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This Article Full Text Full Text (PDF) All Versions of this Article: 586/21/5091    most recent jphysiol.2008.158576v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Bright, D. P. Articles by Brickley, S. G. PubMed PubMed Citation Articles by Bright, D. P. Articles by Brickley, S. G. Related Collections Neuroscience

¹ Biophysics Section, Imperial College London, South Kensington Campus, London SW7 2AZ, UK

We have discovered that adult thalamocortical relay neurones exhibit a sustained enhancement of synaptic inhibition triggered by transient action potential firing of a single thalamic relay neurone. The sustained activity-dependent increase in IPSC frequency (+48.3 ± 11.4%, n = 32) was blocked by chelating calcium inside an individual cell, by scavenging nitric oxide or by blocking NMDA receptor activation in the thalamus. Surprisingly, the tonic inhibition that is known to result from extrasynaptic GABA_A receptor activation in these cells was unaffected by this local form of plasticity. However, tonic inhibition was increased (+131.9 ± 56.5%, n = 13) following widespread changes in GABA release across the thalamus. These data suggest that thalamocortical sleep-state oscillations requiring membrane hyperpolarization will be influenced by global sensing of GABA release acting through extrasynaptic GABA_A receptors. In contrast, local changes in GABA release of the type observed following this novel form of activity-dependent plasticity will influence local integration of sensory information without changing levels of tonic inhibition.

first published online 3 September 2008)
Corresponding author S. G. Brickley: Biophysics Section, Imperial College London, South Kensington Campus, London SW7 2AZ, UK. Email: s.brickley{at}imperial.ac.uk