A hyperpolarizing response induced by glutamate in mouse cerebellar Purkinje cells.
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 Ca(2+)-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.
Inoue
T
T
Department of Physiology, Yamagata University School of Medicine, Japan.
Miyakawa
H
H
Ito
K
K
Mikoshiba
K
K
Kato
H
H
D000818:Animals; D002118:Calcium / Q000502:physiology; D002531:Cerebellum / Q000166:cytology / Q000502:physiology*; D004594:Electrophysiology; D005470:Fluorometry; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D066298:In Vitro Techniques; D007395:Interneurons / Q000187:drug effects; D007478:Iontophoresis; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008813:Mice, Inbred ICR; D015221:Potassium Channels / Q000187:drug effects; D011689:Purkinje Cells / Q000187:drug effects*; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism; D013569:Synapses / Q000187:drug effects; D013779:Tetrodotoxin / Q000494:pharmacology
D005971:Glutamates; D015221:Potassium Channels; D017470:Receptors, Glutamate; D018698:Glutamic Acid; D013779:Tetrodotoxin; D002118:Calcium