GABAergic currents in RT and VB thalamic nuclei follow kinetic pattern of α3- and α1-subunit-containing GABAA receptors

Inhibitory postsynaptic currents (IPSCs) of the thalamic reticular (RT) nucleus are dramatically slower than in the neighboring ventrobasal (VB) neurons. It has been suggested that alpha 3-subunit-containing receptors underlie slow IPSCs in RT neurons, while rapid synaptic currents in the VB nucleus are due to gamma-aminobutyric acid A receptors (GABA(A)Rs), including the alpha 1-subunit. In our recent study [Barberis et al. (2007) Eur. J. Neurosci., 25, 2726-2740] we have found that profound differences in kinetics of currents mediated by alpha 3 beta 2 gamma 2 and alpha 1 beta 2 gamma 3 receptors resulted from distinct binding and desensitization properties. However, a direct comparison between kinetics of neuronal GABA(A)Rs from RT and VB neurons and alpha 3- and alpha 1-subunit-containing receptors has not been made. For this purpose, current responses to ultrafast GABA applications were recorded from patches excised from neurons in VB and RT areas. Deactivation kinetics determined for RT and VB neurons closely resembled that in currents mediated by alpha 3 beta 2 gamma 2 and alpha 1 beta 2 gamma 2 receptors. In RT neurons, currents elicited by non-saturating [GABA] had a remarkably slow onset, a hallmark of alpha 3-subunit-containing receptors. In VB and RT neurons, single-channel currents elicited by brief GABA pulses had similar characteristics to those of alpha 1 beta 2 gamma 2 and alpha 3 beta 2 gamma 2 receptors. However, in stationary conditions, similarity between single-channel currents in neurons and respective recombinant receptors was less apparent. We propose that the non-stationary kinetics of GABAergic currents in VB and RT nuclei mimic that of currents mediated by alpha 1- and alpha 3-subunit-containing receptors. The dissimilarity between stationary kinetics of neuronal and recombinant receptors probably reflects differences between GABA(A)Rs mediating phasic and tonic currents in these neurons.