Many studies have suggested that low ambient GABA concentrations can persistently activate certain GABA_A receptor subtypes, often remote from synapses, to generate a ‘tonic’ inhibition [1]. An as yet unidentified non-vesicular release mechanism is thought to be responsible for generating these low ambient GABA concentrations in cerebellar granule cells [2] calling into question the function of tonic inhibition in the dynamic control of neuronal excitability [2,3]. In this study we have examined the source of the GABA giving rise to a tonic inhibition which has recently been reported in thalamocortical neurons within the dorsal lateral geniculate nucleus (dLGN) in juvenile rats [4]. At physiological temperatures (37-38°C), whole-cell patch-clamp recording in an acute slice preparation from adult C57Bl/6J mice also shows a tonic GABA_A conductance present within the mature dLGN. When normalised to cell capacitance, this conductance has a magnitude of 75.2 ± 20.3 pS/pF (mean ± sem; n=33). Reduction of the extracellular Ca²⁺ concentration from 2 to 1 mM, results in a decrease in the magnitude of this conductance to 6.7 ± 2.9 pS/pF (n=7). Furthermore, this conductance is also significantly reduced (unpaired t test, P<0.05) by the application of 500 nM tetrodotoxin (5.6 ± 2.3 pS/pF, n=7). Therefore, in thalamic relay neurons of the dLGN the tonic GABA_A conductance does appear to be generated by the vesicular release of GABA. Delta subunit containing GABA_A receptors are often associated with this type of conductance. We observe strong delta mRNA labelling within the dLGN, with little evidence of this receptor population in the adjacent ventral LGN (vLGN); another retinorecipient nucleus. Consistent with the absence of delta subunits within the vLGN, no tonic GABA_A conductance was detected in this nucleus (2.5 ± 5.5 pS/pF, n=26). In order to selectively activate these receptors the agonist 4,5,6,7-tetrahydroisothiazolo-[5,4-c]pyridin-3-ol (THIP; 1 μM) was bath applied to thalamic neurons. A clear THIP-activated conductance was elicited in dLGN (2.6 ± 1.0 nS, n=3) whereas, a markedly smaller conductance, with no clear peak associated with THIP application, was observed within the vLGN (0.1 ± 0.1 nS, n=3). Firing properties of LGN cells were then examined following the application of THIP. Hyperpolarising current steps generated high frequency rebound bursts of action potentials, analogous to the ‘burst’ firing mode of thalamic relay cells [5]. In dLGN, application of 1 μM THIP leads to an increase in the latency of these bursts from 29.6 ± 3.3 ms (n=4) to 41.7.± 4.6 ms, whereas there was no effect in vLGN (31.1 ± 8.5 versus 33.1 ± 8.9 ms, n = 6). Therefore, the tonic GABA_A receptor-mediated conductance present in dLGN is capable of altering the timing of high frequency rebound bursts; a key component in the generation of thalamocortical oscillations.