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Mechanisms controlling expression and memory of emotions

開催日 2014/9/11
時間 14:00 - 16:00
会場 Room D(503)
Chairperson(s) 貝淵 弘三 / Kozo Kaibuchi (名古屋大学大学院医学系研究科 / Nagoya University Graduate School of Medicine, Japan)
南 雅文 / Masabumi Minami (北海道大学大学院薬学研究院薬理学研究室 / Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Japan)

Opposing effects of CRF and NPY on neuronal excitability in the BNST: Role in pain-induced aversion

  • S1-D-1-3
  • 南 雅文 / Masabumi Minami:1 
  • 1:北海道大院薬薬理 / Dept Pharmacol, Grad Sch Pharm Sci, Hokkaido Univ, Hokkaido, Japan 

Pain has sensory-discriminative and negative-affective components. Although the neural systems underlying the sensory component of pain have been studied extensively, the mechanisms underlying the affective component of pain are far from being clarified. In the present study, we examined the effects of corticotropin-releasing factor (CRF) and neuropeptide Y (NPY) injected into the dorsolateral bed nucleus of the stria terminalis (dlBNST) on pain-induced aversion and nociceptive behaviors in rats to examine the roles of these peptides in affective and sensory components of pain, respectively. Using a conditioned place aversion (CPA) test, we found that intra-dlBNST injections of CRF receptor antagonists suppressed pain-induced aversion. Intra-dlBNST CRF injection induced CPA even in the absence of pain stimulation. On the other hand, intra-dlBNST NPY injection suppressed pain-induced aversion. Co-administration of NPY inhibited CRF-induced CPA. Furthermore, whole-cell patch-clamp electrophysiology in dlBNST slices revealed that CRF increased neuronal excitability specifically in type II dlBNST neurons, whereas NPY decreased it in these neurons. Excitatory effects of CRF on type II dlBNST neurons were suppressed by NPY. These results have uncovered some of the neuronal mechanisms underlying the affective component of pain by showing opposing effects of intra-dlBNST CRF and NPY in pain-induced aversion and opposing actions of these peptides on neuronal excitability converging on the same target, type II neurons, in the dlBNST.

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