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This Article Full Text Full Text (PDF) All Versions of this Article: 96/1/86    most recent 01282.2005v2 01282.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Glitsch, M. Search for Related Content PubMed PubMed Citation Articles by Glitsch, M.

Selective Inhibition of Spontaneous But Not Ca²⁺-Dependent Release Machinery by Presynaptic Group II mGluRs in Rat Cerebellar Slices

Department of Physiology, Anatomy and Genetics, Oxford University, Oxford, United Kingdom

Submitted 6 December 2005; accepted in final form 9 April 2006

Two main forms of neurotransmitter release are known: action potential-evoked and spontaneous release. Action potential-evoked release depends on Ca²⁺ entry through voltage-gated Ca²⁺ channels, whereas spontaneous release is thought to be Ca²⁺-independent. Generally, spontaneous and action potential-evoked release are believed to use the same release machinery to release neurotransmitter. This study shows, using the whole cell patch-clamp technique in rat cerebellar slices, that at the interneuron- Purkinje cell synapse activation of presynaptic group II metabotropic glutamate receptors suppresses spontaneous GABA release through a mechanism independent of voltage-gated Ca²⁺ channels, store-operated Ca²⁺ channels, and Ca²⁺ release from intracellular Ca²⁺ stores, suggesting that the metabotropic receptors target the release machinery directly. Voltage gated Ca²⁺ channel-independent release following increased presynaptic cAMP production is similarly inhibited by these metabotropic receptors. In contrast, both voltage-gated Ca²⁺ channel-dependent and presynaptic N-methyl-D-aspartate receptor-dependent GABA release were unaffected by activation of group II metabotropic glutamate receptors. Hence, the mechanisms underlying spontaneous and Ca²⁺-dependent GABA release are distinct in that only the former is blocked by group II metabotropic glutamate receptors. Thus the same neurotransmitter, glutamate, can activate or inhibit neurotransmitter release by selecting different receptors that target different release machineries.