Abstract:
: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.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Inoue T,Miyakawa H,Ito K,Mikoshiba K,Kato Hdoi
10.1016/0168-0102(92)90047-gsubject
Has Abstractpub_date
1992-12-01 00:00:00pages
265-71issue
4eissn
0168-0102issn
1872-8111pii
0168-0102(92)90047-Gjournal_volume
15pub_type
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