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“Tobacco smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of tobacco smoke constituents.

The aim of these studies was to investigate if exposure to tobacco smoke leads to nicotine dependence in rats.

The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Somatic signs were recorded from a checklist of nicotine abstinence signs. Nicotine self-administration sessions

were conducted to investigate if tobacco smoke exposure affects the motivation to self-administer nicotine. Nicotinic receptor autoradiography was used to investigate if exposure to tobacco smoke affects central alpha 7 nicotinic acetylcholine MK5108 research buy receptor (nAChR) and non-alpha 7 nAChR levels (primarily alpha 4 beta 2 nAChRs).

The nAChR antagonist mecamylamine dose-dependently elevated the

brain reward thresholds of the rats exposed to tobacco smoke and did not affect the brain reward thresholds of the untreated PRT062607 chemical structure control rats. Furthermore, mecamylamine induced more somatic withdrawal signs in the smoke-exposed rats than in the control rats. Nicotine self-administration was decreased 1 day after the last tobacco smoke exposure sessions and was returned to control levels 5 days later. Tobacco smoke exposure increased the alpha 7 nAChR density in the CA2/3 area and the stratum oriens and increased the non-alpha 7 nAChR density in the dentate gyrus.

Tobacco smoke exposure leads to nicotine dependence as indicated by precipitated affective and somatic withdrawal signs and induces an upregulation of nAChRs in the hippocampus.”
“A number of recent studies suggest 17-DMAG (Alvespimycin) HCl that many biological

species follow a Levy random walk in their search for food. Such a strategy has been shown to be more efficient than classical Brownian motion when resources are scarce. However, current diffusion-reaction models used to describe many ecological systems do not account for the superdiffusive spread of populations due to Levy flights. We have developed a model to simulate the spatial spread of two species competing for the same resources and driven by Levy flights. The model is based on the Lotka-Volterra equations and has been obtained by replacing the second-order diffusion operator by a fractional-order one. Consistent with previous known results, theoretical developments and numerical simulations show that fractional-order diffusion leads to an exponential acceleration of the population fronts and a power-law decay of the fronts’ leading tail. Depending on the skewness of the fractional derivative, we derive catch-up conditions for different types of fronts.