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Home > > Science Meeting Summaries & Special Reports > Frontiers in Addiction Research > Jacob P. Waletzky Memorial Lecture


Header - Frontiers in Addiction Research

JACOB P. WALETZKY MEMORIAL LECTURE

Co-Chairs:

Rita P. Liu, Ph.D.
National Institute on Drug Abuse

Cathrine Sasek, Ph.D.
National Institute on Drug Abuse

Overview

Established in 2003, the Society for Neuroscience Jacob P. Waletzky Memorial Award is given for innovative research in drug addiction and alcoholism. The award is presented to a young scientist within 15 years of obtaining a doctoral degree. The 2007 award recipient is Marina Picciotto, Ph.D.

Studies on the Molecular Basis of Nicotine Addiction and Developmental Responses to Nicotine
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Studies on the Molecular Basis of Nicotine Addiction and Developmental Responses to Nicotine
Marina Picciotto, Ph.D.

Knockout mice lacking the nicotinic acetylcholine receptor (nAChR) beta2 subunit show greatly attenuated nicotine self-administration, place preference, and locomotor activation. Beta2 subunit-containing nAChRs are present throughout the brain in the regions and circuits that mediate these behaviors. We have generated several lines of transgenic mice with inducible beta2 subunit expression in different brain areas. These mice have been tested in behavioral paradigms to establish where in the brain the beta2-containing receptors may act to mediate the effects of nicotine. Using a line of mice with expression of the beta2 subunit restricted to corticothalamic projections, we have established that normal passive avoidance behavior (a fear-associated learning test) requires expression of the beta2 subunit in this pathway during development. Similarly, nicotine exposure during this critical period results in hypersensitive passive avoidance learning in adulthood. Recent studies using diffusion tensor imaging suggest that corticothalamic dysfunction may be responsible for deficits in auditory learning in human subjects exposed to tobacco smoke during development, because changes in white matter in the internal capsule—the tract including both corticothalamic and thalamocortical axons—correlate with impairments in auditory learning. Thus, the maturation of corticothalamic circuits appears to be sensitive to perturbations of nicotinic receptor function, and altered corticothalamic function may be an important anatomical substrate for the behavioral consequences of developmental smoke exposure.


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