A hyperpolarizing response induced by glutamate in mouse cerebellar Purkinje cells

Takafumi Inoue*, Hiroyoshi Miyakawa, Ken ichi Ito, Katsuhiko Mikoshiba, Hiroshi Kato

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


In the vertebrate nervous system, glutamate (Glu) receptors are generally known to cause depolarizing responses. We report here a novel type of Glu response in Purkinje neurons of mouse cerebellar slices, namely glutamate-induced hyperpolarization (GH). This response is not due to activation of inhibitory interneurons, because application of tetrodotoxin (TTX), bicuculline, or strychnine did not abolish GH. In addition, GH persisted in a Ca2+-free or a low-Cl- solution, which rules out the involvement of gK(Ca) or GABAA mechanisms. Quisqualate (Quis) and trans-1-amino-1,3-cyclopentanedicarboxylic acid (tACPD), which are potent and selective agonists, respectively, for the metabotropic Glu receptor (mGluR), failed to induce GH. l-2-Amino-4-phosphonobutyric acid (l-AP4) was also ineffective. Simultaneous recording of electrical activity and intracellular Ca2+ concentration ([Ca2+]i) showed that GH was not accompanied by [Ca2+]i changes. Voltage clamp experiments showed that GH is due to reduction of a tonically active conductance with a reversal potential around 0 mV. Two possible mechanisms are suggested for GH: (1) changes in the desensitized steady state of ionotropic Glu receptors, or (2) a novel Glu-mediated mechanism.

Original languageEnglish
Pages (from-to)265-271
Number of pages7
JournalNeuroscience Research
Issue number4
Publication statusPublished - 1992 Dec
Externally publishedYes


  • Brain slice
  • Cerebellum
  • Glutamate
  • Hyperpolarization
  • Iontophoresis
  • Purkinje cell

ASJC Scopus subject areas

  • Neuroscience(all)


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