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The Journal of Neuroscience, May 1, 1998, 18(9):3195-3205

Calcium-Sensitive Particulate Guanylyl Cyclase as a Modulator of cAMP in Olfactory Receptor Neurons

Cheil Moon¹, Parham Jaberi¹, Annie Otto-Bruc³, Wolfgang Baehr⁵, Krzysztof Palczewski^{3, 4}, and Gabriele V. Ronnett^{1, 2}

Departments of ¹ Neuroscience and ² Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, Departments of ³ Ophthalmology and ⁴ Pharmacology, School of Medicine, University of Washington, Seattle, Washington 98185, and ⁵ Moran Eye Center, University of Utah Health Science Center, Salt Lake City, Utah 84132

The second messengers cAMP and inositol-1,4,5-triphosphate have been implicated in olfaction in various species. The odorant-induced cGMP response was investigated using cilia preparations and olfactory primary cultures. Odorants cause a delayed and sustained elevation of cGMP. A component of this cGMP response is attributable to the activation of one of two kinetically distinct cilial receptor guanylyl cyclases by calcium and a guanylyl cyclase-activating protein (GCAP). cGMP thus formed serves to augment the cAMP signal in a cGMP-dependent protein kinase (PKG) manner by direct activation of adenylate cyclase. cAMP, in turn, activates cAMP-dependent protein kinase (PKA) to negatively regulate guanylyl cyclase, limiting the cGMP signal. These data demonstrate the existence of a regulatory loop in which cGMP can augment a cAMP signal, and in turn cAMP negatively regulates cGMP production via PKA. Thus, a small, localized, odorant-induced cAMP response may be amplified to modulate downstream transduction enzymes or transcriptional events.

Key words: olfaction; signal transduction; guanylyl cyclase; olfactory receptor neuron; cilia; protein kinase

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Copyright © 1998 Society for Neuroscience  0270-6474/98/1893195-11$05.00/0

This article has been cited by other articles:

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