NO inhibits supraoptic oxytocin and vasopressin neurons via activation of GABAergic synaptic inputs

Javier E. Stern, Mike Ludwig

Research output: Contribution to journalArticlepeer-review

122 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)R1815-R1822
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number6 49-6
StatePublished - 2001


  • Bicuculline
  • Hypothalamus
  • Retrodialysis
  • Sodium nitroprusside

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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