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Tytuł:
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Inhibition of Nigrostriatal Dopamine Release by Striatal GABA A and GABA B Receptors.
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Autorzy:
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Lopes EF; Centre for Integrative Neuroscience, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom, and.
Roberts BM; Centre for Integrative Neuroscience, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom, and.
Siddorn RE; Centre for Integrative Neuroscience, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom, and.
Clements MA; Centre for Integrative Neuroscience, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom, and.
Cragg SJ; Centre for Integrative Neuroscience, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, United Kingdom, and .; Oxford Parkinson's Disease Centre, Oxford OX1 3PT, United Kingdom.
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Źródło:
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The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 2019 Feb 06; Vol. 39 (6), pp. 1058-1065. Date of Electronic Publication: 2018 Dec 12.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: Washington, DC : Society for Neuroscience
Original Publication: [Baltimore, Md.] : The Society, c1981-
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MeSH Terms:
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Corpus Striatum/*metabolism
Dopamine/*metabolism
Receptors, GABA-A/*metabolism
Receptors, GABA-B/*metabolism
Substantia Nigra/*metabolism
Animals ; Axons/metabolism ; Cholinergic Antagonists/pharmacology ; Dihydro-beta-Erythroidine/pharmacology ; Electric Stimulation ; GABA Agonists/pharmacology ; GABA Antagonists/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Optogenetics ; Parasympathetic Nervous System/drug effects ; Parasympathetic Nervous System/metabolism ; Receptors, GABA-A/drug effects ; Receptors, GABA-B/drug effects ; gamma-Aminobutyric Acid/metabolism
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References:
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Grant Information:
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G0700932 United Kingdom MRC_ Medical Research Council; G-1504 United Kingdom PUK_ Parkinson's UK; United Kingdom BB_ Biotechnology and Biological Sciences Research Council; MR/K013866/1 United Kingdom MRC_ Medical Research Council; MR/J004324/1 United Kingdom MRC_ Medical Research Council; J-0901 United Kingdom PUK_ Parkinson's UK
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Contributed Indexing:
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Keywords: GABA; dopamine; presynaptic; striatum; voltammetry
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Substance Nomenclature:
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0 (Cholinergic Antagonists)
0 (GABA Agonists)
0 (GABA Antagonists)
0 (Receptors, GABA-A)
0 (Receptors, GABA-B)
23255-54-1 (Dihydro-beta-Erythroidine)
56-12-2 (gamma-Aminobutyric Acid)
VTD58H1Z2X (Dopamine)
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Entry Date(s):
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Date Created: 20181214 Date Completed: 20191211 Latest Revision: 20210211
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Update Code:
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20240105
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PubMed Central ID:
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PMC6363932
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DOI:
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10.1523/JNEUROSCI.2028-18.2018
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PMID:
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30541909
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Nigrostriatal dopamine (DA) is critical to action selection and learning. Axonal DA release is locally influenced by striatal neurotransmitters. Striatal neurons are principally GABAergic projection neurons and interneurons, and a small minority of other neurons are cholinergic interneurons (ChIs). ChIs strongly gate striatal DA release via nicotinic receptors (nAChRs) identified on DA axons. Striatal GABA is thought to modulate DA, but GABA receptors have not been documented conclusively on DA axons. However, ChIs express GABA receptors and are therefore candidates for potential mediators of GABA regulation of DA. We addressed whether striatal GABA and its receptors can modulate DA release directly, independently from ChI regulation, by detecting DA in striatal slices from male mice using fast-scan cyclic voltammetry in the absence of nAChR activation. DA release evoked by single electrical pulses in the presence of the nAChR antagonist dihydro-β-erythroidine was reduced by GABA or agonists of GABA A or GABA B receptors, with effects prevented by selective GABA receptor antagonists. GABA agonists slightly modified the frequency sensitivity of DA release during short stimulus trains. GABA agonists also suppressed DA release evoked by optogenetic stimulation of DA axons. Furthermore, antagonists of GABA A and GABA B receptors together, or GABA B receptors alone, significantly enhanced DA release evoked by either optogenetic or electrical stimuli. These results indicate that striatal GABA can inhibit DA release through GABA A and GABA B receptors and that these actions are not mediated by cholinergic circuits. Furthermore, these data reveal that there is a tonic inhibition of DA release by striatal GABA operating through predominantly GABA B receptors. SIGNIFICANCE STATEMENT The principal inhibitory transmitter in the mammalian striatum, GABA, is thought to modulate striatal dopamine (DA) release, but definitive evidence for GABA receptors on DA axons is lacking. Striatal cholinergic interneurons regulate DA release via axonal nicotinic receptors (nAChRs) and also express GABA receptors, but they have not been eliminated as potentially critical mediators of DA regulation by GABA. Here, we found that GABA A and GABA B receptors inhibit DA release without requiring cholinergic interneurons. Furthermore, ambient levels of GABA inhibited DA release predominantly through GABA B receptors. These findings provide further support for direct inhibition of DA release by GABA receptors and reveal that striatal GABA operates a tonic inhibition on DA output that could critically influence striatal output.
(Copyright © 2019 the authors 0270-6474/19/391058-08$15.00/0.)