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演題詳細

Poster

痛覚、痒み、及びその障害
Pain, Itch and Their Disorders

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

背外側分界条床核におけるコルチコトロピン放出因子による神経情報伝達機構の電気生理学的解析
Electrophysiological analyses of the effects of corticotropin-releasing factor on neuronal excitability in the dorsolateral bed nucleus of the stria terminalis

  • P3-171
  • 兼子 朋之 / Tomoyuki Kaneko:1 井手 聡一郎 / Soichiro Ide:1 原 大樹 / Taiki Hara:1 金田 勝幸 / Katsuyuki Kaneda:1 南 雅文 / Masabumi Minami:1 
  • 1:北海道大学大学院薬学研究院薬理学研究室 / Dept Pharmacol, Grad Sch Pharm Sci, Hokkaido Univ, Sapporo, Japan 

The bed nucleus of the stria terminalis (BNST) is a limbic structure involved in stress responses and negative affective states such as anxiety and fear. Corticotropin-releasing factor (CRF) is also involved in stress responses. Previously, using a conditioned place aversion (CPA) test, we demonstrated that injection of a CRF receptor antagonist into the dorsolateral BNST (dlBNST) suppressed pain-induced aversion. Furthermore, intra-dlBNST CRF injection induced CPA even in the absence of pain stimulation. In the present study, to address cellular mechanisms of CRF-induced CPA, we investigated the effects of CRF on the neuronal excitability in the dlBNST using a whole-cell patch-clamp technique. dlBNST neurons have been categorized into three distinct types (type I-III). We found that CRF depolarized membrane potential specifically in type II dlBNST neurons. Analyses of I-V relationships demonstrated that there may be at least two classes of type II dlBNST neurons, which we designated as type IIa and type IIb, and that CRF depolarized membrane potential by a decrease in potassium conductance and an increase in non-selective cation conductance in the type IIa and type IIb dlBNST neurons, respectively. Depolarizing effects of CRF in type II neurons were blocked by protein kinase A (PKA) inhibitors. Forskolin increased neuronal excitability in type II dlBNST neurons by either a decrease in potassium conductance or an increase in non-selective cation conductance as observed in the CRF-treated type II neurons. In addition, pretreatment with forskolin occluded the depolarizing effects of CRF. These results suggest that depolarizing effects of CRF in type II dlBNST neurons are mediated by an adenylate cyclase-cAMP-PKA pathway.

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