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The Journal of Neuroscience, January 24, 2007, 27(4):818-823; doi:10.1523/JNEUROSCI.4706-06.2007

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Development/Plasticity/Repair
Long-Term Potentiation in the Visual Cortex Requires Both Nitric Oxide Receptor Guanylyl Cyclases

Arash Haghikia,1 * Evanthia Mergia,2 * Andreas Friebe,2 Ulf T. Eysel,1 Doris Koesling,2 and Thomas Mittmann1

1Faculty of Medicine, Institute of Physiology, Department of Neurophysiology, and 2Faculty of Medicine, Institute of Pharmacology and Toxicology, Ruhr-University Bochum, D-44780 Bochum, Germany

Correspondence should be addressed to Doris Koesling, Faculty of Medicine, Institute of Pharmacology and Toxicology, Ruhr-University Bochum, D-44780 Bochum, Germany. Email: doris.koesling{at}ruhr-uni-bochum.de

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.

Key words: LTP; visual cortex; NO; guanylyl cyclase; cGMP; KO


Received Oct. 30, 2006; revised Dec. 18, 2006; accepted Dec. 22, 2006.

Correspondence should be addressed to Doris Koesling, Faculty of Medicine, Institute of Pharmacology and Toxicology, Ruhr-University Bochum, D-44780 Bochum, Germany. Email: doris.koesling{at}ruhr-uni-bochum.de




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