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RAPID COMMUNICATION
1 Centre de Recherche Fernand-Seguin, Montreal, Quebec H1N 3V2, Canada; and 2 Department of Anatomy and Neurobiology, University of California, Irvine, California 92697
Warren, Richard A., Peyman Golshani, and Edward G. Jones. GABAB-receptor-mediated inhibition in developing mouse ventral posterior thalamic nucleus. J. Neurophysiol. 78: 549-553, 1997. Inhibitory postsynaptic potentials (IPSPs) generated by activation of the thalamic reticular nucleus (RTN) were recorded in neurons of the ventral posterior nucleus (VP) in vitro in slices from mice aged postnatal day (P)1-P17. An early IPSP peaking 41 ± 2.5 (SE) ms after electrical stimulation of the internal capsule or RTN was found in 96% of VP neurons. This early IPSP was blocked by bicuculline, showing its dependence on 
-aminobutyric acid-A (GABAA) receptors. A late IPSP peaking 357 ± 27 ms after the stimulus was observed in 22% of VP neurons in control medium but was uncovered in 38% of neurons when bicuculline was added. The late IPSP was blocked by addition of a GABAB antagonist, 2-hydroxysaclofen, to the medium (n = 7); it had a reversal potential of 
98 ± 1.3 mV, 14 mV negative to the early component. In contrast to the early IPSP, whose reversal potential became more negative during postnatal development, the reversal potential of the late IPSP remained constant throughout the postnatal period studied. The most significant change in the late IPSP was shortening in duration, with reduction in latency-to-peak by >400 ms, between P1 and P10. No changes of comparable magnitude were observed in the duration of the earlier GABAA response. These results show that both GABAA and GABAB IPSPs are present very early in the postnatal thalamus and that their characteristics evolve along independent paths during postnatal development.
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