Abstract
Synaptic plasticity leads to long-term changes in neuronal responsiveness, and the molecular mechanisms of plasticity are beginning to be elucidated for the central nervous system (CNS). Watt and Storm show that olfactory neurons activate the extracellular signal-regulated, mitogen-activated protein kinase cascade (ERK) in response to odorant stimuli. This pathway has been implicated in CNS plasticity. Activation of the ERK cascade in olfactory neurons leads to phosphorylation and activation of the cyclic AMP response element binding protein (CREB) through the activation of the CREB kinase pp 90 Rsk. Inhibition of this pathway did not affect primary olfactory signaling measured by electroolfactograms, supporting the hypothesis that the ERK pathway is involved in adaptation to odorant stimulation. In CRE/LacZ transgenic mice, exposure of the mice to the odorant citralva stimulated expression of the reporter gene in a specific layer and zone of the olfactory epithelium. These results provide a molecular mechanism for other physiological and behavioral data that suggest that smells can be learned. W. C. Watt, D. R. Storm, Odorants stimulate the ERK/mitogen-activated protein kinase pathway and activate cAMP-response element-mediated transcription in olfactory sensory neurons. J. Biol. Chem. 276 , 2047-2052 (2001). [Abstract] [Full Text]
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