ナカヤマ ヒサコ   Hisako Nakayama
  中山 寿子
   所属   医学部 医学科
   職種   助教
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 GABAergic activation of an inwardly rectifying K+ current in mouse cerebellar Purkinje cells.
掲載誌名 正式名:The Journal of physiology
略  称:J Physiol
ISSNコード:00223751/14697793
掲載区分国外
巻・号・頁 563(Pt 2),443-457頁
著者・共著者 TABATA Toshihide†, HARUKI Shigeki†, NAKAYAMA Hisako, KANO Masanobu*
発行年月 2005/03
概要 Cerebellar Purkinje cells integrate motor information conveyed by excitatory synaptic inputs from parallel and climbing fibres. Purkinje cells abundantly express B-type G-protein-coupled γ-aminobutyric acid receptors (GABABR) that are assumed to mediate major responses, including postsynaptic modulation of the synaptic inputs. However, the identity and function of effectors operated by GABABR are not fully elucidated. Here we characterized an inwardly rectifying current activated by baclofen (Ibacl), a GABABR agonist, in cultured mouse Purkinje cells using a ruptured-patch whole-cell technique. Ibacl is operated by GABABR via Gi/o-proteins, as it is not inducible in pertussis-toxin-pretreated cells. Ibacl is carried by K+ because its reversal potential shifts with the equilibrium potential of K+. Ibacl is blocked by 10−3m Ba2+ or Cs+, and 10−8m tertiapin-Q. Upon the onset and offset of a hyperpolarizing step, Ibacl is activated and deactivated, respectively, with double-exponential time courses (time constants, <1 ms and 30–80 ms). Based on similarities in the above properties, G-protein-coupled inwardly rectifying K+ (GIRK) channels are thought to be responsible for Ibacl. Perforated-patch recordings from cultured Purkinje cells demonstrate that Ibacl hyperpolarizes the resting potential and the peak level achieved by glutamate-evoked potentials initiated in the dendrites. Moreover, cell-attached recordings from Purkinje cells in cerebellar slices demonstrate that Ibacl impedes spontaneous firing. Therefore, Ibacl may reduce the postsynaptic and intrinsic excitability of Purkinje cells under physiological conditions. These findings give a new insight into the role of GABABR signalling in cerebellar information processing.
DOI 10.1113/jphysiol.2004.081000
PMID 15637097