Phenomenology of a light scalar: the dilaton

We make use of the language of non-linear realizations to analyze electro-weak symmetry breaking scenarios in which a light dilaton emerges from the breaking of a nearly conformal strong dynamics, and compare the phenomenology of the dilaton to that of the well motivated light composite Higgs scenario. We argue that -- in addition to departures in the decay/production rates into massless gauge bosons mediated by the conformal anomaly -- characterizing features of the light dilaton scenario (as well as other scenarios admitting a light CP-even scalar not directly related to the breaking of the electro-weak symmetry) are off-shell events at high invariant mass involving two longitudinally polarized vector bosons and a dilaton, and tree-level flavor violating processes. Accommodating both electro-weak precision measurements and flavor constraints appears especially challenging in the ambiguous scenario in which the Higgs and the dilaton fields strongly mix. We show that warped higgsless models of electro-weak symmetry breaking are explicit and tractable realizations of this limiting case. The relation between the naive radion profile often adopted in the study of holographic realizations of the light dilaton scenario and the actual dynamical dilaton field is clarified in the Appendix.Comment: 21 page

Endogenous cholinergic inputs and local circuit mechanisms govern the phasic mesolimbic dopamine response to nicotine

Nicotine exerts its reinforcing action by stimulating nicotinic acetylcholine receptors (nAChRs) and boosting dopamine (DA) output from the ventral tegmental area (VTA). Recent data have led to a debate about the principal pathway of nicotine action: direct stimulation of the DAergic cells through nAChR activation, or disinhibition mediated through desensitization of nAChRs on GABAergic interneurons. We use a computational model of the VTA circuitry and nAChR function to shed light on this issue. Our model illustrates that the α4β2-containing nAChRs either on DA or GABA cells can mediate the acute effects of nicotine. We account for in vitro as well as in vivo data, and predict the conditions necessary for either direct stimulation or disinhibition to be at the origin of DA activity increases. We propose key experiments to disentangle the contribution of both mechanisms. We show that the rate of endogenous acetylcholine input crucially determines the evoked DA response for both mechanisms. Together our results delineate the mechanisms by which the VTA mediates the acute rewarding properties of nicotine and suggest an acetylcholine dependence hypothesis for nicotine reinforcement.Peer reviewe