Axonal GABAA receptors increase cerebellar granule cell excitability and synaptic activity

Jason R. Pugh, Craig E. Jahr

Research output: Contribution to journalArticle

46 Scopus citations

Abstract

We report that activation of GABAAreceptors on cerebellar granule cell axons modulates both transmitter release and the excitability of the axon and soma. Axonal GABAAreceptors depolarize the axon, increasing its excitability and causing calcium influx at axonal varicosities. GABA-mediated subthreshold depolarizations in the axon spread electrotonically to the soma, promoting orthodromic action potential initiation. When chloride concentrations are unperturbed, GABA iontophoresis elicits spikes and increases excitability of parallel fibers, indicating that GABAAreceptor- mediated responses are normally depolarizing. GABA release from molecular layer interneurons activates parallel fiber GABAAreceptors, and this, in turn, increases release probability at synapses between parallel fibers and molecular layer interneurons. These results describe a positive feedback mechanism whereby transmission from granule cells to Purkinje cells and molecular layer interneurons will be strengthened during granule cell spike bursts evoked by sensory stimulation.

Original languageEnglish (US)
Pages (from-to)565-574
Number of pages10
JournalJournal of Neuroscience
Volume31
Issue number2
DOIs
StatePublished - Jan 12 2011
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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