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Inhibition of nitric oxide synthase does not prevent ocular dominance plasticity in kitten visual cortex.
Author(s) -
Ruthazer E S,
Gillespie D C,
Dawson T M,
Snyder S H,
Stryker M P
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021510
Subject(s) - monocular deprivation , nitric oxide synthase , ocular dominance , kitten , visual cortex , long term potentiation , chemistry , nitroarginine , endocrinology , medicine , nitric oxide , neuroscience , biology , cats , receptor
1. The neural messenger molecule nitric oxide (NO) has been shown to be involved in several forms of plasticity including hippocampal long‐term potentiation. We examined the effects of chronic intracortical infusion of inhibitors of NO synthase (NOS) activity on the plasticity of visual cortical responses following monocular lid suture during the critical period. 2. Single unit recordings (618 cells) made in both the NOS inhibitor‐treated (30 mM NG‐methyl‐L‐arginine (L‐NMMA), or 22 or 2 mM nitro‐L‐arginine (L‐NOArg)) and saline‐treated control hemispheres of barbiturate‐anaesthetized, critical‐period kittens (n = 8) revealed a profound shift in favour of the non‐deprived eye. Shifts were of similar magnitude in hemispheres in which NOS was inhibited and in saline control hemispheres. 3. Subsequent analysis of NOS activity in the same cortical tissue in which recordings had been made showed a pronounced decrease in NOS activity in inhibitor‐treated hemispheres. In the region in which all the single unit recordings were made (< 3 mm from the infusion cannula), 22 mM L‐NOArg resulted in a reduction of NOS activity to 5.55 +/‐ 5.33% of control hemisphere NOS activity levels. L‐NOArg (2 mM) and L‐NMMA (30 mM) also produced clear, but smaller, inhibition of NOS activity. 4. These findings demonstrate that NOS activity is not essential for ocular dominance plasticity in visual cortex.