Heterogeneity of presynaptic muscarinic receptors involved in modulation of transmitter release

Vizi, E.S.; Kobayashi, Osamu; Töröcsik, A.; Kinjo, M.; Nagashima, Hideo; Manabe, N.; Goldiner, Paul L.; Potter, Pamela E.; Foldes, Francis F.

doi:10.1016/0306-4522(89)90048-1

Cited by 73 publications

(33 citation statements)

References 36 publications

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“…Synaptic vesicles (and SLMVs in PC12 cells) package and release neurotransmitters such as acetylcholine, -aminobutyric acid and glutamate, to mediate crosstalk between neurons (Blusztajn and Berse, 2000;Parsons et al, 1993;Vizi et al, 1989;Weihe et al, 1996) and between neuroendocrine cells (Bauerfeind et al, 1993), whereas LDCVs secrete monoamines and various neuropeptides for neurotransmission and to modulate neurophysiological homeostasis. Nonetheless, it is thought that synaptic vesicles and SLMVs share many components (e.g.…”

Section: Discussionmentioning

confidence: 99%

A distinct trans-Golgi network subcompartment for sorting of synaptic and granule proteins in neurons and neuroendocrine cells

Park

Gondré–Lewis

Eiden

et al. 2011

Journal of Cell Science

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SummaryGolgi-to-plasma-membrane trafficking of synaptic-like microvesicle (SLMV) proteins, vesicular acetylcholine transporter (VAChT) and synaptophysin (SYN), and a large dense-core vesicle (LDCV) protein, chromogranin A (CgA), was investigated in undifferentiated neuroendocrine PC12 cells. Live cell imaging and 20°C block-release experiments showed that VAChT-GFP, SYN-GFP and CgA-RFP specifically and transiently cohabitated in a distinct sorting compartment during cold block and then separated into synaptic protein transport vesicles (SPTVs) and LDCVs, after release from temperature block. We found that in this trans-Golgi subcompartment there was colocalization of SPTV and LDCV proteins, most significantly with VAMP4 and Golgin97, and to some degree with TGN46, but not at all with TGN38. Moreover, some SNAP25 and VAMP2, two subunits of the exocytic machinery, were also recruited onto this compartment. Thus, in neuroendocrine cells, synaptic vesicle and LDCV proteins converge briefly in a distinct trans-Golgi network subcompartment before sorting into SPTVs and LDCVs, ultimately for delivery to the plasma membrane. This specialized sorting compartment from which SPTVs and LDCVs bud might facilitate the acquisition of common exocytic machinery needed on the membranes of these vesicles.

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Section: Discussionmentioning

confidence: 99%

A distinct trans-Golgi network subcompartment for sorting of synaptic and granule proteins in neurons and neuroendocrine cells

Park

Gondré–Lewis

Eiden

et al. 2011

Journal of Cell Science

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“…Muscarinic receptors can be found on cholinergic and noncholinergic cells, both as auto-and heteroreceptors. [46][47][48][49] Molecular cloning strategies revealed five different muscarinic receptors (M 1 -M 5 ) that can be distinguished pharmacologically 50 and that are encoded by five different genes (m1-m5). [51][52][53][54] All five subtypes of the muscarinic receptors are found in the human CNS, albeit in regionally varying concentrations.…”

Section: Muscarinic Receptorsmentioning

confidence: 99%

Towards a muscarinic hypothesis of schizophrenia

Raedler

Bymaster

Tandon³

et al. 2006

Mol Psychiatry

247

211

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Although the neurotransmitter dopamine plays a prominent role in the pathogenesis and treatment of schizophrenia, the dopamine hypothesis of schizophrenia fails to explain all aspects of this disorder. It is increasingly evident that the pathology of schizophrenia also involves other neurotransmitter systems. Data from many streams of research including preclinical and clinical pharmacology, treatment studies, post-mortem studies and neuroimaging suggest an important role for the muscarinic cholinergic system in the pathophysiology of schizophrenia. This review will focus on evidence that supports the hypothesis that the muscarinic system is involved in the pathogenesis of schizophrenia and that muscarinic receptors may represent promising novel targets for the treatment of this disorder.

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“…[18] Studies in the guinea pig ileum demonstrated that M1 receptors modulate acetylcholine release from neurons. [19][20][21] M2 receptors are found in the heart. M3 and M4 receptors are reported to be genetically expressed in the smooth muscle, thus facilitating contraction of smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

A comparative study of in vitro contractility between gut tissues of Hirschsprung's disease and other gut malformations

Tiwari¹,

Singh²,

Pandey³

et al. 2017

Natl J Physiol Pharm Pharmacol

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Background: Hirschsprung's disease and other gut malformations commonly present with obstructive features of gut in pediatric age group. Problem of obstruction persists even after resection and anastomosis operation. Aims and Objectives: This in vitro comparative study was performed to assess the gut contractility to chemical mediators such as Acetylcholine and Histamine between Hirschsprung's disease and other gut malformations. Materials and Methods: The longitudinal muscle strips of Hirschsprung's cases and other gut malformations (non-Hirschsprung's cases) were placed in Dales organ bath containing Krebs-Ringer solution, continuously bobbled with 100% O2 at 28°C. Gut contractions were recorded using Power Lab 4/ST system and was analyzed using software CHART-5 for windows. Control contractions were recorded against initial tension of 0.5 g. Subsequently, agonist (acetylcholine, histamine)-induced contractions were recorded before and after appropriate antagonists (atropine, pheniramine). Before values of agonist-induced contractions of Hirschsprung and non-Hirschsprung's cases were compared. Values of agonistinduced contractions obtained after pretreatment with antagonists were also compared between Hirschsprung and nonHirschsprung's cases. Results: Acetylcholine enhanced contractions in non-Hirschsprung's cases and it caused small increase in amplitude of contractions in Hirschsprung's cases. Atropine pretreatment blocked acetylcholine-induced contractions significantly in non-Hirschsprung's cases, whereas it failed to block in the Hirschsprung's cases. Histamine augmented contractions in both Hirschsprung and non-Hirschsprung's cases. H1 antagonist, pheniramine failed to block the contractility in both the cases. Conclusion: Findings of this study suggested that acetylcholine increased gut contractility significantly in non-Hirschsprung's cases involving muscarinic-cholinergic pathways, whereas histamine increased gut contractility in both Hirschsprung's disease and non-Hirschsprung's cases and it is not mediated by H1 receptors.

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Heterogeneity of presynaptic muscarinic receptors involved in modulation of transmitter release

Cited by 73 publications

References 36 publications

A distinct trans-Golgi network subcompartment for sorting of synaptic and granule proteins in neurons and neuroendocrine cells

A distinct trans-Golgi network subcompartment for sorting of synaptic and granule proteins in neurons and neuroendocrine cells

Towards a muscarinic hypothesis of schizophrenia

A comparative study of in vitro contractility between gut tissues of Hirschsprung's disease and other gut malformations

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