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Signal Transduction and Modulation

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Two Distinct Types of Adrenoceptors Modurate Network Activity in The Central Nucleus of Amygdala

  • P3-004
  • 山本 純偉 / Sumii Yamamoto:1 高橋 由香里 / Yukari Takahashi:2 渡部 文子 / Ayako Watabe:2 加藤 総夫 / Fusao Kato:2 
  • 1:筑波大学 / University of Tsukuba 2:慈恵会医科大学 神経生理 / Dept Neurosci, Jikei Univ Sch Med, Tokyo, Japan 

The central nucleus of amygdala (CeA) plays essential role in emotional memory formation. The neurons in the medial division of the central nucleus of amygdala (CeM) receive inhibitory inputs from the lateral and capsular divisions of CeA (CeL and CeC, respectively) and project to the extra-amygdala nuclei involved in emotion-related responses. Noradrenaline (NA), a primary stress hormone in the CNS, has been shown to facilitate emotional memory formation but it remains unexplored how NA affects the synaptic and intrinsic excitability of neurons in the CeM. Last year, we reported NA (50 µM ) dramatically increased the frequency and amplitude of spontaneous IPSC (sIPSC) of CeM neurons in a manner sensitive to propranolol (40 µM ). In addition, NA increased intracellular Ca2+ concentration in a large majority of CeA neurons as visualized with a confocal laser-scanning microscopy-based Ca2+ imaging. A subset of CeL/CeC neurons showed increased intracellular Ca2+ following NA application in a manner sensitive to cyclopiazonic acid (20 µM), an inhibitor of sarcoplasmic reticulum calcium-ATPase and extracellular removal of Ca2+, but not to tetrodotoxin.
Thus, to confirm an involvement of Gq-coupled α-1 receptors, we analyzed the effects of an agonist and an antagonist of α-1 adrenoceptors on sIPSC in CeM neurons. Pharmacologically isolated GABAergic sIPSCs were recorded from neurons in the CeM in acute brain slices prepared from 3-8 weeks-old C57BL/6 mice using whole-cell patch-clamp technique. NA and other drugs were added to external solution and applied in the bath. Phenylephrine (10 µM) reversibly increased sIPSC frequency (P=0.013). Mean event amplitude was increased, which was not significant. Prazosin (10 µM) suppressed the incremental effects of NA on sIPSC frequency and mean event amplitude. Interestingly, the effects of NA on sIPSC in the CeM were sensitive both to propranolol and prazosin. A possible interpretation is that CeM neuron excitability is regulated by inhibitory inputs from the CeL/CeC through α-1 receptor-mediated processes and from unidentified cell populations that are excited by β receptor activation.

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