期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 591, 期 22, 页码 5745-5763出版社
WILEY-BLACKWELL
DOI: 10.1113/jphysiol.2013.258558
关键词
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资金
- JSPS KAKENHI [23890216]
- Japanese Ministry of Education, Culture, Sports, Science and Technology [25293379]
- Dental Research Centre, Nihon University School of Dentistry
- Promotion and Mutual Aid Corporation for Private Schools of Japan
- Uemura Fund
- Grants-in-Aid for Scientific Research [25293379, 23890216, 25861764, 25463150] Funding Source: KAKEN
Medium spiny neurones (MSNs) in the nucleus accumbens (NAc) are the principal neurones whose activities are regulated by GABAergic inputs from MSNs and fast-spiking interneurones (FSNs). Cholinergic interneurones play important roles in the regulation of activity in MSNs; however, how acetylcholine modulates inhibitory synaptic transmission from MSNs/FSNs to MSNs remains unknown. We performed paired whole-cell patch-clamp recordings from MSNs and FSNs in rat NAc shell slice preparations and examined cholinergic effects on unitary inhibitory postsynaptic currents (uIPSCs). Carbachol (1 m) suppressed uIPSC amplitude by 58.3 +/- 8.0% in MSNMSN connections, accompanied by increases in paired-pulse ratio and failure rate, suggesting that acetylcholine reduces the probability of GABA release from the synaptic terminals of MSNs. Carbachol-induced uIPSC suppression was antagonised by 100 m atropine, and was mimicked by pilocarpine (1 m) and acetylcholine (1 m) but not nicotine (1 m). Application of AM251 slightly reduced carbachol-induced uIPSC suppression (30.8 +/- 8.9%), suggesting an involvement of endocannabinoid signalling in muscarinic suppression of uIPSCs. In contrast, FSNMSN connections showed that pilocarpine had little effect on the uIPSC amplitude, whereas both nicotine and acetylcholine facilitated uIPSC amplitude, with decreases in failure rate and paired-pulse ratio, suggesting that nicotine-induced uIPSC facilitation is mediated by presynaptic mechanisms. Miniature IPSC recordings support these hypotheses of presynaptic cholinergic mechanisms. These results suggest a differential role for muscarinic and nicotinic receptors in GABA release, which depends on presynaptic neuronal subtypes in the NAc shell.
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