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The Journal of Neuroscience, March 7, 2007, 27(10):2560-2569; doi:10.1523/JNEUROSCI.5100-06.2007
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Cellular/Molecular
Synaptic Release Generates a Tonic GABAA Receptor-Mediated Conductance That Modulates Burst Precision in Thalamic Relay Neurons
Damian P. Bright,1
M. Isabel Aller,2 and
Stephen G. Brickley1
1Biophysics Section, Blackett Laboratory, Imperial College, London SW7 2AZ, United Kingdom, and 2Instituto de Neurociencias de Alicante, Consejo Superior de Investigaciones Científicas–Universidad Miguel Hernandez, 03550 Sant Joan d'Alacant, Spain
Correspondence should be addressed to Dr. Stephen G. Brickley, Biophysics Section, Blackett Laboratory, Imperial College, South Kensington, London SW7 2AZ, UK. Email: s.brickley{at}imperial.ac.uk
Tonic inhibition has emerged as a key regulator of neuronal excitability in the CNS. Thalamic relay neurons of the dorsal lateral geniculate nucleus (dLGN) exhibit a tonic GABAA receptor (GABAAR)-mediated conductance that is correlated with  -subunit expression. Indeed, consistent with the absence of -subunit expression, no tonic conductance is found in the adjacent ventral LGN. We show that, in contrast to the situation in cerebellar granule cells, thalamic -subunit-containing GABAARs (-GABAARs) do not contribute to a spillover component of IPSCs in dLGN. However, tonic activation of thalamic -GABAARs is sensitive to the global level of inhibition, showing an absolute requirement on the synaptic release of GABA. Thus, the tonic conductance is abolished when transmitter release probability is reduced or action potential-evoked release is blocked. We further show that continuous activation of -GABAARs introduces variability into the timing of low-threshold rebound bursts. Hence, activation of -GABAARs could act to destabilize thalamocortical oscillations and therefore have an important impact on behavioral state.
Key words: GABAA receptor; -subunit; tonic inhibition; synaptic release; thalamic relay neuron; burst firing
Received Nov. 24, 2006;
revised Jan. 10, 2007;
accepted Feb. 1, 2007.
Correspondence should be addressed to Dr. Stephen G. Brickley, Biophysics Section, Blackett Laboratory, Imperial College, South Kensington, London SW7 2AZ, UK. Email: s.brickley{at}imperial.ac.uk
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