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This Article Full Text Full Text (PDF) All Versions of this Article: 295/2/H807    most recent 00259.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Li, D.-P. Articles by Pan, H.-L. PubMed PubMed Citation Articles by Li, D.-P. Articles by Pan, H.-L.

Plasticity of pre- and postsynaptic GABA_B receptor function in the paraventricular nucleus in spontaneously hypertensive rats

¹Department of Critical Care and ²Department of Anesthesiology and Pain Medicine, The University of Texas M. D. Anderson Cancer Center, Houston, Texas

Submitted 12 March 2008 ; accepted in final form 13 June 2008

GABA_B receptor function is upregulated in the paraventricular nucleus (PVN) of the hypothalamus in spontaneously hypertensive rats (SHR), but it is unclear whether this upregulation occurs pre- or postsynaptically. We therefore determined pre- and postsynaptic GABA_B receptor function in retrogradely labeled spinally projecting PVN neurons using whole cell patch-clamp recording in brain slices in SHR and Wistar-Kyoto (WKY) rats. Bath application of the GABA_B receptor agonist baclofen significantly decreased the spontaneous firing activity of labeled PVN neurons in both SHR and WKY rats. However, the magnitude of reduction in the firing rate was significantly greater in SHR than in WKY rats. Furthermore, baclofen produced larger membrane hyperpolarization and outward currents in labeled PVN neurons in SHR than in WKY rats. The baclofen-induced current was abolished by either including G protein inhibitor GDPβS in the pipette solution or bath application of the GABA_B receptor antagonist in both SHR and WKY rats. Blocking N-methyl-D-aspartic acid receptors had no significant effect on baclofen-elicited outward currents in SHR. In addition, baclofen caused significantly greater inhibition of glutamatergic excitatory postsynaptic currents (EPSCs) in labeled PVN neurons in brain slices from SHR than WKY rats. By contrast, baclofen produced significantly less inhibition of GABAergic inhibitory postsynaptic currents (IPSCs) in labeled PVN neurons in SHR than in WKY rats. Although microinjection of the GABA_B antagonist into the PVN increases sympathetic vasomotor tone in SHR, the GABA_B antagonist did not affect EPSCs and IPSCs of the PVN neurons in vitro. These findings suggest that postsynaptic GABA_B receptor function is upregulated in PVN presympathetic neurons in SHR. Whereas presynaptic GABA_B receptor control of glutamatergic synaptic inputs is enhanced, presynaptic GABA_B receptor control of GABAergic inputs in the PVN is attenuated in SHR. Changes in both pre- and postsynaptic GABA_B receptors in the PVN may contribute to the control of sympathetic outflow in hypertension.

autonomic nervous system; synaptic transmission; hypertension; -aminobutyric acid; baclofen