Tatsuro Kumada, Madepalli K.Lakshmana, and Hitoshi Komuroand and Alexandre E. Medina, Thomas E. Krahe, and Ary S. Ramoa
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 hippocampus. Thus, these experiments suggest that multiple pathways can participate in the reinforcing effects of nicotine.