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1 Department of Pharmacology and Toxicology, Wright State University, Dayton, Ohio 45435; and 2 Department of Biomedical Sciences, University of Edinburgh Medical School, Edinburgh E48 9XD, United Kingdom
To study modulatory actions of
nitric oxide (NO) on GABAergic synaptic activity in hypothalamic
magnocellular neurons in the supraoptic nucleus (SON), in vitro and in
vivo electrophysiological recordings were obtained from identified
oxytocin and vasopressin neurons. Whole cell patch-clamp recordings
were obtained in vitro from immunochemically identified oxytocin and
vasopressin neurons. GABAergic synaptic activity was assessed in vitro
by measuring GABAA miniature inhibitory postsynaptic
currents (mIPSCs). The NO donor and precursor sodium nitroprusside
(SNP) and L-arginine, respectively, increased the frequency
and amplitude of GABAA mIPSCs in both cell types
(P 
0.001). Retrodialysis of SNP (50 mM) onto the SON in
vivo inhibited the activity of both neuronal types (P 0.002), an effect that was reduced by retrodialysis of the GABAA-receptor antagonist bicuculline (2 mM, P 0.001). Neurons activated by intravenous infusion of 2 M NaCl were
still strongly inhibited by SNP. These results suggest that NO
inhibition of neuronal excitability in oxytocin and vasopressin neurons
involves pre- and postsynaptic potentiation of GABAergic synaptic
activity in the SON.
sodium nitroprusside; bicuculline; hypothalamus; retrodialysis
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