This week, two groups look at impairments of neuronal migration and synaptic plasticity, respectively, in animal models of fetal alcohol syndrome (FAS). Both studies implicate cAMP signaling but in different ways. Kumada et al. examined granule cell migration in a brain slice preparation of neonatal mouse cerebellum. The authors report that acute alcohol exposure slowed the migration of granule cells. Medina et al. used a ferret model of FAS in which alcohol was injected every other day between postnatal days 10 and 30. Subsequently, ocular dominance plasticity was impaired in FAS animals, an effect that was restored by a phosphodiesterase I inhibitor.
2. Nicotine and Its Sites of
Reinforcement
Satoshi Ikemoto, Mei Qin, and
Zhong-Hua Liu
Ikemoto et al. used an intracranial self-administration
strategy to test for rat
brain regions involved in the reinforcing
effects of nicotine. Rats pressed levers to
receive nicotine injections from chronically
implanted cannulas in the posterior
ventral tegmental area (VTA), the adjacent
central linear nucleus, or the supramammillary
nucleus of the posterior hypothalamus.
However, administration
into a number of surrounding areas was
not self-reinforcing. Pretreatment with a
D2 dopamine receptor antagonist blocked
self-administration of nicotine, consistent
with the role of mesolimbic dopamine
neurons in positive reinforcement. Of
note, the posterior VTA and central linear
nucleus contain dopamine neurons that
project to the medial shell of the nucleus
accumbens and the medial olfactory tubercle,
areas in which dopaminergic drugs
trigger reinforcing effects. However, the
supramammillary nucleus projects to septum
and hippoca
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Contact: Sara Harris
sharris@sfn.org
202-462-6688
Society for Neuroscience
17-Jan-2006