Related Experiment Video
Updated: Aug 17, 2026

Preparation of Acute Brain Slices Using an Optimized N-Methyl-D-glucamine Protective Recovery Method
Published on: February 26, 2018
NO inhibits supraoptic oxytocin and vasopressin neurons via activation of GABAergic synaptic inputs
1Department of Pharmacology and Toxicology, Wright State University, Dayton, Ohio 45435, USA. javier.stern@wright.edu
Abstract:
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 GABA(A) miniature inhibitory postsynaptic currents (mIPSCs). The NO donor and precursor sodium nitroprusside (SNP) and L-arginine, respectively, increased the frequency and amplitude of GABA(A) mIPSCs in both cell types (P < or = 0.001). Retrodialysis of SNP (50 mM) onto the SON in vivo inhibited the activity of both neuronal types (P < or = 0.002), an effect that was reduced by retrodialysis of the GABA(A)-receptor antagonist bicuculline (2 mM, P < or = 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.
More Related Videos
10:44Single Cell Multiplex Reverse Transcription Polymerase Chain Reaction After Patch-clamp
Published on: June 20, 2018
11:04Unraveling the Role of Discrete Areas of the Rat Brain in the Regulation of Ovulation through Reversible Inactivation by Tetrodotoxin Microinjections
Published on: September 3, 2020
Related Concept Videos
Excitatory and Inhibitory Effects of Neurotransmitters
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Drugs Acting on Autonomic Ganglia: Blockers
Adrenergic Agonists: Indirect-Acting Agents
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Drugs Affecting Neurotransmitter Release or Uptake
Neurotransmitters