Ami Cohen

TL;DR: Brain stress response systems are hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence, and to contribute to the development and persistence of addiction.

TL;DR: These results link the brain reward and stress systems in the same brain region to signaling of the negative motivational effects of nicotine withdrawal.

TL;DR: It is demonstrated that the escalation of nicotine intake only occurs in animals given intermittent periods of abstinence with extended access to nicotine, and that inhibition of monoamine oxidase may contribute to theescalation of smoking, thus validating both an animal model of the escalate of smoking behavior and the contribution of monoamines oxidase inhibition to compulsive nicotine-seeking.

TL;DR: It is demonstrated that the model of short access to nicotine self‐administration has limited validity for tobacco dependence and that activation of CRF1 receptors is required for the emergence of abstinence‐induced anxiety‐like behavior, hyperalgesia and excessive nicotine intake.

TL;DR: It is demonstrated that novel animal models of nicotine vapor exposure and escalation of nicotine intake provide a unique opportunity to investigate the neurobiological effects of second-hand nicotine exposure, electronic cigarette use, and the mechanisms that underlie the transition from nicotine use to compulsive nicotine intake.