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Nitric oxide donor sodium nitroprusside inhibits the acetylcholine‐induced K + current in identified Aplysia neurons
Author(s) -
Sawada M.,
Ichinose M.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960401)44:1<21::aid-jnr3>3.0.co;2-k
Subject(s) - sodium nitroprusside , acetylcholine , nitric oxide , chemistry , pharmacology , neuroscience , sodium , medicine , psychology , organic chemistry
The effects of bath‐applied sodium nitroprusside (SNP), a nitric oxide (NO) donor, on an acetylcholine (ACh)‐induced K + current recorded from identified neurons (R9 and R10) of Aplysia kurodai were investigated with conventional voltage‐clamp and pressure ejection techniques. Bath‐applied SNP (25–50 μM) reduced the ACh‐induced K + current in the neurons without affecting the resting membrane conductance and holding current. The suppressing effects of SNP on the current were completely reversible. Intracellular injection of 1 mM guanosine 3′,5′‐cyclic monophosphate (cGMP) or bath‐applied 50 μM 3‐isobutyl‐1‐methylxanthine (IBMX), a nonspecific phosphodiesterase (PDE) inhibitor, also inhibited the ACh‐induced current, thus mimicking the effect of the NO donor on the ACh‐induced current. In contrast, pretreatment with methylene blue (10 μM), an inhibitor of guanylate cyclase, and hemoglobin (50 μM), a nitric oxide scavenger, decreased the SNP‐induced inhibition of the ACh‐induced current. These results suggest that SNP, a NO donor, inhibits the ACh‐induced K + current, and that the mechanism of NO inhibition of the ACh‐induced current recorded from identified Aplysia neurons involves cGMP‐dependent protein kinase. © 1996 Wiley‐Liss, Inc.