Document Detail


Striatal cholinergic interneurons Drive GABA release from dopamine terminals.
MedLine Citation:
PMID:  24613418     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Striatal cholinergic interneurons are implicated in motor control, associative plasticity, and reward-dependent learning. Synchronous activation of cholinergic interneurons triggers large inhibitory synaptic currents in dorsal striatal projection neurons, providing one potential substrate for control of striatal output, but the mechanism for these GABAergic currents is not fully understood. Using optogenetics and whole-cell recordings in brain slices, we find that a large component of these inhibitory responses derive from action-potential-independent disynaptic neurotransmission mediated by nicotinic receptors. Cholinergically driven IPSCs were not affected by ablation of striatal fast-spiking interneurons but were greatly reduced after acute treatment with vesicular monoamine transport inhibitors or selective destruction of dopamine terminals with 6-hydroxydopamine, indicating that GABA release originated from dopamine terminals. These results delineate a mechanism in which striatal cholinergic interneurons can co-opt dopamine terminals to drive GABA release and rapidly inhibit striatal output neurons.
Authors:
Alexandra B Nelson; Nora Hammack; Cindy F Yang; Nirao M Shah; Rebecca P Seal; Anatol C Kreitzer
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural     Date:  2014-03-06
Journal Detail:
Title:  Neuron     Volume:  82     ISSN:  1097-4199     ISO Abbreviation:  Neuron     Publication Date:  2014 Apr 
Date Detail:
Created Date:  2014-04-04     Completed Date:  2014-06-02     Revised Date:  2014-07-16    
Medline Journal Info:
Nlm Unique ID:  8809320     Medline TA:  Neuron     Country:  United States    
Other Details:
Languages:  eng     Pagination:  63-70     Citation Subset:  IM    
Copyright Information:
Copyright © 2014 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / drug effects,  genetics
Animals
Choline O-Acetyltransferase / genetics,  metabolism*
Corpus Striatum / cytology*
Dopamine / metabolism*
Inhibitory Postsynaptic Potentials / drug effects,  genetics
Interneurons / physiology*
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neurotransmitter Agents / pharmacology
Parvalbumins / genetics,  metabolism
Patch-Clamp Techniques
Potassium Channel Blockers / pharmacology
Receptors, Dopamine D1 / genetics,  metabolism
Rhodopsin / genetics
Sodium Channel Blockers / pharmacology
gamma-Aminobutyric Acid / metabolism*
Grant Support
ID/Acronym/Agency:
K08 NS081001/NS/NINDS NIH HHS; K08 NS081001/NS/NINDS NIH HHS; R01 NS049488/NS/NINDS NIH HHS; R01 NS049488/NS/NINDS NIH HHS; R01 NS064984/NS/NINDS NIH HHS; R01 NS064984/NS/NINDS NIH HHS; R01 NS078435/NS/NINDS NIH HHS; R01 NS078435/NS/NINDS NIH HHS; R01 NS082650/NS/NINDS NIH HHS; R01 NS082650/NS/NINDS NIH HHS; R01 NS083872/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Drd1a protein, mouse; 0/Neurotransmitter Agents; 0/Parvalbumins; 0/Potassium Channel Blockers; 0/Receptors, Dopamine D1; 0/Sodium Channel Blockers; 0/channelrhodopsin 2, mouse; 56-12-2/gamma-Aminobutyric Acid; 9009-81-8/Rhodopsin; EC 2.3.1.6/Choline O-Acetyltransferase; VTD58H1Z2X/Dopamine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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