Furthermore, mecamylamine (2 mg/kg) induced more somatic signs in the nicotine-treated rats than in the control rats. Clonidine and propranolol, but not prazosin, decreased the total number of somatic signs associated with nicotine withdrawal.
Blockade of alpha 1-adrenergic
receptors attenuates the deficit in brain reward function associated with nicotine withdrawal. Antagonism of beta-adrenergic receptors or stimulation of alpha 2-adrenergic receptors attenuates the somatic symptoms of nicotine withdrawal.”
“Stressful life events and chronic stressors have been associated with escalations in alcohol drinking. 1 Stress exposure leads to the secretion of glucocorticoids (cortisol in the human; corticosterone (CORT) in the rodent). To model a period of heightened elevations in CURT, the present work assessed the effects of chronic exposure to the stress hormone CORT on alcohol self-administration. Male Long Evans rats were trained to self-administer
a sweetened alcohol solution (2% sucrose/15% alcohol) resulting in moderate levels of daily alcohol intake (0.5-0.7 g/kg). Following stable baseline operant self-administration, rats received CURT in the drinking water for 7 days. A transient increase in alcohol self-administration was observed on the first self-administration session following CURT exposure, and behavior returned to control levels by the second session. Control experiments determined that this increase in alcohol self-administration was specific to alcohol, unrelated to general motor activation, and functionally dissociated from decreased CURT levels at the time of testing. These results indicate that repeated exposure to
heightened levels of stress hormone (e.g., as may be experienced during stressful episodes) has the potential to lead to exacerbated alcohol intake in low to moderate drinkers. Given that maladaptive drinking patterns, such as escalated alcohol drinking following stressful episodes, have the potential to put an individual at risk for future drinking disorders, utilization of this model will be important for examination of neuroadaptations that occur as a consequence of CURT exposure in order to better understand escalated drinking following stressful episodes in nondependent individuals. (C) 2013 Elsevier Ltd. All rights reserved.”
“The adolescent period is characterized by a specific sensitivity to the effects of alcohol, which is believed to contribute to the enhanced risks of alcohol dependence when drinking is initiated early during adolescence. In adolescent rodents, while the reduced sensitivity to the sedative effects of ethanol has been well characterized, its stimulant effects have not yet been extensively studied.
The present study characterized the development of the stimulant and the sedative effects of acute ethanol in male and female Swiss mice from weaning to early adulthood and tested whether both effects are interrelated.