期刊
NEUROPEPTIDES
卷 56, 期 -, 页码 115-123出版社
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.npep.2015.08.008
关键词
Oxytocin; Paraventricular nucleus; Fasting; Feeding; Synaptic plasticity; NMDA receptor; Slice patch clamp; DYNLL2; Proteomics
资金
- Japan Society for the Promotion of Science (JSPS) [23390044, 24659101, 26670453]
- Strategic Research Program for Brain Sciences by the Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT) [10036069]
- MEXT [S1101022, S1311029]
- Salt Science Research Foundation [1434]
- KEIRIN RACE
- Grants-in-Aid for Scientific Research [24659101] Funding Source: KAKEN
The neurons in the hypothalamus regulate food intake and energy metabolism on reception of systemic energy states. Accumulating evidences have indicated that synaptic transmission on the hypothalamic neurons is modulated by the metabolic condition related to fasted/fed states, and that this modulation of synaptic plasticity plays a role in regulation of feeding. It has been shown that oxytocin (Oxt) neurons in the paraventricular nucleus (PVN) of the hypothalamus sense and integrate various peripheral and central signals and thereby induce satiety. However, whether metabolic conditions regulate the synaptic transmission on Oxt neurons in PVN remains unclear. The present study examined whether the fasted/fed states regulate synaptic transmission on Oxt neurons in PVN. The miniature excitatory postsynaptic currents (mEPSCs) onto Oxt neurons in PVN were increased under ad lib fed condition compared to 24 h fasted condition. Furthermore, the NMDA receptor-mediated EPSC on Oxt neurons was increased under fed, compared to fasted, condition. In Oxt neurons, dynein light chain 2 (DYNLL2), a protein suggested to be implicated in the NMDA receptor trafficking to the postsynaptic site, was increased under fed, compared to fasted, condition. The present results suggest that feeding increases excitatory synaptic input on PVN Oxt neurons via mechanisms involving DYNLL2 upregulation and NMDA receptor-mediated synaptic reorganization. (C) 2015 Elsevier Ltd. All rights reserved.
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