Abstract
The inhibitory neurotransmitter GABA activates both ionotropic type A GABA receptors (GABAARs) and metabotropic GABAB receptors (GABABRs). Two independent studies in rat brain slices now show that activation of postsynaptic GABABRs enhances signalling through extrasynaptic GABAARs. Activity-dependent changes in GABA concentration activate postsynaptic GABABRs leading to slow inhibition, whereas high-affinity GABAARs at extrasynaptic sites are activated tonically by ambient GABA. This tonic inhibitory tone has been implicated in synaptic integration, anxiety-related behaviours and seizure susceptibility. Tao et al. show that activation of postsynaptic GABABRs enhances GABAAR-mediated currents caused by exogenous GABA or the GABABR agonist baclofen in dentate gyrus granule cells (DGGCs) but not in CA1 pyramidal neurons or cortical layer 2/3 pyramidal neurons. Connelly et al. report similar crosstalk in thalamocortical neurons of the ventrobasal thalamus and cerebellar granule cells as well as in DGGCs.
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