Journal articles: 'Cholinergic markers'

1

Bartus, R. T. "Cholinergic Markers in Alzheimer Disease." JAMA: The Journal of the American Medical Association 282, no. 23 (December 15, 1999): 2208–9. http://dx.doi.org/10.1001/jama.282.23.2208.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Haroutunian, V., M. Davidson, P. D. Kanof, D. P. Perl, P. Powchik, M. Losonczy, J. McCrystal, D. P. Purohit, L. M. Bierer, and K. L. Davis. "Cortical cholinergic markers in schizophrenia." Schizophrenia Research 12, no. 2 (May 1994): 137–44. http://dx.doi.org/10.1016/0920-9964(94)90071-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Massey, Stephen C., Kevin Blankenship, and Stephen L. Mills. "Cholinergic amacrine cells in the rabbit retina accumulate muscimol." Visual Neuroscience 6, no. 2 (February 1991): 113–17. http://dx.doi.org/10.1017/s0952523800010506.

Full text

Abstract:

AbstractThe cholinergic amacrine cells of the rabbit retina form two mosaics placed symmetrically on either side of the inner plexiform layer. Recently, these cells have been reported to contain immunocytochemical markers for GABA. In this paper, we labeled the cholinergic cells with DAPI, then incubated the retina in [3H]-muscimol, a neuronal marker for GABA. Subsequently, we converted the DAPI fluorescence of the displaced cholinergic matrix to an opaque product by photooxidation in the presence of DAB. Autoradiography showed that all of the displaced cholinergic amacrine cells were labeled with ]3H]-muscimol, thus confirming the immunocytochemical results. The cholinergic cells account for approximately 80% of the cells in the ganglion cell layer which take up ]3H]-muscimol.

APA, Harvard, Vancouver, ISO, and other styles

4

Berger, Michael L., Mario Veitl, Susanne Malessa, Elfriede Sluga, and Oleh Hornykiewicz. "Cholinergic markers in ALS spinal cord." Journal of the Neurological Sciences 108, no. 1 (March 1992): 114–17. http://dx.doi.org/10.1016/0022-510x(92)90196-r.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Perry, E. K., and R. H. Perry. "CNS cholinergic markers and Alzheimer's disease." Neurobiology of Aging 7, no. 5 (September 1986): 390–91. http://dx.doi.org/10.1016/0197-4580(86)90167-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Reale, Marcella, Lucia Velluto, Marta Di Nicola, Chiara D’Angelo, Erica Costantini, Michele Marchioni, Gianluigi Cerroni, and Biancamaria Guarnieri. "Cholinergic Markers and Cytokines in OSA Patients." International Journal of Molecular Sciences 21, no. 9 (May 5, 2020): 3264. http://dx.doi.org/10.3390/ijms21093264.

Full text

Abstract:

The role of inflammation and dysfunction of the cholinergic system in obstructive sleep apnea (OSA) has not exhaustively clarified. Thus, in this study, we explore the non-neuronal cholinergic system and the balance of T helper (Th) 17- and T regulatory (Treg)-related cytokines in OSA patients. The study includes 33 subjects with obstructive sleep apnea and 10 healthy controls (HC). The expression levels of cholinergic system component, RAR-related orphan receptor (RORc), transcription factor forkhead box protein 3 (Foxp3) and cytokines were evaluated. Th17- and Treg-related cytokines, choline levels and acetylcholinesterase (AChE), butyrylcholinesterase (BuChE) activity were quantified in OSA and control subjects. AChE and nicotinic receptor α 7 subunit (α7nAChR) gene expression and serum levels of choline, AChE and BuChE were lower in OSA patients than in the HC group. Compared with the HC group, OSA patients exhibited an increased expression, secretion and serum levels of pro-inflammatory cytokines, a reduced expression, secretion and serum levels of transforming growth factor (TGF)β and reduced Foxp3 mRNA levels. The Th17/Treg-related cytokine ratio was higher in the OSA group. Our results confirm and reinforce the hypothesis that OSA may be considered a systemic inflammatory disease, and that an imbalance of non-neuronal cholinergic and pro/anti-inflammatory cytokines may contribute to development and progression of comorbidities in OSA subjects. The evaluation of Th17/Treg-related cytokine may provide an additional explanation for OSA pathogenesis and clinical features, opening new directions for the OSA management.

APA, Harvard, Vancouver, ISO, and other styles

7

Volgin, Denys V., Irma Rukhadze, and Leszek Kubin. "Hypoglossal premotor neurons of the intermediate medullary reticular region express cholinergic markers." Journal of Applied Physiology 105, no. 5 (November 2008): 1576–84. http://dx.doi.org/10.1152/japplphysiol.90670.2008.

Full text

Abstract:

The inspiratory drive to hypoglossal (XII) motoneurons originates in the caudal medullary intermediate reticular (IRt) region. This drive is mainly glutamatergic, but little is known about the neurochemical features of IRt XII premotor neurons. Prompted by the evidence that XII motoneuronal activity is controlled by both muscarinic (M) and nicotinic cholinergic inputs and that the IRt region contains cells that express choline acetyltransferase (ChAT), a marker of cholinergic neurons, we investigated whether some IRt XII premotor neurons are cholinergic. In seven rats, we applied single-cell reverse transcription-polymerase chain reaction to acutely dissociated IRt neurons retrogradely labeled from the XII nucleus. We found that over half (21/37) of such neurons expressed mRNA for ChAT and one-third (13/37) also had M2 receptor mRNA. In contrast, among the IRt neurons not retrogradely labeled, only 4 of 29 expressed ChAT mRNA ( P < 0.0008) and only 3 of 29 expressed M2 receptor mRNA ( P < 0.04). The distributions of other cholinergic receptor mRNAs (M1, M3, M4, M5, and nicotinic α4-subunit) did not differ between IRt XII premotor neurons and unlabeled IRt neurons. In an additional three rats with retrograde tracers injected into the XII nucleus and ChAT immunohistochemistry, 5–11% of IRt XII premotor neurons located at, and caudal to, the area postrema were ChAT positive, and 27–48% of ChAT-positive caudal IRt neurons were retrogradely labeled from the XII nucleus. Thus the pre- and postsynaptic cholinergic effects previously described in XII motoneurons may originate, at least in part, in medullary IRt neurons.

APA, Harvard, Vancouver, ISO, and other styles

8

Adem, Abdu, Agneta Nordberg, Gösta Bucht, and Bengt Winblad. "Extraneural cholinergic markers in Alzheimer's and Parkinson's disease." Progress in Neuro-Psychopharmacology and Biological Psychiatry 10, no. 3-5 (January 1986): 247–57. http://dx.doi.org/10.1016/0278-5846(86)90005-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Marinova, Desislava M., Miroslav L. Dobrev, Tihomir R. Rashev, Iskren K. Gerasimov, Vladislav Nankov, and Stefan V. Trifonov. "ACETYLCHOLINE AND ITS SYNTHESIZING ENZYME CHOLINE ACETYLTRANSPHERASE IN THE ENTERIC NERVOUS SYSTEM." Journal of IMAB - Annual Proceeding (Scientific Papers) 28, no. 4 (November 9, 2022): 4671–75. http://dx.doi.org/10.5272/jimab.2022284.4671.

Full text

Abstract:

The enteric nervous system is the largest and most complex division of the peripheral nervous system. Located in the wall of the gastrointestinal tract, it is a regulatory and coordination unit of the nervous system. Neurochemical, pharmacological, and functional studies describe three main classes of neurons in the enteric nervous system– primary afferent, interneurons and motor neurons. These are grouped in ganglia, which are connected and form plexuses. Acetylcholine is a major neurotransmitter that plays a pivotal role in the enteric nervous system and several non-neuronal structures. Internal cholinergic neurons and vagus terminals in the enteric nervous system use acetylcholine as the main excitatory neurotransmitter, regulating motility and mucosal function in the digestive system. The enzyme choline acetyltransferase (ChAT) that catalyzes the synthesis of acetylcholine represents the most specific cholinergic marker. Recent markers used to visualize cholinergic structures are the splicing variants of ChAT mRNA that are transcribed from the ChAT gene. Different alternatively spliced ChAT mRNA variants are transcribed in many animal species, including humans. In the mouse, seven variants in the 5’-noncoding region and two variants that differ in their coding region are described. Morphological, genetic and molecular analysis of ChAT and its splicing variants, as the most reliable and frequently used marker for cholinergic structures, would contribute to a better understanding of the physiological and pathological states of cholinergic neurons in the enteric nervous system.

APA, Harvard, Vancouver, ISO, and other styles

10

Gil-Bea, Francisco Javier, Mónica García-Alloza, Jon Domínguez, Beatriz Marcos, and María Javier Ramírez. "Evaluation of cholinergic markers in Alzheimer's disease and in a model of cholinergic deficit." Neuroscience Letters 375, no. 1 (February 2005): 37–41. http://dx.doi.org/10.1016/j.neulet.2004.10.062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Corsetti, Veronica, Carla Perrone-Capano, Michael Sebastian Salazar Intriago, Elisabetta Botticelli, Giancarlo Poiana, Gabriella Augusti-Tocco, Stefano Biagioni, and Ada Maria Tata. "Expression of Cholinergic Markers and Characterization of Splice Variants during Ontogenesis of Rat Dorsal Root Ganglia Neurons." International Journal of Molecular Sciences 22, no. 11 (May 23, 2021): 5499. http://dx.doi.org/10.3390/ijms22115499.

Full text

Abstract:

Dorsal root ganglia (DRG) neurons synthesize acetylcholine (ACh), in addition to their peptidergic nature. They also release ACh and are cholinoceptive, as they express cholinergic receptors. During gangliogenesis, ACh plays an important role in neuronal differentiation, modulating neuritic outgrowth and neurospecific gene expression. Starting from these data, we studied the expression of choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) expression in rat DRG neurons. ChAT and VAChT genes are arranged in a “cholinergic locus”, and several splice variants have been described. Using selective primers, we characterized splice variants of these cholinergic markers, demonstrating that rat DRGs express R1, R2, M, and N variants for ChAT and V1, V2, R1, and R2 splice variants for VAChT. Moreover, by RT-PCR analysis, we observed a progressive decrease in ChAT and VAChT transcripts from the late embryonic developmental stage (E18) to postnatal P2 and P15 and in the adult DRG. Interestingly, Western blot analyses and activity assays demonstrated that ChAT levels significantly increased during DRG ontogenesis. The modulated expression of different ChAT and VAChT splice variants during development suggests a possible differential regulation of cholinergic marker expression in sensory neurons and confirms multiple roles for ACh in DRG neurons, both in the embryo stage and postnatally.

APA, Harvard, Vancouver, ISO, and other styles

12

Martinelli, Ilenia, Daniele Tomassoni, Proshanta Roy, Francesco Amenta, and Seyed Khosrow Tayebati. "Altered Brain Cholinergic and Synaptic Markers in Obese Zucker Rats." Cells 10, no. 10 (September 24, 2021): 2528. http://dx.doi.org/10.3390/cells10102528.

Full text

Abstract:

The association between obesity and loss of cognitive performance has been recognized. Although there are data regarding the metabolic alterations in obese conditions and the development of neuroinflammation, no clear evidence concerning obesity-related cholinergic and synaptic impairments in the frontal cortex and hippocampus has been reported yet. Here, we investigate different cholinergic and synaptic markers in 12-, 16-, and 20-week-old obese Zucker rats (OZRs) compared with lean littermate rats (LZRs), using immunochemical and immunohistochemical analysis. Consequently, OZRs showed body weight gain, hypertension, and dysmetabolism. In 20-week-old OZRs, the reduction of vesicular acetylcholine transporter (VAChT) and alpha7 nicotinic acetylcholine receptors (α7nAChR) occurred both in the frontal cortex and in the hippocampus, suggesting a cognitive dysfunction due to obesity and aging. Among the muscarinic receptors analyzed, the level of expression of type 1 (mAChR1) was lower in the hippocampus of the older OZRs. Finally, we showed synaptic dysfunctions in OZRs, with a reduction of synaptophysin (SYP) and synaptic vesicle glycoprotein 2B (SV2B) in 20-week-old OZRs, both in the frontal cortex and in the hippocampus. Taken together, our data suggest specific alterations of cholinergic and synaptic markers that can be targeted to prevent cognitive deficits related to obesity and aging.

APA, Harvard, Vancouver, ISO, and other styles

13

Dorn, Roland, Bernhard Loy, Georg Dechant, and Galina Apostolova. "Neurogenomics of the Sympathetic Neurotransmitter Switch Indicates That Different Mechanisms Steer Cholinergic Differentiation in Rat and Chicken Models." Dataset Papers in Neuroscience 2013 (September 26, 2013): 1–9. http://dx.doi.org/10.7167/2013/520930.

Full text

Abstract:

Vertebrate sympathetic neurons have the remarkable potential to switch their neurotransmitter phenotype from noradrenergic to cholinergic—a phenomenon that has been intensively studied in rat and chicken models. In both species, loss of noradrenergic markers and concomitant upregulation of cholinergic markers occurs in response to neuropoietic cytokines such as ciliary neurotrophic factor (CNTF). However, other aspects of the neurotransmitter switch including developmental timing, target tissues of cholinergic neurons, and dependence on neurotrophic factors differ between the two species. Here we compare CNTF-triggered transcriptome changes in both species by using DNA microarrays. CNTF induced changes in 1130 out of 16084 analyzed genomic loci in rat sympathetic neurons. When this set of genes was compared to CNTF-induced changes in the chicken transcriptome, a surprisingly small overlap was found—only 94 genes were regulated in the same direction in chicken and rat. The differential responses of the transcriptome to neuropoietic cytokines provide additional evidence that the cholinergic switch, although conserved during vertebrate evolution, is a heterogeneous phenomenon and may result from differential cellular mechanisms.

APA, Harvard, Vancouver, ISO, and other styles

14

Teipel, Stefan J., Martin Dyrba, Tommaso Ballarini, Frederic Brosseron, Davide Bruno, Katharina Buerger, Nicoleta-Carmen Cosma, et al. "Association of Cholinergic Basal Forebrain Volume and Functional Connectivity with Markers of Inflammatory Response in the Alzheimer’s Disease Spectrum." Journal of Alzheimer's Disease 85, no. 3 (February 1, 2022): 1267–82. http://dx.doi.org/10.3233/jad-215196.

Full text

Abstract:

Background: Inflammation has been described as a key pathogenic event in Alzheimer’s disease (AD), downstream of amyloid and tau pathology. Preclinical and clinical data suggest that the cholinergic basal forebrain may moderate inflammatory response to different pathologies. Objective: To study the association of cholinergic basal forebrain volume and functional connectivity with measures of neuroinflammation in people from the AD spectrum. Methods: We studied 261 cases from the DELCODE cohort, including people with subjective cognitive decline, mild cognitive impairment, AD dementia, first degree relatives, and healthy controls. Using Bayesian ANCOVA, we tested associations of MRI indices of cholinergic basal forebrain volume and functional connectivity with cerebrospinal fluid (CSF) levels of sTREM2 as a marker of microglia activation, and serum levels of complement C3. Using Bayesian elastic net regression, we determined associations between basal forebrain measures and a large inflammation marker panel from CSF and serum. Results: We found anecdotal to moderate evidence in favor of the absence of an effect of basal forebrain volume and functional connectivity on CSF sTREM2 and serum C3 levels both in Aβ42/ptau-positive and negative cases. Bayesian elastic net regression identified several CSF and serum markers of inflammation that were associated with basal forebrain volume and functional connectivity. The effect sizes were moderate to small. Conclusion: Our data-driven analyses generate the hypothesis that cholinergic basal forebrain may be involved in the neuroinflammation response to Aβ42 and phospho-tau pathology in people from the AD spectrum. This hypothesis needs to be tested in independent samples.

APA, Harvard, Vancouver, ISO, and other styles

15

Nordberg, Agneta. "Biological markers and the cholinergic hypothesis in Alzheimer's disease." Acta Neurologica Scandinavica 85, S139 (September 1992): 54–58. http://dx.doi.org/10.1111/j.1600-0404.1992.tb04455.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Sparks, D. L., and W. R. Markesbery. "Altered Serotonergic and Cholinergic Synaptic Markers in Pick's Disease." Archives of Neurology 48, no. 8 (August 1, 1991): 796–99. http://dx.doi.org/10.1001/archneur.1991.00530200032014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Aubert, I., W. Rowe, M. J. Meaney, S. Gauthier, and R. Quirion. "Cholinergic markers in aged cognitively impaired long-evans rats." Neuroscience 67, no. 2 (July 1995): 277–92. http://dx.doi.org/10.1016/0306-4522(95)00056-o.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Kumar, U., and Å. Sellström. "Development of cholinergic markers in the neuroblastoma, N1E-115." Journal of Neuroscience Research 27, no. 1 (September 1990): 99–105. http://dx.doi.org/10.1002/jnr.490270115.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Müller, Martijn L. T. M., Nicolaas I. Bohnen, Vikas Kotagal, Peter J. H. Scott, Robert A. Koeppe, Kirk A. Frey, and Roger L. Albin. "Clinical markers for identifying cholinergic deficits in Parkinson's disease." Movement Disorders 30, no. 2 (November 12, 2014): 269–73. http://dx.doi.org/10.1002/mds.26061.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Djemil, Sarra, Claire R. Ressel, Amanda K. Schneeweisi, S. Abdel-Ghani, and Daniel T. S. Pak. "66108 Central Cholinergic Synapse Formation in Optimized Primary Septal “Hippocampal Co” cultures." Journal of Clinical and Translational Science 5, s1 (March 2021): 3–4. http://dx.doi.org/10.1017/cts.2021.411.

Full text

Abstract:

ABSTRACT IMPACT: Optimization of primary septal-hippocampal co-cultures facilitates studying central cholinergic synapse formation and dysfunction OBJECTIVES/GOALS: Septal cholinergic innervation to the hippocampus is critical for normal learning and memory and is severely degenerated in Alzheimer’s disease. To understand the molecular events underlying this loss, we optimized a primary septal-hippocampal co-culture system that facilitates the study of central cholinergic synapses. METHODS/STUDY POPULATION: We developed an optimized in vitro septal-hippocampal co-culture system modified from previously published protocols. Briefly, hippocampal and septal tissue were harvested from embryonic day 19 (E19) Sprague-Dawley rats, digested with 0.1% trypsin, and an equal number of cells from each region plated onto coverslips coated with poly-D-lysine and laminin at a final density of 300 cells/mm2. We use immunostaining with validated primary antibodies and a fluorescent binding assay, together with confocal microscopy, to determine the structure of cholinergic synapses that are 1) native, 2) mammalian, 3) CNS derived, 4) comprised of physiological synaptic partners, and 5) developmentally mature. RESULTS/ANTICIPATED RESULTS: After DIV21, co-cultures maintained a healthy morphology. A subpopulation of neurons strongly expressed the cholinergic markers vesicular ACh transporter (vAChT), choline acetyltransferase (ChAT), and the high-affinity choline transporter (ChT1), whereas most neurons lacked vAChT expression and were presumably glutamatergic or GABAergic. The percentage of cholinergic neurons attained in the co-culture is ˜5-7%. The size of these cholinergic neurons is strikingly similar to that reported for BFCNs in the intact brain (mean 30μm, range 18-43μm). All sampled cholinergic neurons (28/28 neurons) also expressed molecular machinery necessary for GABA release. Staining for a cholinergic postsynaptic marker shows that 63% of the contacts made with are synaptic. DISCUSSION/SIGNIFICANCE OF FINDINGS: Primary septal-hippocampal co-cultured neurons have not been exploited extensively in the field, perhaps due to the difficulty in maintaining such cultures for extended periods. Here, we optimized an in vitro septal-hippocampal co-culture system, a powerful tool to comprehensively analyze central cholinergic synapse formation and dysfunction.

APA, Harvard, Vancouver, ISO, and other styles

21

Quirion, Rémi, Dalia M. Araujo, Paul A. Lapchak, David Seto, and Jean-Guy Chabot. "Growth Factors and Lymphokines: Modulators of Cholinergic Neuronal Activity." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S3 (August 1991): 390–93. http://dx.doi.org/10.1017/s0317167100032510.

Full text

Abstract:

ABSTRACT:It is well known that various markers of the cholinergic synapse are altered in Alzheimer's Disease. Much interest is currently focussing on the evaluation of the possible efficacy of certain growth factors, especially nerve growth factor (NGF), to reduce or reverse cholinergic neuronal losses. Here we report that other growth factors (epidermal growth factor and insulin-like growth factor I) and a lymphokine, interleukin-2, are able to block acetylcholine release in the rat hippocampus. This suggests that while certain growth factors like NGF may have positive effects on the cholinergic neuron, others may act as “negative” factors on this neuronal population.

APA, Harvard, Vancouver, ISO, and other styles

22

Djemil, Sarra, Claire R. Ressel, and Daniel T. S. Pak. "4303 Optimization of primary septal-hippocampal co-cultures to study central cholinergic synapse formation and dysfunction." Journal of Clinical and Translational Science 4, s1 (June 2020): 14. http://dx.doi.org/10.1017/cts.2020.86.

Full text

Abstract:

OBJECTIVES/GOALS: Septal cholinergic innervation to the hippocampus is critical for normal learning and memory and is severely degenerated in Alzheimer’s disease. To understand the molecular events underlying this loss, we optimized a primary septal-hippocampal co-culture system that facilitates study of central cholinergic synapses. METHODS/STUDY POPULATION: We developed an optimized in vitro septal-hippocampal co-culture system modified from previous published protocols. Briefly, hippocampal and septal tissue were harvested from embryonic day 19 (E19) Sprague-Dawley rats, digested with 0.1% trypsin, and an equal number of cells from each region plated onto coverslips coated with poly-D-lysine and laminin at a final density of 300 cells/mm2. We use immunostaining with validated primary antibodies and a fluorescent binding assay, together with confocal microscopy, to determine the structure of cholinergic synapses that are 1) native, 2) mammalian, 3) CNS derived, 4) comprised of physiological synaptic partners, and 5) developmentally mature. RESULTS/ANTICIPATED RESULTS: After DIV21, co-cultures maintained a healthy morphology. A subpopulation of neurons strongly expressed the cholinergic markers vesicular ACh transporter (vAChT), choline acetyltransferase (ChAT), and the high-affinity choline transporter (ChT1), whereas most neurons lacked vAChT expression and were presumably glutamatergic or GABAergic. The percentage of cholinergic neurons in the co-culture attained up to ~5-7%, depending on conditions such as embryo age at dissection or ratio of septal to hippocampal cells. We also report on cholinergic synapse structure by examining postsynaptic markers (excitatory and inhibitory) and staining for nicotinic acetylcholine receptor subunits. DISCUSSION/SIGNIFICANCE OF IMPACT: Primary septal-hippocampal co-cultured neurons have not been exploited extensively in the field, perhaps due to the difficulty in maintaining such cultures for extended periods. Here, we optimized an in vitro septal-hippocampal co-culture system, a powerful tool to comprehensively analyze central cholinergic synapse formation and dysfunction.

APA, Harvard, Vancouver, ISO, and other styles

23

Gatta, Valentina, Guadalupe Mengod, Marcella Reale, and Ada Maria Tata. "Possible Correlation between Cholinergic System Alterations and Neuro/Inflammation in Multiple Sclerosis." Biomedicines 8, no. 6 (June 8, 2020): 153. http://dx.doi.org/10.3390/biomedicines8060153.

Full text

Abstract:

Multiple sclerosis (MS) is an autoimmune and demyelinating disease of the central nervous system. Although the etiology of MS is still unknown, both genetic and environmental factors contribute to the pathogenesis of the disease. Acetylcholine participates in the modulation of central and peripheral inflammation. The cells of the immune system, as well as microglia, astrocytes and oligodendrocytes express cholinergic markers and receptors of muscarinic and nicotinic type. The role played by acetylcholine in MS has been recently investigated. In the present review, we summarize the evidence indicating the cholinergic dysfunction in serum and cerebrospinal fluid of relapsing–remitting (RR)-MS patients and in the brains of the MS animal model experimental autoimmune encephalomyelitis (EAE). The correlation between the increased activity of the cholinergic hydrolyzing enzymes acetylcholinesterase and butyrylcholinesterase, the reduced levels of acetylcholine and the increase of pro-inflammatory cytokines production were recently described in immune cells of MS patients. Moreover, the genetic polymorphisms for both hydrolyzing enzymes and the possible correlation with the altered levels of their enzymatic activity have been also reported. Finally, the changes in cholinergic markers expression in the central nervous system of EAE mice in peak and chronic phases suggest the involvement of the acetylcholine also in neuro-inflammatory processes.

APA, Harvard, Vancouver, ISO, and other styles

24

Williams, Lawrence R., R. Jane Rylett, Hylan C. Moises, and Andrew H. Tang. "Exogenous NGF Affects Cholinergic Transmitter Function and Y-Maze Behavior in Aged Fischer 344 Male Rats." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S3 (August 1991): 403–7. http://dx.doi.org/10.1017/s0317167100032546.

Full text

Abstract:

ABSTRACT:Chronic ICV administration of NGF stimulates the activity of the cholinergic neuronal markers, HACU and ChAT, as well as the evoked release of both endogenous and newly synthesized acetylcholine in the brain of aging Fischer 344 male rats. However, the pattern of cholinergic phenotype stimulation indicates an age-related differential regulation of ChAT, HACU, and ACh release between specific brain areas, with the largest.effects found in the striatum. NGF treatment also increases the effectiveness of neurotransmission between basal forebrain cholinergic neurons and postsynaptic amygdaloid target neurons. The stimulation of central cholinergic transmitter function after NGF treatment affects behavior in a Y-maze brightness discrimination paradigm. NGF treatment does not affect the cognitive measure of brightness discrimination, but reduces the number of avoidance attempts, a measure of motor function.

APA, Harvard, Vancouver, ISO, and other styles

25

Egashira, Toru, Fumie Murayama, Yoshihira Kimba, and Yasumitsu Yamanaka. "Age-related decrements of cholinergic markers in aged rat brain." Japanese Journal of Pharmacology 52 (1990): 74. http://dx.doi.org/10.1016/s0021-5198(19)55050-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Greco, Mary Ann, Meredith Magner, David Overstreet, and Priyattam J. Shiromani. "Expression of cholinergic markers in the pons of Flinders rats." Molecular Brain Research 55, no. 2 (April 1998): 232–36. http://dx.doi.org/10.1016/s0169-328x(98)00002-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Rodríguez-Ithurralde, Daniel, and Oscar Vincent. "Excitotoxicity and cholinergic chemical markers during programmed motor neurone death." Journal of the Neurological Sciences 124 (July 1994): 52–53. http://dx.doi.org/10.1016/0022-510x(94)90176-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Yufu, Fumie, Toru Egashira, and Yasumitsu Yamanaka. "Age-Related Changes of Cholinergic Markers in the Rat Brain." Japanese Journal of Pharmacology 66, no. 2 (1994): 247–56. http://dx.doi.org/10.1254/jjp.66.247.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

John, Jebin Jacob, Niranjan L. Gujar, G. B. K. S. Prasad, and Rahul Bhattacharya. "Dose and Time-dependent Alterations in Various Cholinergic and Non-cholinergic Markers after Organophosphate Poisoning: Possible Role in Diagnosis." Defence Life Science Journal 1, no. 2 (October 7, 2016): 171. http://dx.doi.org/10.14429/dlsj.1.10746.

Full text

Abstract:

Toxicity of organophosphates (OP) is mainly ascribed to inhibition of acetylcholinesterase (AChE) enzyme at the cholinergic synapses. This results in cholinergic crisis leading to various muscarinic, nicotinic and central effects. Additionally, there are several non-cholinergic effects of OP which are likely to exacerbate the toxicity and complicate diagnosis. The present study reports the dose (0.125 - 4.0 LD50) and time (1 h - 14 d)- dependent acute effect of diisopropyl phosphorofluoridate (DFP) on mice body weight, organ-body weight index (brain), butyrylcholinesterase (BChE) and β-glucoronidase (BG) activity in plasma, AChE activity, reduced glutathione (GSH) and malondialdehyde (MDA) levels in brain, and DNA damage in brain (agarose gel electrophoresis) and blood (comet assay). The study reveals a dose and time- dependent BChE inhibition up to 24 h and AChE inhibition up to 7 d. However, elevated BG levels were observed up to 1 h only after 1.0, 2.0, and 4.0 LD50 DFP. Diminished GSH levels up to 24 h and increased MDA levels at 4 h indicated oxidative stress. None of the treatments produced any DNA damage in soft tissues. In addition to cholinesterase, the study suggests possible relevance of measuring BG levels (non-cholinergic marker) in the diagnosis of OP poisoning.

APA, Harvard, Vancouver, ISO, and other styles

30

El-Defrawy, S. R., R. J. Boegman, K. Jhamandas, and R. J. Beninger. "The neurotoxic actions of quinolinic acid in the central nervous system." Canadian Journal of Physiology and Pharmacology 64, no. 3 (March 1, 1986): 369–75. http://dx.doi.org/10.1139/y86-060.

Full text

Abstract:

Excitotoxins such as kainic acid, ibotenic acid, and quinolinic acid are a group of molecules structurally related to glutamate or aspartate. They are capable of exciting neurons and producing axon sparing neuronal degeneration. Quinolinic acid (QUIN), an endogenous metabolite of the amino acid, tryptophan, has been detected in brain and its concentration increases with age. The content of QUIN in the brain and the activity of the enzymes involved in its synthesis and metabolism show a regional distribution. The neuroexcitatory action of QUIN is antagonized by magnesium (Mg2+) and the aminophosphonates, proposed N-methyl-D-aspartate (NMDA) receptor antagonists, suggesting that QUIN acts at the Mg2+-sensitive NMDA receptor. Like its excitatory effects, QUIN's neurotoxic actions in the striatum are antagonized by the aminophosphonates. This suggests that QUIN neurotoxicity involves the NMDA receptor and (or) another receptor sensitive to the aminophosphonates. The neuroexcitatory and neurotoxic effects of QUIN are antagonized by kynurenic acid (KYN), another metabolite of tryptophan. QUIN toxicity is dependent on excitatory amino acid afferents and shows a regional variation in the brain. Local injection of QUIN into the nucleus basalis magnocellularis (NBM) results in a dose-dependent reduction in cortical cholinergic markers including the evoked release of acetylcholine. A significant reduction in cortical cholinergic function is maintained over a 3-month period. Coinjection of an equimolar ratio of QUIN and KYN into the NBM results in complete protection against QUIN-induced neurodegeneration and decreases in cortical cholinergic markers. In contrast, focal injections of QUIN into the frontoparietal cortex do not alter cortical cholinergic function. Animals showing central cholinergic hypofunction induced by QUIN could serve as experimental models for testing pharmacological agents aimed at improving the function of damaged cholinergic neurons.

APA, Harvard, Vancouver, ISO, and other styles

31

Zhou, Xiaoxin, Jian Lu, Tong Wu, Xuliang Jiang, Weitian Tian, Wanbing Dai, Siyi Qi, Xuemei Chen, Jiaqiang Zhang, and Diansan Su. "Multiple Anesthesia/Surgery Cannot Impair Reference Memory in Adult Mice." Mediators of Inflammation 2020 (March 7, 2020): 1–8. http://dx.doi.org/10.1155/2020/3736912.

Full text

Abstract:

Postoperative cognitive dysfunction increases mortality and morbidity in perioperative patients. Numerous studies have demonstrated that multiple surgery/anesthesia during the neurodevelopmental period affects cognitive function, whereas a single anesthesia/surgery rarely causes cognitive dysfunction in adults. However, whether adults who undergo multiple anesthesia/surgery over a short period will experience cognitive dysfunction remains unclear. In this study, central nervous system inflammation and changes in cholinergic markers were investigated in adult mice subjected to multiple laparotomy procedures over a short period of time. The results showed that despite the increased expression of IL-6 and TNF-α in the hippocampus after multiple operations and the activation of microglia, multiple anesthesia/surgery did not cause a decline in cognitive function in adult mice. There were no changes in the cholinergic markers after multiple anesthesia/surgery.

APA, Harvard, Vancouver, ISO, and other styles

32

Kuol, Nyanbol, Majid Davidson, Jimsheena Karakkat, Rhiannon T. Filippone, Margaret Veale, Rodney Luwor, Sarah Fraser, Vasso Apostolopoulos, and Kulmira Nurgali. "Blocking Muscarinic Receptor 3 Attenuates Tumor Growth and Decreases Immunosuppressive and Cholinergic Markers in an Orthotopic Mouse Model of Colorectal Cancer." International Journal of Molecular Sciences 24, no. 1 (December 29, 2022): 596. http://dx.doi.org/10.3390/ijms24010596.

Full text

Abstract:

Tumor cells have evolved to express immunosuppressive molecules allowing their evasion from the host’s immune system. These molecules include programmed death ligands 1 and 2 (PD-L1 and PD-L2). Cancer cells can also produce acetylcholine (ACh), which plays a role in tumor development. Moreover, tumor innervation can stimulate vascularization leading to tumor growth and metastasis. The effects of atropine and muscarinic receptor 3 (M3R) blocker, 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP), on cancer growth and spread were evaluated in vitro using murine colon cancer cell line, CT-26, and in vivo in an orthotopic mouse model of colorectal cancer. In the in vitro model, atropine and 4-DAMP significantly inhibited CT-26 cell proliferation in a dose dependent manner and induced apoptosis. Atropine attenuated immunosuppressive markers and M3R via inhibition of EGFR/AKT/ERK signaling pathways. However, 4-DAMP showed no effect on the expression of PD-L1, PD-L2, and choline acetyltransferase (ChAT) on CT-26 cells but attenuated M3R by suppressing the phosphorylation of AKT and ERK. Blocking of M3R in vivo decreased tumor growth and expression of immunosuppressive, cholinergic, and angiogenic markers through inhibition of AKT and ERK, leading to an improved immune response against cancer. The expression of immunosuppressive and cholinergic markers may hold potential in determining prognosis and treatment regimens for colorectal cancer patients. This study’s results demonstrate that blocking M3R has pronounced antitumor effects via several mechanisms, including inhibition of immunosuppressive molecules, enhancement of antitumor immune response, and suppression of tumor angiogenesis via suppression of the AKT/ERK signaling pathway. These findings suggest a crosstalk between the cholinergic and immune systems during cancer development. In addition, the cholinergic system influences cancer evasion from the host’s immunity.

APA, Harvard, Vancouver, ISO, and other styles

33

Kirby, Michael, and Brian A. Lawlor. "Biologic Markers and Neurochemical Correlates of Agitation and Psychosis in Dementia." Journal of Geriatric Psychiatry and Neurology 8, no. 1 (October 1995): S2—S7. http://dx.doi.org/10.1177/089198879500800102.

Full text

Abstract:

Behavioral and psychiatric symptoms frequently accompany the cognitive deterioration of dementia occurring in up to 80% of both community-based and nursing home patients. In Alzheimer's disease (AD), behavioral complications may develop at any stage of the disease process and tend to follow a more unpredictable course than the core cognitive symptoms. Over the past 15 years, our knowledge of the biologic and neurochemical basis of dementia, and of AD in particular, has increased significantly. Great emphasis has been placed on the cholinergic system abnormalities in the context of the cognitive impairment in AD and on the psychopharmalogic enhancement of cholinergic transmission in AD. However deficits in other neurotransmitter systems, such as the noradrenergic, serotonergic, and dopaminergic systems, also occur and may contribute to the core cognitive symptoms of AD. More recently, there has been increased interest in the biologic and neurochemical basis of behavioral and psychiatric disturbances in dementia. This article reviews the evidence for biologic and neurochemical correlates of psychosis and agitation in dementia, and discusses the treatment implications for these findings. ( J Geriatr Psychiatry Neurol 1995; 8(suppl 1):S2-S7).

APA, Harvard, Vancouver, ISO, and other styles

34

Hu, Haibei, Qiang Chen, Siqi Zheng, Shan Du, Siqin Ding, and Yongzhi Lun. "Transcriptome Analysis Revealed Potential Neuro-Immune Interaction in Papillary Thyroid Carcinoma Tissues." Diseases 11, no. 1 (January 4, 2023): 9. http://dx.doi.org/10.3390/diseases11010009.

Full text

Abstract:

Background: A recent study reported that papillary thyroid carcinoma (PTC) was associated with increased adrenergic nerve density. Meanwhile, emerging evidence suggested that tumor-innervating nerves might play a role in shaping the tumor microenvironment. We aimed to explore the potential interaction between neuronal markers and tumor microenvironmental signatures through a transcriptomic approach. Methods: mRNA sequencing was conducted using five pairs of PTC and adjacent normal tissues. The Gene Set Variation Analysis (GSVA) was performed to calculate enrichment scores of gene sets related to tumor-infiltrating immune cells and the tumor microenvironment. The potential interaction was tested using the expression levels of a series of neuronal markers and gene set enrichment scores. Results: PTC tissues were associated with increased enrichment scores of CD8 T cells, cancer-associated fibroblasts, mast cells, and checkpoint molecules. The neuronal marker for cholinergic neurons was positively correlated with CD8 T cell activation, while markers for serotonergic and dopaminergic neurons showed an inverse correlation. Conclusion: Distinct neuronal markers exerted different correlations with tumor microenvironmental signatures. Tumor-innervating nerves might play a role in the formation of the PTC microenvironment.

APA, Harvard, Vancouver, ISO, and other styles

35

Sparks, D. Larry, and John C. Hunsaker. "Sudden Infant Death Syndrome: Altered Aminergic-Cholinergic Synaptic Markers in Hypothalamus." Journal of Child Neurology 6, no. 4 (October 1991): 335–39. http://dx.doi.org/10.1177/088307389100600409.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Castro, Veronica S. P., Aleksandro S. Da Silva, Márcio M. Costa, Francine C. Paim, Sydney H. Alves, Sonia T. A. Lopes, Cássia B. Silva, et al. "Cholinergic enzymes and inflammatory markers in rats infected by Sporothrix schenckii." Microbial Pathogenesis 97 (August 2016): 94–102. http://dx.doi.org/10.1016/j.micpath.2016.05.020.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Sugaya, K., R. Greene, D. Personett, M. Robbins, C. Kent, D. Bryan, E. Skiba, M. Gallagher, and M. McKinney. "Septo-hippocampal cholinergic and neurotrophin markers in age-induced cognitive decline." Neurobiology of Aging 19, no. 4 (July 1998): 351–61. http://dx.doi.org/10.1016/s0197-4580(98)00072-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Wevers, Andrea. "Localisation of pre- and postsynaptic cholinergic markers in the human brain." Behavioural Brain Research 221, no. 2 (August 2011): 341–55. http://dx.doi.org/10.1016/j.bbr.2010.02.025.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Henderson, Zaineb. "Lamellar bodies are markers of cholinergic neurons in ferret nucleus basalis." Journal of Neurocytology 18, no. 1 (February 1989): 95–103. http://dx.doi.org/10.1007/bf01188428.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Thiriet, G., J. Kempf, and A. Ebel. "Expression of cholinergic markers in the developing chick embryo spinal cord." International Journal of Developmental Neuroscience 4, no. 5 (1986): 451–59. http://dx.doi.org/10.1016/0736-5748(86)90027-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Donat, Cornelius K., Martin U. Schuhmann, Cornelia Voigt, Karen Nieber, Winnie Deuther-Conrad, and Peter Brust. "Time-dependent alterations of cholinergic markers after experimental traumatic brain injury." Brain Research 1246 (December 2008): 167–77. http://dx.doi.org/10.1016/j.brainres.2008.09.059.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Davis, Kenneth L. "Cholinergic Markers in Elderly Patients With Early Signs of Alzheimer Disease." JAMA 281, no. 15 (April 21, 1999): 1401. http://dx.doi.org/10.1001/jama.281.15.1401.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Martinelli, Ilenia, Seyed Khosrow Tayebati, Proshanta Roy, Maria Vittoria Micioni Di Bonaventura, Michele Moruzzi, Carlo Cifani, Francesco Amenta, and Daniele Tomassoni. "Obesity-Related Brain Cholinergic System Impairment in High-Fat-Diet-Fed Rats." Nutrients 14, no. 6 (March 15, 2022): 1243. http://dx.doi.org/10.3390/nu14061243.

Full text

Abstract:

A link between obesity and cerebral health is receiving growing recognition. Here, we investigate in the frontal cortex and hippocampus the potential involvement of cholinergic markers in brain alterations previously reported in rats with obesity induced by diet (DIO) after long-term exposure (17 weeks) to a high-fat diet (HFD) in comparison with animals fed with a standard diet (CHOW). The obesity developed after 5 weeks of HFD. Bodyweight, systolic blood pressure, glycemia, and insulin levels were increased in DIO rats compared to the CHOW group. Measurements of malondialdehyde (MDA) provided lipid peroxidation in HFD-fed rats. Western blot and immunohistochemical techniques were performed. Our results showed a higher expression of choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) in obese rats but not the VAChT expression in the frontal cortex after 17 weeks of HFD. Furthermore, the acetylcholinesterase (AChE) enzyme was downregulated in HFD both in the frontal cortex and hippocampus. In the brain regions analyzed, it was reported a modulation of certain cholinergic receptors expressed pre- and post-synaptically (alpha7 nicotinic receptor and muscarinic receptor subtype 1). Collectively, these findings point out precise changes of cholinergic markers that can be targeted to prevent cerebral injuries related to obesity.

APA, Harvard, Vancouver, ISO, and other styles

44

Bottini, Gabriella, Manuela Berlingeri, Stefania Basilico, Serena Passoni, Laura Danelli, Nadia Colombo, Maurizio Sberna, Massimo Franceschi, Roberto Sterzi, and Eraldo Paulesu. "GOOD or BAD Responder? Behavioural and Neuroanatomical Markers of Clinical Response to Donepezil in Dementia." Behavioural Neurology 25, no. 2 (2012): 61–72. http://dx.doi.org/10.1155/2012/538542.

Full text

Abstract:

We explored the neuropsychological and neuromorphometrical differences between probable Alzheimer's disease patients showing a good or a bad response to nine months treatment with donepezil. Before treatment, the neuropsychological profile of the two patient groups was perfectly matched. By the ninth month after treatment, theBAD-respondersshowed a decline of the MMSE score together with a progressive impairment of executive functions. A voxel-based morphometry investigation (VBM), at the time of the second neuropsychological assessment, showed that theBAD-respondershad larger grey and white matter atrophies involving the substantia innominata of Meynert bilaterally, the ventral part of caudate nuclei and the left uncinate fasciculus, brain areas belonging to the cholinergic pathways. A more widespread degeneration of the central cholinergic pathways may explain the lack of donepezil efficacy in those patients not responding to a treatment that operates on the grounds that some degree of endogeneous release of acetylcholine is still available.

APA, Harvard, Vancouver, ISO, and other styles

45

Jang, Soomi, Young-Hoon Kang, Imran Ullah, Sharath Shivakumar, Gyu-Jin Rho, Yeong-Cheol Cho, Iel-Yong Sung, and Bong-Wook Park. "Cholinergic Nerve Differentiation of Mesenchymal Stem Cells Derived from Long-Term Cryopreserved Human Dental Pulp In Vitro and Analysis of Their Motor Nerve Regeneration Potential In Vivo." International Journal of Molecular Sciences 19, no. 8 (August 17, 2018): 2434. http://dx.doi.org/10.3390/ijms19082434.

Full text

Abstract:

The reduction of choline acetyltransferase, caused by the loss of cholinergic neurons, leads to the absence of acetylcholine (Ach), which is related to motor nerve degeneration. The aims of the present study were to evaluate the in vitro cholinergic nerve differentiation potential of mesenchymal stem cells from cryopreserved human dental pulp (hDPSCs-cryo) and to analyze the scale of in vivo motor nerve regeneration. The hDPSCs-cryo were isolated and cultured from cryopreserved dental pulp tissues, and thereafter differentiated into cholinergic neurons using tricyclodecane-9-yl-xanthogenate (D609). Differentiated cholinergic neurons (DF-chN) were transplanted into rats to address sciatic nerve defects, and the scale of in vivo motor nerve regeneration was analyzed. During in vitro differentiation, the cells showed neuron-like morphological changes including axonal fibers and neuron body development, and revealed high expression of cholinergic neuron-specific markers at both the messenger RNA (mRNA) and protein levels. Importantly, DF-chN showed significant Ach secretion ability. At eight weeks after DF-chN transplantation in rats with sciatic nerve defects, notably increased behavioral activities were detected with an open-field test, with enhanced low-affinity nerve growth factor receptor (p75NGFR) expression detected using immunohistochemistry. These results demonstrate that stem cells from cryopreserved dental pulp can successfully differentiate into cholinergic neurons in vitro and enhance motor nerve regeneration when transplanted in vivo. Additionally, this study suggests that long-term preservation of dental pulp tissue is worthwhile for use as an autologous cell resource in the field of nerve regeneration, including cholinergic nerves.

APA, Harvard, Vancouver, ISO, and other styles

46

Roßner, S., Reinhard Schliebs, J. R. Perez-Polo, R. G. Wiley, and V. Bigl. "Differential changes in cholinergic markers from selected brain regions after specific immunolesion of the rat cholinergic basal forebrain system." Journal of Neuroscience Research 40, no. 1 (January 1, 1995): 31–43. http://dx.doi.org/10.1002/jnr.490400105.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Barbelivien, Alexandra, Claire Vaussy, Yannick Marchalant, Eric Maubert, Nathalie Bertrand, Alain Beley, Simon Roussel, Eric T. MacKenzie, and François Dauphin. "Degeneration of the Basalocortical Pathway from the Cortex Induces a Functional Increase in Galaninergic Markers in the Nucleus Basalis Magnocellularis of the Rat." Journal of Cerebral Blood Flow & Metabolism 24, no. 11 (November 2004): 1255–66. http://dx.doi.org/10.1097/01.wcb.0000139447.69413.05.

Full text

Abstract:

The present work aimed 1) to evaluate whether an increase in galanin or galanin receptors could be induced in the nucleus basalis magnocellularis (nbm) by degeneration of the basalocortical neurons from the cortex and 2) to analyze the consequences of such an increase on cortical activity. First, a mild ischemic insult to the frontoparietal cortex was performed to induce the degeneration of the basalocortical system; galanin immunoreactivity, galanin binding sites, and cholinergic muscarinic receptors were quantified through immunocytochemistry and autoradiography. Second, galanin infusions in the nbm were undertaken to mimic a local increase of the galaninergic innervation; cortical acetylcholine release, cerebral glucose use, and cerebral blood flow were then measured as indices of cortical activity. As a result of the cortical ischemic lesion, the postsynaptic M1 and presynaptic M2 muscarinic receptors were found to be reduced in the altered cortex. In contrast, galaninergic binding capacity and fiber density were found to be increased in the ipsilateral nbm in parallel with a local decrease in the cholinergic markers such as the muscarinic M1 receptor density. Galanin infusion into the nbm inhibited the cortical acetylcholine release and cerebral blood flow increases elicited by the activation of the cholinergic basalocortical system but failed to affect acetylcholine release, cerebral blood flow, and cerebral glucose use when injected alone in the nbm. These results demonstrate that degeneration of the basalocortical system from the cortex induces an increase in galaninergic markers in the nbm, a result that might suggest that the galaninergic overexpression described in the basal forebrain of patients with Alzheimer's disease can result from a degeneration of the cholinergic basalocortical system from the cortex. Because galanin was found to reduce the activity of the basalocortical cholinergic system only when this one is activated, galanin might exert its role rather during activation deficits than under resting conditions such as the resting cortical hypometabolism, which is characteristic of Alzheimer's disease.

APA, Harvard, Vancouver, ISO, and other styles

48

Muñoz, Sonia Sanz, Martin Engel, Rachelle Balez, Dzung Do-Ha, Mauricio Castro Cabral-da-Silva, Damian Hernández, Tracey Berg, et al. "A Simple Differentiation Protocol for Generation of Induced Pluripotent Stem Cell-Derived Basal Forebrain-Like Cholinergic Neurons for Alzheimer’s Disease and Frontotemporal Dementia Disease Modeling." Cells 9, no. 9 (September 2, 2020): 2018. http://dx.doi.org/10.3390/cells9092018.

Full text

Abstract:

The study of neurodegenerative diseases using pluripotent stem cells requires new methods to assess neurodevelopment and neurodegeneration of specific neuronal subtypes. The cholinergic system, characterized by its use of the neurotransmitter acetylcholine, is one of the first to degenerate in Alzheimer’s disease and is also affected in frontotemporal dementia. We developed a differentiation protocol to generate basal forebrain-like cholinergic neurons (BFCNs) from induced pluripotent stem cells (iPSCs) aided by the use of small molecule inhibitors and growth factors. Ten iPSC lines were successfully differentiated into BFCNs using this protocol. The neuronal cultures were characterised through RNA and protein expression, and functional analysis of neurons was confirmed by whole-cell patch clamp. We have developed a reliable protocol using only small molecule inhibitors and growth factors, while avoiding transfection or cell sorting methods, to achieve a BFCN culture that expresses the characteristic markers of cholinergic neurons.

APA, Harvard, Vancouver, ISO, and other styles

49

Brandstätter, J. H., U. Greferath, T. Euler, and H. Wässle. "Co-stratification of GABAA receptors with the directionally selective circuitry of the rat retina." Visual Neuroscience 12, no. 2 (March 1995): 345–58. http://dx.doi.org/10.1017/s0952523800008026.

Full text

Abstract:

AbstractDirection-selective (DS) ganglion cells of the mammalian retina have their dendrites in the inner plexiform layer (IPL) confined to two narrow strata. The same strata are also occupied by the dendrites of cholinergic amacrine cells which are probably presynaptic to the DS ganglion cells. GABA is known to play a crucial role in creating DS responses. We examined the types of GABAA receptors expressed by the cholinergic amacrine cells and also those expressed by their presynaptic and postsynaptic neurons, by applying immunocytochemical markers to vertical sections of rat retinas. Double-labelling experiments with antibodies against choline acetyltransferase (ChAT) and specific antibodies against different GABAA receptor subunits were performed. Cholinergic amacrine cells seem to express an unusual combination of GABAA receptor subunits consisting of α2-, β1-, β2/3-, γ2-, and δ-subunits. Bipolar cells, which could provide synaptic input to the DS circuitry, were stained with antibodies against the glutamate transporter GLT-1. The axon terminals of these bipolar cells are narrowly stratified in close proximity to the dendritic plexus of displaced cholinergic amacrine cells. The retinal distribution of synaptoporin, a synaptic vesicle associated protein, was studied. Strong reduction of immunolabelling was observed in the two cholinergic strata. The anatomical findings are discussed in the context of models of the DS circuitry of the mammalian retina.

APA, Harvard, Vancouver, ISO, and other styles

50

Patel, Phenil J., William S. Messer, and Richard A. Hudson. "Inhibition and inactivation of presynaptic cholinergic markers using redox-reactive choline analogs." Journal of Medicinal Chemistry 36, no. 13 (June 1993): 1893–901. http://dx.doi.org/10.1021/jm00065a012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Cholinergic markers'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles