Striatal muscarinic receptors promote activity dependence of dopamine transmission via distinct receptor subtypes on cholinergic interneurons in ventral versus dorsal striatum.Reportar como inadecuado




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Reference: Threlfell, S, Clements, MA, Khodai, T et al., (2010). Striatal muscarinic receptors promote activity dependence of dopamine transmission via distinct receptor subtypes on cholinergic interneurons in ventral versus dorsal striatum. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (9), 3398-3408.Citable link to this page:

 

Striatal muscarinic receptors promote activity dependence of dopamine transmission via distinct receptor subtypes on cholinergic interneurons in ventral versus dorsal striatum.

Abstract: Striatal dopamine (DA) and acetylcholine (ACh) regulate motivated behaviors and striatal plasticity. Interactions between these neurotransmitters may be important, through synchronous changes in parent neuron activities and reciprocal presynaptic regulation of release. How DA signaling is regulated by striatal muscarinic receptors (mAChRs) is unresolved; contradictory reports indicate suppression or facilitation, implicating several mAChR subtypes on various neurons. We investigated whether mAChR regulation of DA signaling varies with presynaptic activity and identified the mAChRs responsible in sensorimotor- versus limbic-associated striatum. We detected DA in real time at carbon fiber microelectrodes in mouse striatal slices. Broad-spectrum mAChR agonists [oxotremorine-M, APET (arecaidine propargyl ester tosylate)] decreased DA release evoked by low-frequency stimuli (1-10 Hz, four pulses) but increased the sensitivity of DA release to presynaptic activity, even enhancing release by high frequencies (e.g., >25 Hz for four pulses). These bidirectional effects depended on ACh input to striatal nicotinic receptors (nAChRs) on DA axons but not GABA or glutamate input. In caudate-putamen (CPu), knock-out of M(2)- or M(4)-mAChRs (not M(5)) prevented mAChR control of DA, indicating that M(2)- and M(4)-mAChRs are required. In nucleus accumbens (NAc) core or shell, mAChR function was prevented in M(4)-knock-outs, but not M(2)- or M(5)-knock-outs. These data indicate that striatal mAChRs, by inhibiting ACh release from cholinergic interneurons and thus modifying nAChR activity, offer variable control of DA release probability that promotes how DA release reflects activation of dopaminergic axons. Furthermore, different coupling of striatal M(2)/M(4)-mAChRs to the control of DA release in CPu versus NAc suggests targets to influence DA/ACh function differentially between striatal domains.

Publication status:Published

Bibliographic Details

Journal: The Journal of neuroscience : the official journal of the Society for Neurosciencesee more from them

Issue Date: 2010-3

pages:3398-3408Identifiers

Urn: uuid:362f74b0-a473-4098-ad95-ab3770e7c946

Source identifier: 113596

Eissn: 1529-2401

Doi: https://doi.org/10.1523/jneurosci.5620-09.2010

Issn: 0270-6474 Item Description

Type: Journal article;

Language: eng Keywords: Animals Mice, Inbred C57BL Mice, Knockout Mice Basal Ganglia Neostriatum Nucleus Accumbens Interneurons Acetylcholine Dopamine Muscarinic Agonists Receptors, Muscarinic Receptor, Muscarinic M2 Receptor, Muscarinic M4 Receptors, Nicotinic Patch-Clamp Techniques Synaptic Transmission Presynaptic Terminals Organ Culture Techniques Corpus Striatum Electrophysiology Tiny URL: pubs:113596

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Autor: Threlfell, S - institutionUniversity of Oxford Oxford, MSD, Physiology Anatomy and Genetics - - - Clements, MA - - - Khodai, T -

Fuente: https://ora.ox.ac.uk/objects/uuid:362f74b0-a473-4098-ad95-ab3770e7c946



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