions. The models fitted on TMS data revealed a slowed down re-acquisition (sessions-2) compared to the control condition ([Formula: see text]). The plasticity parameters characterizing each model significantly differ among conditions, and thus mechanistically explain these response changes. Importantly, the model was able to capture the alteration in EBCC consolidation caused by TMS and showed that TMS affected plasticity at cortical synapses thereby altering the fast learning phase. This, secondarily, also affected plasticity in deep cerebellar nuclei altering learning dynamics in the entire sensory-motor loop. This observation reveals dynamic redistribution of changes over the entire network and suggests how TMS affects local circuit computation and memory processing in the cerebellum.
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Hotton, Jenna. "Neuroplasticity and Post-Synaptic Rebound-Induced Spiking at Purkinje Cell-Deep Cerebellar Nuclei Synapses." McGill Science Undergraduate Research Journal 9, no. 1 (April 30, 2014): 50–55. http://dx.doi.org/10.26443/msurj.v9i1.160.
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Background: Within the cerebellum white matter are located four pairs of nuclei, collectively known as the deep cerebellar nuclei (DCN) (1). In the cerebellum, signal integration from pre-cerebellar structures via excitatory parallel fibers and climbing fibers in the cerebellar cortex occurs in GABAergic Purkinje cells (PC) (2). The main target of these PC cells is the DCN (2) and approximately 85% of GABAergic input on the DCN is from PCs (3). Furthermore, PCs outnumber DCN neurons (26:1) (2). Therefore, despite receiving substantial inhibition from Purkinje cells, DCN neurons are still active at rest showing regular spiking or spontaneous bursts (4). DCN neurons fire spontaneously at approximately 10-50 Hz (5). Given this unique anatomy of PC-DCN synapses, characterization of this synaptic circuit is important in understanding the overall role of the DCN in the brain.
Methods: The findings of 28 studies, including a few reviews, are reported in this paper. Studies selected focused principally on characterization of DCN circuitry properties and the role these properties have in the functioning of the DCN. Most studies employed in vivo and/or in vitro cellular recordings in rodents, among other models. Studies ranged from 1984 to 2013.
Summary: This review outlines current findings on the forms of plasticity found in the DCN, the function of the DCN and the connections between the DCN and other brain regions. In short, neurons in the DCN demonstrate both synaptic and non-synaptic plasticity. Cerebellar involvement in motor activity has been extensively studied therefore, not surprisingly; DCN neurons form connections with the motor cortex but also the prefrontal cortex. PC input on the DCN influences spike rate and timing through fluctuations in PC synchrony, and rebound depolarization.
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Zhou, Joy, Meike E. Van der Heijden, Luis E. Salazar Leon, Tao Lin, Lauren N. Miterko, Dominic J. Kizek, Ross M. Perez, Matea Pavešković, Amanda M. Brown, and Roy V. Sillitoe. "Propranolol Modulates Cerebellar Circuit Activity and Reduces Tremor." Cells 11, no. 23 (December 1, 2022): 3889. http://dx.doi.org/10.3390/cells11233889.
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Tremor is the most common movement disorder. Several drugs reduce tremor severity, but no cures are available. Propranolol, a β-adrenergic receptor blocker, is the leading treatment for tremor. However, the in vivo circuit mechanisms by which propranolol decreases tremor remain unclear. Here, we test whether propranolol modulates activity in the cerebellum, a key node in the tremor network. We investigated the effects of propranolol in healthy control mice and Car8wdl/wdl mice, which exhibit pathophysiological tremor and ataxia due to cerebellar dysfunction. Propranolol reduced physiological tremor in control mice and reduced pathophysiological tremor in Car8wdl/wdl mice to control levels. Open field and footprinting assays showed that propranolol did not correct ataxia in Car8wdl/wdl mice. In vivo recordings in awake mice revealed that propranolol modulates the spiking activity of control and Car8wdl/wdl Purkinje cells. Recordings in cerebellar nuclei neurons, the targets of Purkinje cells, also revealed altered activity in propranolol-treated control and Car8wdl/wdl mice. Next, we tested whether propranolol reduces tremor through β1 and β2 adrenergic receptors. Propranolol did not change tremor amplitude or cerebellar nuclei activity in β1 and β2 null mice or Car8wdl/wdl mice lacking β1 and β2 receptor function. These data show that propranolol can modulate cerebellar circuit activity through β-adrenergic receptors and may contribute to tremor therapeutics.
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Anchisi, Davide, Bibiana Scelfo, and Filippo Tempia. "Postsynaptic Currents in Deep Cerebellar Nuclei." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 323–31. http://dx.doi.org/10.1152/jn.2001.85.1.323.
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Postsynaptic currents were studied by whole cell recordings in visually identified large neurons of the deep cerebellar nuclei (DCN) in slices of 4- to 11-day-old mice. Spontaneous postsynaptic currents were abolished by the GABAA receptor antagonist bicuculline and had a single-exponential decay with a mean time constant of 13.6 ± 3.2 (SD) ms. Excitatory postsynaptic currents (EPSCs) were evoked in 48/56 neurons recorded. The addition of AMPA and N-methyl-d-aspartate (NMDA) receptor antagonists together completely abolished all synaptic responses. In 1 mM [Mg2+]o and at a holding potential of −60 mV, the peak amplitude of the NMDA component of the EPSC (NMDA-EPSC) was 83.2 ± 21.2% of the AMPA component (AMPA-EPSC). This indicates that in DCN neurons, at a physiological [Mg2+]o and at the resting membrane potential, NMDA receptors contribute to the synaptic signal. AMPA-EPSCs had a linear current-voltage relationship with a reversal potential of +2.3 ± 0.4 mV and a single-exponential decay with a voltage-dependent time constant that at −60 mV was 7.1 ± 3.3 ms. In 10 μM glycine and 1 mM [Mg2+]o, the I-V relationship of NMDA-EPSCs had a reversal potential of −0.5 ± 3.3 mV and a maximal inward current at −33.4 ± 5.8 mV. The apparent dissociation constant ( K D) of Mg2+ for the NMDA receptor-channel at −60 mV, measured by varying [Mg2+]o, was 135.5 ± 55.3 μM, and when measured by fitting the I-V curves with a theoretical function, it was 169.9 ± 119.5 μM. Thus in the DCN, NMDA receptors have a sensitivity to Mg2+ that corresponds to subunits that are weakly blocked by this ion (ε3 and ε4) of which the DCN express ε4. NMDA-EPSCs had a double-exponential decay with voltage-dependent time constants that at −60 mV were 20.2 ± 8.9 and 136.4 ± 62.8 ms. At positive voltages, the time constants were slower and their contributions were about equal, while in the negative slope conductance region of the I-V curve, the faster time constant became predominant, conferring faster kinetics to the EPSC. The weak sensitivity to Mg2+ of NMDA receptors, together with a relatively fast kinetics, provide DCN neurons with strong excitatory inputs in which fast dynamic signals are relatively well preserved.
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Witter, Laurens, Chris I. De Zeeuw, Tom J. H. Ruigrok, and Freek E. Hoebeek. "The Cerebellar Nuclei Take Center Stage." Cerebellum 10, no. 4 (January 29, 2011): 633–36. http://dx.doi.org/10.1007/s12311-010-0245-y.
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Gornati, Simona V., Carmen B. Schäfer, Oscar H. J. Eelkman Rooda, Alex L. Nigg, Chris I. De Zeeuw, and Freek E. Hoebeek. "Differentiating Cerebellar Impact on Thalamic Nuclei." Cell Reports 23, no. 9 (May 2018): 2690–704. http://dx.doi.org/10.1016/j.celrep.2018.04.098.
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Cohen, Dana. "The cerebellar nuclei take center stage." Current Opinion in Behavioral Sciences 57 (June 2024): 101362. http://dx.doi.org/10.1016/j.cobeha.2024.101362.
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Kakei, Shinji, Takahiro Ishikawa, Jongho Lee, Takeru Honda, and Donna S. Hoffman. "Physiological and Morphological Principles Underpinning Recruitment of the Cerebellar Reserve." CNS & Neurological Disorders - Drug Targets 17, no. 3 (June 19, 2018): 184–92. http://dx.doi.org/10.2174/1871527317666180315164429.
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Background: In order to optimize outcomes of novel therapies for cerebellar ataxias (CAs), it is desirable to start these therapies while declined functions are restorable: i.e. while the so-called cerebellar reserve remains. Objective: In this mini-review, we tried to define and discuss the cerebellar reserve from physiological and morphological points of view. Method: The cerebellar neuron circuitry is designed to generate spatiotemporally organized outputs, regardless of the region. Therefore, the cerebellar reserve may be defined as a mechanism to restore its proper input-output organization of the cerebellar neuron circuitry, when it is damaged. Then, the following four components are essential for recruitment of the cerebellar reserve: operational local neuron circuitry; proper combination of mossy fiber inputs to be integrated; climbing fiber inputs to instruct favorable reorganization of the integration; deep cerebellar nuclei to generate reorganized outputs. Results: We discussed three topics related to these resources, 1) principles of generating organized cerebellar outputs, 2) redundant mossy fiber inputs to the cerebellum, 3) plasticity of the cerebellar neuron circuitry. Conclusion: To make most of the cerebellar reserve, it is desirable to start any intervention as early as possible when the cerebellar cell loss is minimal or even negligible. Therefore, an ideal future therapy for degenerative cerebellar diseases should start before consuming the cerebellar reserve at all. In the meantime, our real challenge is to establish a reliable method to identify the decrease in the cerebellar reserve as early as possible.
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IWANIUK, ANDREW N., JANELLE M. P. PAKAN, CRISTIÁN GUTIÉRREZ-IBÁÑEZ, and DOUGLAS R. WYLIE. "Expression of calcium-binding proteins in cerebellar- and inferior olivary-projecting neurons in the nucleus lentiformis mesencephali of pigeons." Visual Neuroscience 26, no. 3 (May 2009): 341–47. http://dx.doi.org/10.1017/s0952523809090087.
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AbstractIn the avian brain, the optokinetic response is controlled by two retinal-recipient nuclei: the nucleus of the basal optic root (nBOR) of the accessory optic system and the pretectal nucleus lentiformis mesencephali (LM). Although considered sister nuclei because of their similar response properties and function, there are both similarities and differences with respect to efferent projections and neurochemistry. Both nBOR and LM project to the cerebellum (Cb) directly as mossy fibers but also indirectly via the inferior olive (IO). In a previous report, we showed that the cerebellar- and inferior olivary-projecting neurons in nBOR of pigeons differentially express the calcium-binding proteins calretinin (CR) and parvalbumin (PV). Both CR and PV are expressed in the somata of LM neurons, although the latter is not as prevalent, and whether expression of CR and PV reflects cerebellar and IO projections is not known. In this report, by combining retrograde neuronal tracing from the Cb and IO with fluorescent immunohistochemistry, we examined the expression of these calcium-binding proteins in the pigeon LM. Half (52%) of the cerebellar-projecting neurons were CR+ve, but only 15% were PV+ve. Almost all (>95%) these PV+ve cells also expressed CR. In contrast, few of the IO-projecting neurons expressed CR or PV (≤5%). This is strikingly similar to what we observed in nBOR and reveals that calcium-binding protein expression is concordant with projection patterns in two nuclei that share similar functions.
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Salmi, Juha, Karen Johanne Pallesen, Tuomas Neuvonen, Elvira Brattico, Antti Korvenoja, Oili Salonen, and Synnöve Carlson. "Cognitive and Motor Loops of the Human Cerebro-cerebellar System." Journal of Cognitive Neuroscience 22, no. 11 (November 2010): 2663–76. http://dx.doi.org/10.1162/jocn.2009.21382.
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We applied fMRI and diffusion-weighted MRI to study the segregation of cognitive and motor functions in the human cerebro-cerebellar system. Our fMRI results show that a load increase in a nonverbal auditory working memory task is associated with enhanced brain activity in the parietal, dorsal premotor, and lateral prefrontal cortices and in lobules VII–VIII of the posterior cerebellum, whereas a sensory-motor control task activated the motor/somatosensory, medial prefrontal, and posterior cingulate cortices and lobules V/VI of the anterior cerebellum. The load-dependent activity in the crus I/II had a specific relationship with cognitive performance: This activity correlated negatively with load-dependent increase in RTs. This correlation between brain activity and RTs was not observed in the sensory-motor task in the activated cerebellar regions. Furthermore, probabilistic tractography analysis of the diffusion-weighted MRI data suggests that the tracts between the cerebral and the cerebellar areas exhibiting cognitive load-dependent and sensory-motor activity are mainly projected via separated pontine (feed-forward tracts) and thalamic (feedback tracts) nuclei. The tractography results also indicate that the crus I/II in the posterior cerebellum is linked with the lateral prefrontal areas activated by cognitive load increase, whereas the anterior cerebellar lobe is not. The current results support the view that cognitive and motor functions are segregated in the cerebellum. On the basis of these results and theories of the function of the cerebellum, we suggest that the posterior cerebellar activity during a demanding cognitive task is involved with optimization of the response speed.
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Plumel, Marine, Stéphanie Dumont, Pauline Maes, Cristina Sandu, Marie-Paule Felder-Schmittbuhl, Etienne Challet, and Fabrice Bertile. "Circadian Analysis of the Mouse Cerebellum Proteome." International Journal of Molecular Sciences 20, no. 8 (April 15, 2019): 1852. http://dx.doi.org/10.3390/ijms20081852.
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The cerebellum contains a circadian clock, generating internal temporal signals. The daily oscillations of cerebellar proteins were investigated in mice using a large-scale two-dimensional difference in gel electrophoresis (2D-DIGE). Analysis of 2D-DIGE gels highlighted the rhythmic variation in the intensity of 27/588 protein spots (5%) over 24 h based on cosinor regression. Notably, the rhythmic expression of most abundant cerebellar proteins was clustered in two main phases (i.e., midday and midnight), leading to bimodal distribution. Only six proteins identified here to be rhythmic in the cerebellum are also known to oscillate in the suprachiasmatic nuclei, including two proteins involved in the synapse activity (Synapsin 2 [SYN2] and vesicle-fusing ATPase [NSF]), two others participating in carbohydrate metabolism (triosephosphate isomerase (TPI1] and alpha-enolase [ENO1]), Glutamine synthetase (GLUL), as well as Tubulin alpha (TUBA4A). Most oscillating cerebellar proteins were not previously identified in circadian proteomic analyses of any tissue. Strikingly, the daily accumulation of mitochondrial proteins was clustered to the mid-resting phase, as previously observed for distinct mitochondrial proteins in the liver. Moreover, a number of rhythmic proteins, such as SYN2, NSF and TPI1, were associated with non-rhythmic mRNAs, indicating widespread post-transcriptional control in cerebellar oscillations. Thus, this study highlights extensive rhythmic aspects of the cerebellar proteome.
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Kurtaj, Lavdim, Vjosa Shatri, and Ilir Limani. "Cerebellar Model Controller with new Model of Granule Cell-golgi Cell Building Blocks and Two-phase Learning Acquires Multitude of Generalization Capabilities in Controlling Robot Joint without Exponential Growth in Complexity." International Journal of Electrical and Computer Engineering (IJECE) 8, no. 6 (December 1, 2018): 4292. http://dx.doi.org/10.11591/ijece.v8i6.pp4292-4309.
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Processing in the cerebellum is roughly described as feed forward processing of incoming information over three layers of the cerebellar cortex that send intermediate output to deep cerebellar nuclei, the only output from the cerebellum. Beside this main picture there are several feedback routes, mainly not included in models. In this paper we use new model for neuronal circuit of the cerebellar granule cell layer, as collection of idealized granule cell–golgi cell building blocks with capability of generating multi-dimensional receptive fields modulated by separate input coming to lower dendrite tree of Golgi cell. Resulting cerebellar model controller with two-phase learning will acquire multitude of generalization capabilities when used as robot joint controller. This will usually require more than one Purkinje cell per output. Functionality of granule cell-Golgi cell building block was evaluated with simulations using Simulink single compartment spiking neuronal model. Trained averaging cerebellar model controller attains very good tracking results for wide range of unlearned slower and faster trajectories, with additional improvements by relearning at faster trajectories. Inclusion of new dynamical effects to the controller results with linear growth in complexity for inputs targeting lower dendrite tree of Golgi cell, important for control applications in robotics, but not only.
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Fox, J., R. Duncan, P. Friday, B. Klein, and W. Scarratt. "Cerebello-Olivary and Lateral (Accessory) Cuneate Degeneration in a Juvenile American Miniature Horse." Veterinary Pathology 37, no. 3 (May 2000): 271–74. http://dx.doi.org/10.1354/vp.37-3-271.
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A 12-month-old American Miniature horse colt was presented to the Virginia Tech Veterinary Teaching Hospital with a 7-month history of progressive ataxia. Physical examination revealed a head intention tremor, base-wide stance, and ataxia. Necropsy findings were confined to the brain. There were bilateral areas of liquefactive necrosis and cavitation corresponding to the dorsal accessory olivary and lateral (accessory) cuneate nuclei. Cerebellar folia of the dorsal vermis were thin. Microscopically, the cerebellar cortex was characterized by patchy areas of Purkinje cell loss with associated variable thinning of the molecular and granule cell layers and astrogliosis. Dorsal accessory olivary and lateral cuneate nuclei were cavitated and had mild glial response around their periphery. Additionally, a focus of necrosis and neuropil vacuolization was found in the right putamen. These findings indicate the presence of a neurodegenerative disorder centered, but not confined to, the cerebellum and its connections in this American Miniature horse colt.
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Lu, Xiaofeng, Okihide Hikosaka, and Shigehiro Miyachi. "Role of Monkey Cerebellar Nuclei in Skill for Sequential Movement." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2245–54. http://dx.doi.org/10.1152/jn.1998.79.5.2245.
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Lu, Xiaofeng, Okihide Hikosaka, and Shigehiro Miyachi. Role of monkey cerebellar nuclei in skill for sequential movement. J. Neurophysiol. 79: 2245–2254, 1998. To examine whether the cerebellum is involved in learning and memory of visuomotor sequences, we trained two monkeys on a sequential button press task and inactivated different portions of the cerebellar nuclei by injecting a small amount of muscimol (γ-aminobutyric acid agonist). Before the injection experiments started, the monkeys had learned a set of sequences ( n = 21 and 12) extensively. After each injection, we had the monkeys perform the learned sequences and, in addition, learn new sequences. We found deficits in learning/memory by the injections into the dorsal and central part of the dentate nucleus. The number of errors increased significantly for the learned sequences but not for the new sequences. This effect was present only when the hand ipsilateral to the muscimol injection was used. Consistent with this result, anticipatory saccades, the occurrence of which is correlated closely with motor skill, also became less frequent particularly when the ipsilateral hand was used. No effect on learning/memory was observed after injections into the ventral or lateral parts of the dentate nucleus, interpositus nucleus, or fastigial nucleus. In contrast, hand movements became slower after ipsilateral injections at all of the injection sites. These results suggest that, among the cerebellar nuclei, the dentate nucleus, especially its dorsal and central regions, is related to the storage and/or retrieval of long-term memory for motor skill.
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Schreurs, Bernard G., Deidre E. O’Dell, and Desheng Wang. "The Role of Cerebellar Intrinsic Neuronal Excitability, Synaptic Plasticity, and Perineuronal Nets in Eyeblink Conditioning." Biology 13, no. 3 (March 21, 2024): 200. http://dx.doi.org/10.3390/biology13030200.
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Evidence is strong that, in addition to fine motor control, there is an important role for the cerebellum in cognition and emotion. The deep nuclei of the mammalian cerebellum also contain the highest density of perineural nets—mesh-like structures that surround neurons—in the brain, and it appears there may be a connection between these nets and cognitive processes, particularly learning and memory. Here, we review how the cerebellum is involved in eyeblink conditioning—a particularly well-understood form of learning and memory—and focus on the role of perineuronal nets in intrinsic membrane excitability and synaptic plasticity that underlie eyeblink conditioning. We explore the development and role of perineuronal nets and the in vivo and in vitro evidence that manipulations of the perineuronal net in the deep cerebellar nuclei affect eyeblink conditioning. Together, these findings provide evidence of an important role for perineuronal net in learning and memory.
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Pundt, L. L., E. A. Jörn, J. A. Conrad, and W. C. Low. "Organization and Histochemical Phenotype of Human Fetal Cerebellar Cells following Transplantation into the Cerebellum of Nude Mice." Cell Transplantation 6, no. 5 (September 1997): 479–89. http://dx.doi.org/10.1177/096368979700600507.
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Previous rodent studies have demonstrated the capacity of cerebellar transplants to organize into trilaminar cell layers typically observed in the normal cerebellum. In Purkinje Cell (PC)-deficient animals, PCs will migrate into the host and form synaptic connections. Recently, fetal cerebellar grafts transplanted into the Purkinje cell degeneration (pcd) mutant mouse were shown to result in an improvement of motor behaviors. These studies indicate the potential therapeutic use of neural transplantation in patients with cerebellar degeneration. In the present study, human fetal cerebellar tissue (8.5 wk postconception) was dissociated and transplanted into the normal cerebellum of nude mice. Six months following transplantation, histological analysis revealed donor cells in recipient mice. Immunostaining for the 28 kDa calcium-binding protein (calbindin) revealed the presence of donor PCs that were organized in discrete cellular layers within the transplant neuropil. In most cases the dendritic processes were oriented in a planar fashion perpendicular to the transplant cell layer. Human neurofilament immunostaining revealed bundles of donor fibers within the core of the transplant and/or at the periphery. These bundles were found to be calbindin positive (PC fibers). Three animals provided evidence of donor PC axon growth ventrally into host white matter, and in one case, this ventral migration reached the deep cerebellar nuclei. Most notable was the development of a pronounced folia-like organization by the implanted cell suspensions. Glial processes within the grafts were aligned perpendicular to the long axis of the transplant folia. These results demonstrate the capacity of human fetal cerebellar cell suspension to reorganize into cell layers typical of the normal cerebellum following transplantation into the rodent cerebellum, and develop an organotypic folia-like organization.
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Joaquim, Andrei Fernandes. "Severe Cerebellar Degeneration and Chiari I Malformation - Speculative pathophysiology based on a systematic review." Revista da Associação Médica Brasileira 66, no. 3 (March 2020): 375–79. http://dx.doi.org/10.1590/1806-9282.66.3.375.
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SUMMARY BACKGROUND Symptomatic Chiari Type I Malformation (CM) is treated with posterior fossa decompression with or without duroplasty. We have noticed some cases with concomitant severe cerebellar ataxia due to cerebellar atrophy. The aim of this study is to review the literature of CM associated with severe cerebellar atrophy and discuss its potential physiopathology. METHODS A systematic literature review in the Pubmed Database was performed using the following key-terms: “cerebellar atrophy Chiari”, and “cerebellar degeneration Chiari”. Articles reporting the presence of cerebellar degeneration/atrophy associated with CM were included. RESULTS We found only six studies directly discussing the association of cerebellar atrophy with CM, with a total of seven cases. We added one case of our own practice for additional discussion. Only speculative causes were described to justify cerebellar atrophy. The potential causes of cerebellar atrophy were diffuse cerebellar ischemia from chronic compression of small vessels (the most mentioned speculative cause), chronic raised intracranial pressure due to CSF block, chronic venous hypertension, and association with platybasia with ventral compression of the brainstem resulting in injury of the inferior olivary nuclei leading to mutual trophic effects in the cerebellum. Additionally, it is not impossible to rule out a degenerative cause for cerebellar atrophy without a causative reason. CONCLUSIONS Severe cerebellar atrophy is found in some patients with CM. Although chronic ischemia due to compression is the most presumed cause, other etiologies were proposed. The real reasons for cerebellar degeneration are not known. Further studies are necessary.
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Walia, Pushpinder, Abhishek Ghosh, Shubhmohan Singh, and Anirban Dutta. "Portable Neuroimaging-Guided Noninvasive Brain Stimulation of the Cortico-Cerebello-Thalamo-Cortical Loop—Hypothesis and Theory in Cannabis Use Disorder." Brain Sciences 12, no. 4 (March 26, 2022): 445. http://dx.doi.org/10.3390/brainsci12040445.
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Background: Maladaptive neuroplasticity-related learned response in substance use disorder (SUD) can be ameliorated using noninvasive brain stimulation (NIBS); however, inter-individual variability needs to be addressed for clinical translation. Objective: Our first objective was to develop a hypothesis for NIBS for learned response in SUD based on a competing neurobehavioral decision systems model. The next objective was to develop the theory by conducting a computational simulation of NIBS of the cortico-cerebello-thalamo-cortical (CCTC) loop in cannabis use disorder (CUD)-related dysfunctional “cue-reactivity”—a construct closely related to “craving”—that is a core symptom. Our third objective was to test the feasibility of a neuroimaging-guided rational NIBS approach in healthy humans. Methods: “Cue-reactivity” can be measured using behavioral paradigms and portable neuroimaging, including functional near-infrared spectroscopy (fNIRS) and electroencephalogram (EEG) metrics of sensorimotor gating. Therefore, we conducted a computational simulation of NIBS, including transcranial direct current stimulation (tDCS) and transcranial alternating current stimulation (tACS) of the cerebellar cortex and deep cerebellar nuclei (DCN) of the CCTC loop for its postulated effects on fNIRS and EEG metrics. We also developed a rational neuroimaging-guided NIBS approach for the cerebellar lobule (VII) and prefrontal cortex based on a healthy human study. Results: Simulation of cerebellar tDCS induced gamma oscillations in the cerebral cortex, while transcranial temporal interference stimulation induced a gamma-to-beta frequency shift. A preliminary healthy human study (N = 10) found that 2 mA cerebellar tDCS evoked similar oxyhemoglobin (HbO) response in the range of 5 × 10−6 M across the cerebellum and PFC brain regions (α = 0.01); however, infra-slow (0.01–0.10 Hz) prefrontal cortex HbO-driven phase–amplitude-coupled (PAC; 4 Hz, ±2 mA (max)) cerebellar tACS evoked HbO levels in the range of 10−7 M that were statistically different (α = 0.01) across these brain regions. Conclusion: Our healthy human study showed the feasibility of fNIRS of cerebellum and PFC and closed-loop fNIRS-driven ctACS at 4 Hz, which may facilitate cerebellar cognitive function via the frontoparietal network. Future work needs to combine fNIRS with EEG for multi-modal imaging for closed-loop NIBS during operant conditioning.
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Pastor, M. A., C. Vidaurre, M. A. Fernández-Seara, A. Villanueva, and K. J. Friston. "Frequency-Specific Coupling in the Cortico-Cerebellar Auditory System." Journal of Neurophysiology 100, no. 4 (October 2008): 1699–705. http://dx.doi.org/10.1152/jn.01156.2007.
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Induced oscillatory activity in the auditory cortex peaks at around 40 Hz in humans. Using regional cerebral blood flow and positron emission tomography we previously confirmed frequency-selective cortical responses to 40-Hz tones in auditory primary cortices and concomitant bilateral activation of the cerebellar hemispheres. In this study, using functional magnetic resonance imaging (fMRI) we estimated the influence of 40-Hz auditory stimulation on the coupling between auditory cortex and superior temporal sulcus (STS) and Crus II, using a dynamic causal model of the interactions between medial geniculate nuclei, auditory superior temporal gyrus (STG)/STS, and the cerebellar Crus II auditory region. Specifically, we tested the hypothesis that 40-Hz-selective responses in the cerebellar Crus II auditory region could be explained by frequency-specific enabling of interactions in the auditory cortico–cerebellar–thalamic loop. Our model comparison results suggest that input from auditory STG/STS to cerebellum is enhanced selectively at gamma-band frequencies around 40 Hz.