RAPID COMMUNICATION GABAB-Receptor-Mediated Inhibition in Developing Mouse Ventral Posterior Thalamic Nucleus

Warren, Richard A., Peyman Golshani, and Edward G. Jones. or seizurelike activity do not occur in human infants (Aicardi GABAB-receptor-mediated inhibition in developing mouse ventral 1994) or in infant animal models (Marescaux et al. 1992b). posterior thalamic nucleus. J. Neurophysiol. 78: 549–553, 1997. This may be related to immaturity of the membrane and Inhibitory postsynaptic potentials (IPSPs) generated by activation synaptic properties of thalamic relay and reticular neurons of the thalamic reticular nucleus (RTN) were recorded in neurons during early postnatal life; in mice these only reach the adult of the ventral posterior nucleus (VP) in vitro in slices from mice state and permit full development of thalamic oscillations aged postnatal day (P)1–P17. An early IPSP peaking 41 { 2.5 toward the end of the second postnatal week (Warren and (SE) ms after electrical stimulation of the internal capsule or RTN Jones 1997). was found in 96% of VP neurons. This early IPSP was blocked Generation of rebound bursts in relay neurons is largely by bicuculline, showing its dependence on g-aminobutyric acid-A (GABAA) receptors. A late IPSP peaking 357 { 27 ms after the dependent on inhibition by the reticular nucleus through faststimulus was observed in 22% of VP neurons in control medium acting, ionotropic GABAA receptors (Bal et al. 1995a; Hubut was uncovered in 38% of neurons when bicuculline was added. guenard and Prince 1994a; Warren et al. 1994). The role of The late IPSP was blocked by addition of a GABAB antagonist, GABAB receptors may be more limited normally because 2-hydroxysaclofen, to the medium (n Å 7); it had a reversal potenGABAB antagonists reportedly do not affect intrathalamic tial of 098 { 1.3 mV, 14 mV negative to the early component. In oscillations in vitro (Bal et al. 1995a; Warren et al. 1994). contrast to the early IPSP, whose reversal potential became more Nevertheless, GABAB receptor binding can be demonnegative during postnatal development, the reversal potential of strated in mouse thalamus in early postnatal life (e.g., Lin the late IPSP remained constant throughout the postnatal period et al. 1993), and typical, GABAB-mediated slow inhibitory studied. The most significant change in the late IPSP was shortenpostsynaptic potentials (IPSPs) and presynaptic GABAB efing in duration, with reduction in latency-to-peak by ú400 ms, between P1 and P10. No changes of comparable magnitude were fects occur in thalamic neurons of rats¢8 days old (Huguenobserved in the duration of the earlier GABAA response. These ard and Prince 1994a; Ulrich and Huguenard 1996) and results show that both GABAA and GABAB IPSPs are present very under certain conditions in carnivores (Bal et al. 1995a; von early in the postnatal thalamus and that their characteristics evolve Krosigk et al. 1993). It was not possible to demonstrate along independent paths during postnatal development. GABAB-mediated IPSPs in earlier studies in mice (Warren and Jones 1997; Warren et al. 1994). In the present study we report their presence in ventral posterior nucleus (VP) I N T R O D U C T I O N neurons from birth. Low-frequency oscillations in the interconnected network of thalamic and cortical neurons are accompaniments of