|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Cellular Neurophysiology, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan
2 Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan
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
-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 103
M Ba2+ or Cs+, and 108
M 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 3080 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.
(Received 11 December 2004;
accepted after revision 4 January 2005;
first published online 6 January 2005)
Corresponding author M. Kano: Department of Cellular Neurophysiology, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. Email: mkano{at}med.kanazawa-u.ac.jp
This article has been cited by other articles:
![]() |
Y. Kamikubo, T. Tabata, S. Kakizawa, D. Kawakami, M. Watanabe, A. Ogura, M. Iino, and M. Kano Postsynaptic GABAB receptor signalling enhances LTD in mouse cerebellar Purkinje cells J. Physiol., December 1, 2007; 585(2): 549 - 563. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Tabata, D. Kawakami, K. Hashimoto, H. Kassai, T. Yoshida, Y. Hashimotodani, B. B. Fredholm, Y. Sekino, A. Aiba, and M. Kano G protein-independent neuromodulatory action of adenosine on metabotropic glutamate signalling in mouse cerebellar Purkinje cells J. Physiol., June 1, 2007; 581(2): 693 - 708. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |