Marina R. Picciotto

TL;DR: In this article, the authors investigated the contribution of the high-affinity neuronal nicotinic acetylcholine receptor to the effects of nicotine on the mesolimbic dopamine system in mice lacking the β2 subunit of this receptor.

TL;DR: Action of cholinergic signaling on cellular and synaptic properties of neurons in several brain areas are identified and consequences of this signaling on behaviors related to drug abuse, attention, food intake, and affect are discussed.

TL;DR: It is shown that in mice and rats, ghrelin bound to neurons of the VTA, where it triggered increased dopamine neuronal activity, synapse formation, and dopamine turnover in the nucleus accumbens in a GHSR-dependent manner, suggesting that the mesolimbic reward circuitry is targeted by peripheral gh Relin to influence physiological mechanisms related to feeding.

TL;DR: A new, experimentally based compilation of species-specific dose selection for studies on the in vivo effects of nicotine, addressing issues related to genetic background, age, acute vs chronic exposure, route of administration, and behavioral responses is provided.

TL;DR: It is reported here that high-affinity binding sites for nicotine are absent from the brains of mice homozygous for the β2-subunit mutation, and electrophysiological recording from brain slices reveals that thalamic neurons from these mice do not respond to nicotine application.