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Journal articles on the topic 'Synaptic learning mechanisms'

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Published: 4 June 2021

Last updated: 19 February 2022

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Li, Y., E. G. Meloni, W. A. Carlezon, et al. "Learning and reconsolidation implicate different synaptic mechanisms." Proceedings of the National Academy of Sciences 110, no. 12 (2013): 4798–803. http://dx.doi.org/10.1073/pnas.1217878110.

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Mameli, Manuel, and Christian Lüscher. "Synaptic plasticity and addiction: Learning mechanisms gone awry." Neuropharmacology 61, no. 7 (2011): 1052–59. http://dx.doi.org/10.1016/j.neuropharm.2011.01.036.

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DOUPE, ALLISON J., MICHELE M. SOLIS, RHEA KIMPO, and CHARLOTTE A. BOETTIGER. "Cellular, Circuit, and Synaptic Mechanisms in Song Learning." Annals of the New York Academy of Sciences 1016, no. 1 (2004): 495–523. http://dx.doi.org/10.1196/annals.1298.035.

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Carey, Megan R. "Synaptic mechanisms of sensorimotor learning in the cerebellum." Current Opinion in Neurobiology 21, no. 4 (2011): 609–15. http://dx.doi.org/10.1016/j.conb.2011.06.011.

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Sánchez-Montañés, Manuel A., Paul F. M. J. Verschure, and Peter König. "Local and Global Gating of Synaptic Plasticity." Neural Computation 12, no. 3 (2000): 519–29. http://dx.doi.org/10.1162/089976600300015682.

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Mechanisms influencing learning in neural networks are usually investigated on either a local or a global scale. The former relates to synaptic processes, the latter to unspecific modulatory systems. Here we study the interaction of a local learning rule that evaluates coincidences of pre- and postsynaptic action potentials and a global modulatory mechanism, such as the action of the basal forebrain onto cortical neurons. The simulations demonstrate that the interaction of these mechanisms leads to a learning rule supporting fast learning rates, stability, and flexibility. Furthermore, the simulations generate two experimentally testable predictions on the dependence of backpropagating action potential on basal forebrain activity and the relative timing of the activity of inhibitory and excitatory neurons in the neocortex.

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Saar, Drorit, Iris Reuveni, and Edi Barkai. "Mechanisms underlying rule learning-induced enhancement of excitatory and inhibitory synaptic transmission." Journal of Neurophysiology 107, no. 4 (2012): 1222–29. http://dx.doi.org/10.1152/jn.00356.2011.

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Training rats to perform rapidly and efficiently in an olfactory discrimination task results in robust enhancement of excitatory and inhibitory synaptic connectivity in the rat piriform cortex, which is maintained for days after training. To explore the mechanisms by which such synaptic enhancement occurs, we recorded spontaneous miniature excitatory and inhibitory synaptic events in identified piriform cortex neurons from odor-trained, pseudo-trained, and naive rats. We show that olfactory discrimination learning induces profound enhancement in the averaged amplitude of AMPA receptor-mediated miniature synaptic events in piriform cortex pyramidal neurons. Such physiological modifications are apparent at least 4 days after learning completion and outlast learning-induced modifications in the number of spines on these neurons. Also, the averaged amplitude of GABAA receptor-mediated miniature inhibitory synaptic events was significantly enhanced following odor discrimination training. For both excitatory and inhibitory transmission, an increase in miniature postsynaptic current amplitude was evident in most of the recorded neurons; however, some neurons showed an exceptionally great increase in the amplitude of miniature events. For both excitatory and inhibitory transmission, the frequency of spontaneous synaptic events was not modified after learning. These results suggest that olfactory discrimination learning-induced enhancement of synaptic transmission in cortical neurons is mediated by postsynaptic modulation of AMPA receptor-dependent currents and balanced by long-lasting modulation of postsynaptic GABAA receptor-mediated currents.

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Orpwood, Roger D. "Mechanisms of association learning in the post-synaptic neurone." Journal of Theoretical Biology 143, no. 2 (1990): 145–62. http://dx.doi.org/10.1016/s0022-5193(05)80265-6.

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NORDEEN, KATHY W., and ERNEST J. NORDEEN. "Synaptic and Molecular Mechanisms Regulating Plasticity during Early Learning." Annals of the New York Academy of Sciences 1016, no. 1 (2004): 416–37. http://dx.doi.org/10.1196/annals.1298.018.

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Isokawa, Masako. "Cellular Signal Mechanisms of Reward-Related Plasticity in the Hippocampus." Neural Plasticity 2012 (2012): 1–18. http://dx.doi.org/10.1155/2012/945373.

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The hippocampus has the extraordinary capacity to process and store information. Consequently, there is an intense interest in the mechanisms that underline learning and memory. Synaptic plasticity has been hypothesized to be the neuronal substrate for learning. Ca2+and Ca2+-activated kinases control cellular processes of most forms of hippocampal synapse plasticity. In this paper, I aim to integrate our current understanding of Ca2+-mediated synaptic plasticity and metaplasticity in motivational and reward-related learning in the hippocampus. I will introduce two representative neuromodulators that are widely studied in reward-related learning (e.g., ghrelin and endocannabinoids) and show how they might contribute to hippocampal neuron activities and Ca2+-mediated signaling processes in synaptic plasticity. Additionally, I will discuss functional significance of these two systems and their signaling pathways for its relevance to maladaptive reward learning leading to addiction.

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Kfir, Adi, Naama Ohad-Giwnewer, Luna Jammal, Drorit Saar, David Golomb, and Edi Barkai. "Learning-induced modulation of the GABAB-mediated inhibitory synaptic transmission: mechanisms and functional significance." Journal of Neurophysiology 111, no. 10 (2014): 2029–38. http://dx.doi.org/10.1152/jn.00004.2014.

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Complex olfactory-discrimination (OD) learning results in a series of intrinsic and excitatory synaptic modifications in piriform cortex pyramidal neurons that enhance the circuit excitability. Such overexcitation must be balanced to prevent runway activity while maintaining the efficient ability to store memories. We showed previously that OD learning is accompanied by enhancement of the GABAA-mediated inhibition. Here we show that GABAB-mediated inhibition is also enhanced after learning and study the mechanism underlying such enhancement and explore its functional role. We show that presynaptic, GABAB-mediated synaptic inhibition is enhanced after learning. In contrast, the population-average postsynaptic GABAB-mediated synaptic inhibition is unchanged, but its standard deviation is enhanced. Learning-induced reduction in paired pulse facilitation in the glutamatergic synapses interconnecting pyramidal neurons was abolished by application of the GABAB antagonist CGP55845 but not by blocking G protein-gated inwardly rectifying potassium channels only, indicating enhanced suppression of excitatory synaptic release via presynaptic GABAB-receptor activation. In addition, the correlation between the strengths of the early (GABAA-mediated) and late (GABAB-mediated) synaptic inhibition was much stronger for each particular neuron after learning. Consequently, GABAB-mediated inhibition was also more efficient in controlling epileptic-like activity induced by blocking GABAA receptors. We suggest that complex OD learning is accompanied by enhancement of the GABAB-mediated inhibition that enables the cortical network to store memories, while preventing uncontrolled activity.

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Tan, Han L., Shu-Ling Chiu, Qianwen Zhu, and Richard L. Huganir. "GRIP1 regulates synaptic plasticity and learning and memory." Proceedings of the National Academy of Sciences 117, no. 40 (2020): 25085–91. http://dx.doi.org/10.1073/pnas.2014827117.

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Hebbian plasticity is a key mechanism for higher brain functions, such as learning and memory. This form of synaptic plasticity primarily involves the regulation of synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) abundance and properties, whereby AMPARs are inserted into synapses during long-term potentiation (LTP) or removed during long-term depression (LTD). The molecular mechanisms underlying AMPAR trafficking remain elusive, however. Here we show that glutamate receptor interacting protein 1 (GRIP1), an AMPAR-binding protein shown to regulate the trafficking and synaptic targeting of AMPARs, is required for LTP and learning and memory. GRIP1 is recruited into synapses during LTP, and deletion of Grip1 in neurons blocks synaptic AMPAR accumulation induced by glycine-mediated depolarization. In addition, Grip1 knockout mice exhibit impaired hippocampal LTP, as well as deficits in learning and memory. Mechanistically, we find that phosphorylation of serine-880 of the GluA2 AMPAR subunit (GluA2-S880) is decreased while phosphorylation of tyrosine-876 on GluA2 (GluA2-Y876) is elevated during chemically induced LTP. This enhances the strength of the GRIP1–AMPAR association and, subsequently, the insertion of AMPARs into the postsynaptic membrane. Together, these results demonstrate an essential role of GRIP1 in regulating AMPAR trafficking during synaptic plasticity and learning and memory.

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Avchalumov, Yosef, and Chitra D. Mandyam. "Synaptic Plasticity and its Modulation by Alcohol." Brain Plasticity 6, no. 1 (2020): 103–11. http://dx.doi.org/10.3233/bpl-190089.

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Alcohol is one of the oldest pharmacological agents used for its sedative/hypnotic effects, and alcohol abuse and alcohol use disorder (AUD) continues to be major public health issue. AUD is strongly indicated to be a brain disorder, and the molecular and cellular mechanism/s by which alcohol produces its effects in the brain are only now beginning to be understood. In the brain, synaptic plasticity or strengthening or weakening of synapses, can be enhanced or reduced by a variety of stimulation paradigms. Synaptic plasticity is thought to be responsible for important processes involved in the cellular mechanisms of learning and memory. Long-term potentiation (LTP) is a form of synaptic plasticity, and occurs via N-methyl-D-aspartate type glutamate receptor (NMDAR or GluN) dependent and independent mechanisms. In particular, NMDARs are a major target of alcohol, and are implicated in different types of learning and memory. Therefore, understanding the effect of alcohol on synaptic plasticity and transmission mediated by glutamatergic signaling is becoming important, and this will help us understand the significant contribution of the glutamatergic system in AUD. In the first part of this review, we will briefly discuss the mechanisms underlying long term synaptic plasticity in the dorsal striatum, neocortex and the hippocampus. In the second part we will discuss how alcohol (ethanol, EtOH) can modulate long term synaptic plasticity in these three brain regions, mainly from neurophysiological and electrophysiological studies. Taken together, understanding the mechanism(s) underlying alcohol induced changes in brain function may lead to the development of more effective therapeutic agents to reduce AUDs.

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Zakharova, E. I., Z. I. Storozheva, A. M. Dudchenko, and A. A. Kubatiev. "Chronic Cerebral Ischaemia Forms New Cholinergic Mechanisms of Learning and Memory." International Journal of Alzheimer's Disease 2010 (2010): 1–17. http://dx.doi.org/10.4061/2010/954589.

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The purpose of this research was a comparative analysis of cholinergic synaptic organization following learning and memory in normal and chronic cerebral ischaemic rats in the Morris water maze model. Choline acetyltransferase and protein content were determined in subpopulations of presynapses of “light” and “heavy” synaptosomal fractions of the cortex and the hippocampus, and the cholinergic projective and intrinsic systems of the brain structures were taken into consideration. We found a strong involvement of cholinergic systems, both projective and intrinsic, in all forms of cognition. Each form of cognition had an individual cholinergic molecular profile and the cholinergic synaptic compositions in the ischaemic rat brains differed significantly from normal ones. Our data demonstrated that under ischaemic conditions, instead of damaged connections new key synaptic relationships, which were stable against pathological influences and able to restore damaged cognitive functions, arose. The plasticity of neurochemical links in the individual organization of certain types of cognition gave a new input into brain pathology and can be used in the future for alternative corrections of vascular and other degenerative dementias.

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Lovinger, David M., and Karina P. Abrahao. "Synaptic plasticity mechanisms common to learning and alcohol use disorder." Learning & Memory 25, no. 9 (2018): 425–34. http://dx.doi.org/10.1101/lm.046722.117.

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Lombroso, Paul, and Marilee Ogren. "Learning and Memory, Part II: Molecular Mechanisms of Synaptic Plasticity." Journal of the American Academy of Child & Adolescent Psychiatry 48, no. 1 (2009): 5–9. http://dx.doi.org/10.1097/chi.0b013e318190c4b3.

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Hüning, Harald, Helmut Glünder, and Günther Palm. "Synaptic Delay Learning in Pulse-Coupled Neurons." Neural Computation 10, no. 3 (1998): 555–65. http://dx.doi.org/10.1162/089976698300017665.

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We present rules for the unsupervised learning of coincidence between excitatory postsynaptic potentials (EPSPs) by the adjustment of post-synaptic delays between the transmitter binding and the opening of ion channels. Starting from a gradient descent scheme, we develop a robust and more biological threshold rule by which EPSPs from different synapses can be gradually pulled into coincidence. The synaptic delay changes are determined from the summed potential—at the site where the coincidence is to be established—and from postulated synaptic learning functions that accompany the individual EPSPs. According to our scheme, templates for the detection of spatiotemporal patterns of synaptic activation can be learned, which is demonstrated by computer simulation. Finally, we discuss possible relations to biological mechanisms.

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Triesch, Jochen. "Synergies Between Intrinsic and Synaptic Plasticity Mechanisms." Neural Computation 19, no. 4 (2007): 885–909. http://dx.doi.org/10.1162/neco.2007.19.4.885.

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We propose a model of intrinsic plasticity for a continuous activation model neuron based on information theory. We then show how intrinsic and synaptic plasticity mechanisms interact and allow the neuron to discover heavy-tailed directions in the input. We also demonstrate that intrinsic plasticity may be an alternative explanation for the sliding threshold postulated in the BCM theory of synaptic plasticity. We present a theoretical analysis of the interaction of intrinsic plasticity with different Hebbian learning rules for the case of clustered inputs. Finally, we perform experiments on the “bars” problem, a popular nonlinear independent component analysis problem.

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Bazzari, Amjad, and H. Parri. "Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: A Steered-Glutamatergic Perspective." Brain Sciences 9, no. 11 (2019): 300. http://dx.doi.org/10.3390/brainsci9110300.

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The molecular pathways underlying the induction and maintenance of long-term synaptic plasticity have been extensively investigated revealing various mechanisms by which neurons control their synaptic strength. The dynamic nature of neuronal connections combined with plasticity-mediated long-lasting structural and functional alterations provide valuable insights into neuronal encoding processes as molecular substrates of not only learning and memory but potentially other sensory, motor and behavioural functions that reflect previous experience. However, one key element receiving little attention in the study of synaptic plasticity is the role of neuromodulators, which are known to orchestrate neuronal activity on brain-wide, network and synaptic scales. We aim to review current evidence on the mechanisms by which certain modulators, namely dopamine, acetylcholine, noradrenaline and serotonin, control synaptic plasticity induction through corresponding metabotropic receptors in a pathway-specific manner. Lastly, we propose that neuromodulators control plasticity outcomes through steering glutamatergic transmission, thereby gating its induction and maintenance.

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Xue, Renhao, David A. Ruhl, Joseph S. Briguglio, Alexander G. Figueroa, Robert A. Pearce, and Edwin R. Chapman. "Doc2-mediated superpriming supports synaptic augmentation." Proceedings of the National Academy of Sciences 115, no. 24 (2018): E5605—E5613. http://dx.doi.org/10.1073/pnas.1802104115.

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Various forms of synaptic plasticity underlie aspects of learning and memory. Synaptic augmentation is a form of short-term plasticity characterized by synaptic enhancement that persists for seconds following specific patterns of stimulation. The mechanisms underlying this form of plasticity are unclear but are thought to involve residual presynaptic Ca2+. Here, we report that augmentation was reduced in cultured mouse hippocampal neurons lacking the Ca2+ sensor, Doc2; other forms of short-term enhancement were unaffected. Doc2 binds Ca2+ and munc13 and translocates to the plasma membrane to drive augmentation. The underlying mechanism was not associated with changes in readily releasable pool size or Ca2+ dynamics, but rather resulted from superpriming a subset of synaptic vesicles. Hence, Doc2 forms part of the Ca2+-sensing apparatus for synaptic augmentation via a mechanism that is molecularly distinct from other forms of short-term plasticity.

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Silva, Mariline M., Beatriz Rodrigues, Joana Fernandes, et al. "MicroRNA-186-5p controls GluA2 surface expression and synaptic scaling in hippocampal neurons." Proceedings of the National Academy of Sciences 116, no. 12 (2019): 5727–36. http://dx.doi.org/10.1073/pnas.1900338116.

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Homeostatic synaptic scaling is a negative feedback response to fluctuations in synaptic strength induced by developmental or learning-related processes, which maintains neuronal activity stable. Although several components of the synaptic scaling apparatus have been characterized, the intrinsic regulatory mechanisms promoting scaling remain largely unknown. MicroRNAs may contribute to posttranscriptional control of mRNAs implicated in different stages of synaptic scaling, but their role in these mechanisms is still undervalued. Here, we report that chronic blockade of glutamate receptors of the AMPA and NMDA types in hippocampal neurons in culture induces changes in the neuronal mRNA and miRNA transcriptomes, leading to synaptic upscaling. Specifically, we show that synaptic activity blockade persistently down-regulates miR-186-5p. Moreover, we describe a conserved miR-186-5p-binding site within the 3′UTR of the mRNA encoding the AMPA receptor GluA2 subunit, and demonstrate that GluA2 is a direct target of miR-186-5p. Overexpression of miR-186 decreased GluA2 surface levels, increased synaptic expression of GluA2-lacking AMPA receptors, and blocked synaptic scaling, whereas inhibition of miR-186-5p increased GluA2 surface levels and the amplitude and frequency of AMPA receptor-mediated currents, and mimicked excitatory synaptic scaling induced by synaptic inactivity. Our findings elucidate an activity-dependent miRNA-mediated mechanism for regulation of AMPA receptor expression.

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Benjamin, Paul, R. "Non-synaptic neuronal mechanisms of learning and memory in gastropod molluscs." Frontiers in Bioscience Volume, no. 13 (2008): 4051. http://dx.doi.org/10.2741/2993.

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Reuveni, Iris, Longnian Lin, and Edi Barkai. "Complex-learning Induced Modifications in Synaptic Inhibition: Mechanisms and Functional Significance." Neuroscience 381 (June 2018): 105–14. http://dx.doi.org/10.1016/j.neuroscience.2018.04.023.

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Luchkina, Natalia V., and Vadim Y. Bolshakov. "Mechanisms of fear learning and extinction: synaptic plasticity–fear memory connection." Psychopharmacology 236, no. 1 (2018): 163–82. http://dx.doi.org/10.1007/s00213-018-5104-4.

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Weitlauf, Carl, and Danny Winder. "Calcineurin, Synaptic Plasticity, and Memory." Scientific World JOURNAL 1 (2001): 530–33. http://dx.doi.org/10.1100/tsw.2001.259.

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A long-held hypothesis in neuroscience holds that learning and memory mechanisms involve lasting changes in synaptic weights. Multiple mechanisms for producing such changes exist, of which NMDA-receptor–dependent long-term potentiation (LTP) is the most widely studied. Curiously, the relatively simple hypothesis that LTP plays a role in learning and memory has proven difficult to test. A current experimental strategy is to generate genetically altered mice with mutations in genes thought to be involved in LTP and assess the effects of these mutations both on LTP and animal behavior[1,2]. A difficulty associated with these approaches has been that they are not temporally or spatially refined. To alleviate this problem, Dr. Isabelle Mansuy and colleagues used an inducible and reversible transgene expression system in which transgene expression could be controlled on a week-to-week timescale to assess the effects of genetic reduction of the activity of a protein phosphatase known as calcineurin or PP2B in adult mouse forebrain[3,4].

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Giachello, Carlo Natale Giuseppe, Pier Giorgio Montarolo, and Mirella Ghirardi. "Synaptic Functions of Invertebrate Varicosities: What Molecular Mechanisms Lie Beneath." Neural Plasticity 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/670821.

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In mammalian brain, the cellular and molecular events occurring in both synapse formation and plasticity are difficult to study due to the large number of factors involved in these processes and because the contribution of each component is not well defined. Invertebrates, such asDrosophila, Aplysia, Helix, Lymnaea,andHelisoma, have proven to be useful models for studying synaptic assembly and elementary forms of learning. Simple nervous system, cellular accessibility, and genetic simplicity are some examples of the invertebrate advantages that allowed to improve our knowledge about evolutionary neuronal conserved mechanisms. In this paper, we present an overview of progresses that elucidates cellular and molecular mechanisms underlying synaptogenesis and synapse plasticity in invertebrate varicosities and their validation in vertebrates. In particular, the role of invertebrate synapsin in the formation of presynaptic terminals and the cell-to-cell interactions that induce specific structural and functional changes in their respective targets will be analyzed.

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Volmer, Romain, Christine M. A. Prat, Gwendal Le Masson, André Garenne, and Daniel Gonzalez-Dunia. "Borna Disease Virus Infection Impairs Synaptic Plasticity." Journal of Virology 81, no. 16 (2007): 8833–37. http://dx.doi.org/10.1128/jvi.00612-07.

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ABSTRACT The mechanisms whereby Borna disease virus (BDV) can impair neuronal function and lead to neurobehavioral disease are not well understood. To analyze the electrophysiological properties of neurons infected with BDV, we used cultures of neurons grown on multielectrode arrays, allowing a real-time monitoring of the electrical activity across the network shaped by synaptic transmission. Although infection did not affect spontaneous neuronal activity, it selectively blocked activity-dependent enhancement of neuronal network activity, one form of synaptic plasticity thought to be important for learning and memory. These findings highlight the original mechanism of the neuronal dysfunction caused by noncytolytic infection with BDV.

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Sun, Linlin, Hang Zhou, Joseph Cichon, and Guang Yang. "Experience and sleep-dependent synaptic plasticity: from structure to activity." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1799 (2020): 20190234. http://dx.doi.org/10.1098/rstb.2019.0234.

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Synaptic plasticity is important for learning and memory. With increasing evidence linking sleep states to changes in synaptic strength, an emerging view is that sleep promotes learning and memory by facilitating experience-induced synaptic plasticity. In this review, we summarize the recent progress on the function of sleep in regulating cortical synaptic plasticity. Specifically, we outline the electroencephalogram signatures of sleep states (e.g. slow-wave sleep, rapid eye movement sleep, spindles), sleep state-dependent changes in gene and synaptic protein expression, synaptic morphology, and neuronal and network activity. We highlight studies showing that post-experience sleep potentiates experience-induced synaptic changes and discuss the potential mechanisms that may link sleep-related brain activity to synaptic structural remodelling. We conclude that both synapse formation or strengthening and elimination or weakening occur across sleep. This sleep-dependent synaptic plasticity plays an important role in neuronal circuit refinement during development and after learning, while sleep disorders may contribute to or exacerbate the development of common neurological diseases. This article is part of the Theo Murphy meeting issue ‘Memory reactivation: replaying events past, present and future’.

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Dur-e-Ahmad, Muhammad. "MODELING CALCIUM DYNAMICS AND INHIBITION BASED SYNAPTIC PLASTICITY IN DENDRITIC SPINES." Mathematical Modelling and Analysis 19, no. 5 (2014): 676–95. http://dx.doi.org/10.3846/13926292.2014.980865.

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Inhibitory synapses through GABAergic channels not only change spine's calcium dynamics but also modulate postsynaptic current mediated through glutamate receptors. However the mechanism and extent to which these inhibitory synapses can modulate postsynaptic potential is not clearly understood. We propose a mathematical model to explain this phenomenon which encompasses both presynaptic and postsynaptic mechanisms. Further this model also elaborates the effect of these channels in synaptic calcium dynamics and learning mechanism.

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Yu, Wendou, and Bingwei Lu. "Synapses and Dendritic Spines as Pathogenic Targets in Alzheimer’s Disease." Neural Plasticity 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/247150.

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Synapses are sites of cell-cell contacts that transmit electrical or chemical signals in the brain. Dendritic spines are protrusions on dendritic shaft where excitatory synapses are located. Synapses and dendritic spines are dynamic structures whose plasticity is thought to underlie learning and memory. No wonder neurobiologists are intensively studying mechanisms governing the structural and functional plasticity of synapses and dendritic spines in an effort to understand and eventually treat neurological disorders manifesting learning and memory deficits. One of the best-studied brain disorders that prominently feature synaptic and dendritic spine pathology is Alzheimer’s disease (AD). Recent studies have revealed molecular mechanisms underlying the synapse and spine pathology in AD, including a role for mislocalized tau in the postsynaptic compartment. Synaptic and dendritic spine pathology is also observed in other neurodegenerative disease. It is possible that some common pathogenic mechanisms may underlie the synaptic and dendritic spine pathology in neurodegenerative diseases.

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Hochner, Binyamin, Euan R. Brown, Marina Langella, Tal Shomrat, and Graziano Fiorito. "A Learning and Memory Area in the Octopus Brain Manifests a Vertebrate-Like Long-Term Potentiation." Journal of Neurophysiology 90, no. 5 (2003): 3547–54. http://dx.doi.org/10.1152/jn.00645.2003.

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Cellular mechanisms underlying learning and memory were investigated in the octopus using a brain slice preparation of the vertical lobe, an area of the octopus brain involved in learning and memory. Field potential recordings revealed long-term potentiation (LTP) of glutamatergic synaptic field potentials similar to that in vertebrates. These findings suggest that convergent evolution has led to the selection of similar activity-dependent synaptic processes that mediate complex forms of learning and memory in vertebrates and invertebrates.

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Gandolfi, Daniela, Albertino Bigiani, Carlo Adolfo Porro, and Jonathan Mapelli. "Inhibitory Plasticity: From Molecules to Computation and Beyond." International Journal of Molecular Sciences 21, no. 5 (2020): 1805. http://dx.doi.org/10.3390/ijms21051805.

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Synaptic plasticity is the cellular and molecular counterpart of learning and memory and, since its first discovery, the analysis of the mechanisms underlying long-term changes of synaptic strength has been almost exclusively focused on excitatory connections. Conversely, inhibition was considered as a fixed controller of circuit excitability. Only recently, inhibitory networks were shown to be finely regulated by a wide number of mechanisms residing in their synaptic connections. Here, we review recent findings on the forms of inhibitory plasticity (IP) that have been discovered and characterized in different brain areas. In particular, we focus our attention on the molecular pathways involved in the induction and expression mechanisms leading to changes in synaptic efficacy, and we discuss, from the computational perspective, how IP can contribute to the emergence of functional properties of brain circuits.

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Schrader, Laura, and Michael J. Friedlander. "Developmental regulation of synaptic mechanisms that may contribute to learning and memory." Mental Retardation and Developmental Disabilities Research Reviews 5, no. 1 (1999): 60–71. http://dx.doi.org/10.1002/(sici)1098-2779(1999)5:1<60::aid-mrdd7>3.0.co;2-1.

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Schmidt, John T. "Activity-dependent synaptic stabilization in development and learning: How similar the mechanisms?" Cellular and Molecular Neurobiology 5, no. 1-2 (1985): 1–3. http://dx.doi.org/10.1007/bf00711082.

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Thompson, John A., and David J. Perkel. "Endocannabinoids mediate synaptic plasticity at glutamatergic synapses on spiny neurons within a basal ganglia nucleus necessary for song learning." Journal of Neurophysiology 105, no. 3 (2011): 1159–69. http://dx.doi.org/10.1152/jn.00676.2010.

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Activation of type 1 cannabinoid receptors (CB1R) in many central nervous system structures induces both short- and long-term changes in synaptic transmission. Within mammalian striatum, endocannabinoids (eCB) are one of several mechanisms that induce synaptic plasticity at glutamatergic terminals onto medium spiny neurons. Striatal synaptic plasticity may contribute a critical component of adaptive motor coordination and procedural learning. Songbirds are advantageous for studying the neural mechanisms of motor learning because they possess a neural pathway necessary for song learning and adult song plasticity that includes a striato-pallidal nucleus, area X (homologous to a portion of mammalian basal ganglia). Recent findings suggest that eCBs contribute to vocal development. For example, dense CB1R expression in song control nuclei peaks around the closure of the sensori-motor integration phase of song development. Also, systemic administration of a CB1R agonist during vocal development impairs song learning. Here we test whether activation of CB1R alters excitatory synaptic input on spiny neurons in area X of adult male zebra finches. Application of the CB1R agonist WIN55212–2 decreased excitatory postsynaptic current (EPSC) amplitude; that decrease was blocked by the CB1R antagonist AM251. Guided by eCB experiments in mammalian striatum, we tested and verified that at least two mechanisms indirectly activate CB1Rs through eCBs in area X. First, activation of group I metabotropic glutamate receptors with the agonist 3,5-dihydroxyphenylglycine (DHPG) induced a CB1R-mediated reduction in EPSC amplitude. Second, we observed that a 10 s postsynaptic depolarization induced a calcium-mediated, eCB-dependent decrease in synaptic strength that resisted rescue with late CB1R blockade. Together, these results show that eCB modulation occurs at inputs to area X spiny neurons and could influence motor learning and production.

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Zhuo, M. "Cortical Mechanisms for Emotional Fear and Chronic Pain." European Psychiatry 24, S1 (2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70318-9.

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Investigation of molecular and cellular mechanisms of synaptic plasticity is the major focus of many neuroscientists. There are two major reasons for searching new genes and molecules contributing to central plasticity: first, it provides basic neural mechanism for learning and memory, a key function of the brain; second, it provides new targets for treating brain-related disease. Here, I propose that LTP in the anterior cingulate cortex (ACC) as a synaptic model for emotional fear and chronic pain in the brain. Integrative approaches including genetic, neurobiological and physiological methods are used to investigate the roles of cortical neurons and microglia in synaptic LTP, fear and chronic pain. We have identified several key calcium-stimulated signaling molecules including AC1, CaMKIV and FMRP for AMPA receptor mediated cingulate LTP, trace fear memory, and chronic pain. By contrast, microglia only contributes to changes in spinal dorsal horn, but not in the cortex. Our findings strongly suggest that ACC LTP may serve as a cellular model for studying central sensitization that related to fear and chronic pain, as well as pain-related cognitive emotional disorders.

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Matamales, Miriam. "Neuronal activity-regulated gene transcription: how are distant synaptic signals conveyed to the nucleus?" F1000Research 1 (December 19, 2012): 69. http://dx.doi.org/10.12688/f1000research.1-69.v1.

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Synaptic activity can trigger gene expression programs that are required for the stable change of neuronal properties, a process that is essential for learning and memory. Currently, it is still unclear how the stimulation of dendritic synapses can be coupled to transcription in the nucleus in a timely way given that large distances can separate these two cellular compartments. Although several mechanisms have been proposed to explain long distance communication between synapses and the nucleus, the possible co-existence of these models and their relevance in physiological conditions remain elusive. One model suggests that synaptic activation triggers the translocation to the nucleus of certain transcription regulators localised at postsynaptic sites that function as synapto-nuclear messengers. Alternatively, it has been hypothesised that synaptic activity initiates propagating regenerative intracellular calcium waves that spread through dendrites into the nucleus where nuclear transcription machinery is thereby regulated. It has also been postulated that membrane depolarisation of voltage-gated calcium channels on the somatic membrane is sufficient to increase intracellular calcium concentration and activate transcription without the need for transported signals from distant synapses. Here I provide a critical overview of the suggested mechanisms for coupling synaptic stimulation to transcription, the underlying assumptions behind them and their plausible physiological significance.

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Cuestas Torres, Diana Marcela, and Fernando P. Cardenas. "Synaptic plasticity in Alzheimer’s disease and healthy aging." Reviews in the Neurosciences 31, no. 3 (2020): 245–68. http://dx.doi.org/10.1515/revneuro-2019-0058.

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AbstractThe strength and efficiency of synaptic connections are affected by the environment or the experience of the individual. This property, called synaptic plasticity, is directly related to memory and learning processes and has been modeled at the cellular level. These types of cellular memory and learning models include specific stimulation protocols that generate a long-term strengthening of the synapses, called long-term potentiation, or a weakening of the said long-term synapses, called long-term depression. Although, for decades, researchers have believed that the main cause of the cognitive deficit that characterizes Alzheimer’s disease (AD) and aging was the loss of neurons, the hypothesis of an imbalance in the cellular and molecular mechanisms of synaptic plasticity underlying this deficit is currently widely accepted. An understanding of the molecular and cellular changes underlying the process of synaptic plasticity during the development of AD and aging will direct future studies to specific targets, resulting in the development of much more efficient and specific therapeutic strategies. In this review, we classify, discuss, and describe the main findings related to changes in the neurophysiological mechanisms of synaptic plasticity in excitatory synapses underlying AD and aging. In addition, we suggest possible mechanisms in which aging can become a high-risk factor for the development of AD and how its development could be prevented or slowed.

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Deco, Gustavo, and Edmund T. Rolls. "Sequential Memory: A Putative Neural and Synaptic Dynamical Mechanism." Journal of Cognitive Neuroscience 17, no. 2 (2005): 294–307. http://dx.doi.org/10.1162/0898929053124875.

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A key issue in the neurophysiology of cognition is the problem of sequential learning. Sequential learning refers to the ability to encode and represent the temporal order of discrete elements occurring in a sequence. We show that the short-term memory for a sequence of items can be implemented in an autoassociation neural network. Each item is one of the attractor states of the network. The autoassociation network is implemented at the level of integrate-and-fire neurons so that the contributions of different biophysical mechanisms to sequence learning can be investigated. It is shown that if it is a property of the synapses or neurons that support each attractor state that they adapt, then everytime the network is made quiescent (e.g., by inhibition), then the attractor state that emerges next is the next item in the sequence. We show with numerical simulations implementations of the mechanisms using (1) a sodium inactivation-based spike-frequency-adaptation mechanism, (2) a Ca2+-activated K+ current, and (3) short-term synaptic depression, with sequences of up to three items. The network does not need repeated training on a particular sequence and will repeat the items in the order that they were last presented. The time between the items in a sequence is not fixed, allowing the items to be read out as required over a period of up to many seconds. The network thus uses adaptation rather than associative synaptic modification to recall the order of the items in a recently presented sequence.

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Afonso, Pedro, Pasqualino De Luca, Rafael S. Carvalho, et al. "BDNF increases synaptic NMDA receptor abundance by enhancing the local translation of Pyk2 in cultured hippocampal neurons." Science Signaling 12, no. 586 (2019): eaav3577. http://dx.doi.org/10.1126/scisignal.aav3577.

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The effects of brain-derived neurotrophic factor (BDNF) in long-term synaptic potentiation (LTP) are thought to underlie learning and memory formation and are partly mediated by local protein synthesis. Here, we investigated the mechanisms that mediate BDNF-induced alterations in the synaptic proteome that are coupled to synaptic strengthening. BDNF induced the synaptic accumulation of GluN2B-containing NMDA receptors (NMDARs) and increased the amplitude of NMDAR-mediated miniature excitatory postsynaptic currents (mEPSCs) in cultured rat hippocampal neurons by a mechanism requiring activation of the protein tyrosine kinase Pyk2 and dependent on cellular protein synthesis. Single-particle tracking using quantum dot imaging revealed that the increase in the abundance of synaptic NMDAR currents correlated with their enhanced stability in the synaptic compartment. Furthermore, BDNF increased the local synthesis of Pyk2 at the synapse, and the observed increase in Pyk2 protein abundance along dendrites of cultured hippocampal neurons was mediated by a mechanism dependent on the ribonucleoprotein hnRNP K, which bound to Pyk2 mRNA and dissociated from it upon BDNF application. Knocking down hnRNP K reduced the BDNF-induced synaptic synthesis of Pyk2 protein, whereas its overexpression enhanced it. Together, these findings indicate that hnRNP K mediates the synaptic distribution of Pyk2 synthesis, and hence the synaptic incorporation of GluN2B-containing NMDARs, induced by BDNF, which may affect LTP and synaptic plasticity.

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Drouet, Valérie, and Suzanne Lesage. "Synaptojanin 1 Mutation in Parkinson’s Disease Brings Further Insight into the Neuropathological Mechanisms." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/289728.

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Synaptojanin 1 (SYNJ1) is a phosphoinositide phosphatase highly expressed in nerve terminals. Its two phosphatase domains dephosphorylate phosphoinositides present in membranes, while its proline-rich domain directs protein-protein interactions with synaptic components, leading to efficient recycling of synaptic vesicles in neurons. Triplication of SYNJ1 in Down’s syndrome is responsible for higher level of phosphoinositides, enlarged endosomes, and learning deficits. SYNJ1 downregulation in Alzheimer’s disease models is protective towards amyloid-beta peptide (Aβ) toxicity. One missense mutation in one of SYNJ1 functional domains was recently incriminated in an autosomal recessive form of early-onset Parkinson’s disease (PD). In the third decade of life, these patients develop progressive Parkinsonism with bradykinesia, dystonia, and variable atypical symptoms such as cognitive decline, seizures, and eyelid apraxia. The identification of this new gene, together with the fact that most of the known PD proteins play a role in synaptic vesicle recycling and lipid metabolism, points out that synaptic maintenance is a key player in PD pathological mechanisms. Studying PD genes as a network regulating synaptic activity could bring insight into understanding the neuropathological processes of PD and help identify new genes at fault in this devastating disorder.

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Briz, Victor, and Michel Baudry. "Calpains: Master Regulators of Synaptic Plasticity." Neuroscientist 23, no. 3 (2016): 221–31. http://dx.doi.org/10.1177/1073858416649178.

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Although calpain was proposed to participate in synaptic plasticity and learning and memory more than 30 years ago, the mechanisms underlying its activation and the roles of different substrates have remained elusive. Recent findings have provided evidence that the two major calpain isoforms in the brain, calpain-1 and calpain-2, play opposite functions in synaptic plasticity. In particular, while calpain-1 activation is the initial trigger for certain forms of synaptic plasticity, that is, long-term potentiation, calpain-2 activation restricts the extent of plasticity. Moreover, while calpain-1 rapidly cleaves regulatory and cytoskeletal proteins, calpain-2-mediated stimulation of local protein synthesis reestablishes protein homeostasis. These findings have important implications for our understanding of learning and memory and disorders associated with impairment in these processes.

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Ben Zablah, Youssif, Haiwang Zhang, Radu Gugustea, and Zhengping Jia. "LIM-Kinases in Synaptic Plasticity, Memory, and Brain Diseases." Cells 10, no. 8 (2021): 2079. http://dx.doi.org/10.3390/cells10082079.

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Learning and memory require structural and functional modifications of synaptic connections, and synaptic deficits are believed to underlie many brain disorders. The LIM-domain-containing protein kinases (LIMK1 and LIMK2) are key regulators of the actin cytoskeleton by affecting the actin-binding protein, cofilin. In addition, LIMK1 is implicated in the regulation of gene expression by interacting with the cAMP-response element-binding protein. Accumulating evidence indicates that LIMKs are critically involved in brain function and dysfunction. In this paper, we will review studies on the roles and underlying mechanisms of LIMKs in the regulation of long-term potentiation (LTP) and depression (LTD), the most extensively studied forms of long-lasting synaptic plasticity widely regarded as cellular mechanisms underlying learning and memory. We will also discuss the involvement of LIMKs in the regulation of the dendritic spine, the structural basis of synaptic plasticity, and memory formation. Finally, we will discuss recent progress on investigations of LIMKs in neurological and mental disorders, including Alzheimer’s, Parkinson’s, Williams–Beuren syndrome, schizophrenia, and autism spectrum disorders.

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Birbaumer, Niels, and Herta Flor. "A leg to stand on: Learning creates pain." Behavioral and Brain Sciences 20, no. 3 (1997): 441–42. http://dx.doi.org/10.1017/s0140525x97251496.

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The persistence of both inflammatory and neuropathic pain can only be explained when learning processes are taken into account in addition to sensitizing mechanisms. Learning processes such as classical and operant conditioning create memories for pain that are based on altered synaptic connections in supraspinal structures and persist without peripheral input. [coderre & katz; dickenson; wiesenfeld-hallin et al.]

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Horn, David, Nir Levy, and Eytan Ruppin. "Memory Maintenance via Neuronal Regulation." Neural Computation 10, no. 1 (1998): 1–18. http://dx.doi.org/10.1162/089976698300017863.

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Since their conception half a century ago, Hebbian cell assemblies have become a basic term in the neurosciences, and the idea that learning takes place through synaptic modifications has been accepted as a fundamental paradigm. As synapses undergo continuous metabolic turnover, adopting the stance that memories are engraved in the synaptic matrix raises a fundamental problem: How can memories be maintained for very long time periods? We present a novel solution to this long-standing question, based on biological evidence of neuronal regulation mechanisms that act to maintain neuronal activity. Our mechanism is developed within the framework of a neural model of associative memory. It is operative in conjunction with random activation of the memory system and is able to counterbalance degradation of synaptic weights and normalize the basins of attraction of all memories. Over long time periods, when the variance of the degradation process becomes important, the memory system stabilizes if its synapses are appropriately bounded. Thus, the remnant memory system is obtained by a dynamic process of synaptic selection and growth driven by neuronal regulatory mechanisms. Our model is a specific realization of dynamic stabilization of neural circuitry, which is often assumed to take place during sleep.

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Hulme, Sarah R., Owen D. Jones, Clarke R. Raymond, Pankaj Sah, and Wickliffe C. Abraham. "Mechanisms of heterosynaptic metaplasticity." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1633 (2014): 20130148. http://dx.doi.org/10.1098/rstb.2013.0148.

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Synaptic plasticity is fundamental to the neural processes underlying learning and memory. Interestingly, synaptic plasticity itself can be dynamically regulated by prior activity, in a process termed ‘metaplasticity’, which can be expressed both homosynaptically and heterosynaptically. Here, we focus on heterosynaptic metaplasticity, particularly long-range interactions between synapses spread across dendritic compartments, and review evidence for intra cellular versus inter cellular signalling pathways leading to this effect. Of particular interest is our previously reported finding that priming stimulation in stratum oriens of area CA1 in the hippocampal slice heterosynaptically inhibits subsequent long-term potentiation and facilitates long-term depression in stratum radiatum. As we have excluded the most likely intracellular signalling pathways that might mediate this long-range heterosynaptic effect, we consider the hypothesis that intercellular communication may be critically involved. This hypothesis is supported by the finding that extracellular ATP hydrolysis, and activation of adenosine A2 receptors are required to induce the metaplastic state. Moreover, delivery of the priming stimulation in stratum oriens elicited astrocytic calcium responses in stratum radiatum. Both the astrocytic responses and the metaplasticity were blocked by gap junction inhibitors. Taken together, these findings support a novel intercellular communication system, possibly involving astrocytes, being required for this type of heterosynaptic metaplasticity.

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Song, Chenghui, Julia A. Detert, Megha Sehgal, and James R. Moyer. "Trace fear conditioning enhances synaptic and intrinsic plasticity in rat hippocampus." Journal of Neurophysiology 107, no. 12 (2012): 3397–408. http://dx.doi.org/10.1152/jn.00692.2011.

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Experience-dependent synaptic and intrinsic plasticity are thought to be important substrates for learning-related changes in behavior. The present study combined trace fear conditioning with both extracellular and intracellular hippocampal recordings to study learning-related synaptic and intrinsic plasticity. Rats received one session of trace fear conditioning, followed by a brief conditioned stimulus (CS) test the next day. To relate behavioral performance with measures of hippocampal CA1 physiology, brain slices were prepared within 1 h of the CS test. In trace-conditioned rats, both synaptic plasticity and intrinsic excitability were significantly correlated with behavior such that better learning corresponded with enhanced long-term potentiation (LTP; r = 0.64, P < 0.05) and a smaller postburst afterhyperpolarization (AHP; r = −0.62, P < 0.05). Such correlations were not observed in pseudoconditioned rats, whose physiological data were comparable to those of poor learners and naive and chamber-exposed control rats. In addition, acquisition of trace fear conditioning did not enhance basal synaptic responses. Thus these data suggest that within the hippocampus both synaptic and intrinsic mechanisms are involved in the acquisition of trace fear conditioning.

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Kida, Hiroyuki, and Dai Mitsushima. "Mechanisms of motor learning mediated by synaptic plasticity in rat primary motor cortex." Neuroscience Research 128 (March 2018): 14–18. http://dx.doi.org/10.1016/j.neures.2017.09.008.

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Sandi, Carmen. "The Role and Mechanisms of Action of Glucocorticoid Involvement in Memory Storage." Neural Plasticity 6, no. 3 (1998): 41–52. http://dx.doi.org/10.1155/np.1998.41.

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Adrenal steroid hormones modulate learning and memory processes by interacting with specific glucocorticoid receptors at different brain areas. In this article, certain components of the physiological response to stress elicited by learning situations are proposed to form an integral aspect of the neurobiological mechanism underlying memory formation. By reviewing the work carried out in different learning models in chicks (passive avoidance learning) and rats (spatial orientation in the Morris water maze and contextual fear conditioning), a role for brain corticosterone action through the glucocorticoid receptor type on the mechanisms of memory consolidation is hypothesized. Evidence is also presented to relate post-training corticosterone levels to the strength of memory storage. Finally, the possible molecular mechanisms that might mediate the influences of glucocorticoids in synaptic plasticity subserving long-term memory formation are considered, mainly by focusing on studies implicating a steroid action through (i) glutamatergic transmission and (ii) cell adhesion molecules.

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Hanley, J. G. "Molecular mechanisms for regulation of AMPAR trafficking by PICK1." Biochemical Society Transactions 34, no. 5 (2006): 931–35. http://dx.doi.org/10.1042/bst0340931.

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AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor trafficking is a fundamental mechanism for regulating synaptic strength, and hence may underlie cellular processes involved in learning and memory. PICK1 (protein that interacts with protein C-kinase) has recently emerged as a key regulator of AMPAR (AMPA receptor) traffic, and the precise molecular mechanisms of PICK1's action are just beginning to be unravelled. In this review, I summarize recent findings that describe some important molecular characteristics of PICK1 with respect to AMPAR cell biology.

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Tanaka, Shigeru, and Masanobu Miyashita. "Constraint on the Number of Synaptic Inputs to a Visual Cortical Neuron Controls Receptive Field Formation." Neural Computation 21, no. 9 (2009): 2554–80. http://dx.doi.org/10.1162/neco.2009.04-08-752.

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To date, Hebbian learning combined with some form of constraint on synaptic inputs has been demonstrated to describe well the development of neural networks. The previous models revealed mathematically the importance of synaptic constraints to reproduce orientation selectivity in the visual cortical neurons, but biological mechanisms underlying such constraints remain unclear. In this study, we addressed this issue by formulating a synaptic constraint based on activity-dependent mechanisms of synaptic changes. Particularly, considering metabotropic glutamate receptor-mediated long-term depression, we derived synaptic constraint that suppresses the number of inputs from individual presynaptic neurons. We performed computer simulations of the activity-dependent self-organization of geniculocortical inputs with the synaptic constraint and examined the formation of receptive fields (RFs) of model visual cortical neurons. When we changed the magnitude of the synaptic constraint, we found the emergence of distinct RF structures such as concentric RFs, simple-cell-like RFs, and double-oriented RFs and also a gradual transition between spatiotemporal separable and inseparable RFs. Thus, the model based on the synaptic constraint derived from biological consideration can account systematically for the repertoire of RF structures observed in the primary visual cortices of different species for the first time.

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