Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 4, Pages 818-823Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4706-06.2007
Keywords
LTP; visual cortex; NO; guanylyl cyclase; cGMP; KO
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The role of nitric oxide (NO)/cGMP signaling in long-term potentiation (LTP) has been a lingering matter of debate. Within the cascade, the NO receptor guanylyl cyclase (GC), the cGMP-forming enzyme that is stimulated by NO, plays a key role. Two isoforms of GC (alpha(2)-GC, alpha(1)-GC) exist. To evaluate their contribution to synaptic plasticity, we analyzed knock-out mice lacking either one of the GC isoforms. We found that LTP induced in the visual cortex is NO dependent in the wild-type mice, absent in either of the GC isoform-deficient mice, and restored with application of a cGMP analog in both strains. The requirement of both NO receptor GCs for LTP indicates the existence of two distinct NO/cGMP-mediated pathways, which have to work in concert for expression of LTP.
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