Nicotine administration interacts with housing conditions to alter social and non-social behaviors in male and female Long-Evans rats

Abstract

Despite the fact that the anxiety-relieving effects of smoking are widely reported by smokers, human laboratory studies have not found consistent evidence for this effect. In animals, contrasting results also have been reported, with Sprague-Dawley rats unaffected by nicotine in behavioral tests of anxiety but with other rat strains (e.g., Wistar, Fischer-344) displaying behaviors indicative of anxiolysis. The present experiment used the social interaction test to evaluate effects of nicotine (12 mg/kg/day) chronically administered via minipump on social and non-social behaviors in 48 male and 48 female Long-Evans rats--a strain that has not previously been evaluated and that is known to differ from Sprague-Dawleys in other behavioral responses to nicotine. Because environmental conditions can alter behavioral effects of drugs, animals lived in either individual or same-sex group housing. Social interactions were measured on day 10 of drug administration and social behaviors (touch, follow, sniff-other, wrestle) as well as non-social behaviors (anxiety-related behaviors: freezing, grooming-self; exploratory behavior: moving) were scored. Group housing decreased social behaviors and increased anxiety-related behaviors. Nicotine's effects depended upon housing condition, such that nicotine further decreased social behaviors and increased anxiety-related behaviors of group-housed animals, with weaker effects in single-housed animals. Overall, the results suggest that nicotine's effects are modified by environmental conditions, and that nicotine administration at this dosage and in this particular rat strain results in anxiogenic effects.

Age differences in the spontaneous acquisition of nicotine self-administration in male Wistar and Long–Evans rats

“…One possible factor that may contribute to this observation is a difference in sensitivity to some of nicotine's effects. For example, nicotine may have greater anxiolytic effects in Wistar rats (Brioni et al 1994), whereas the opposite, i.e., anxiogenesis, is reported for LE rats (Scheufele et al 2000). Interestingly, Irvine et al (2001) report that rats may self-administer nicotine because of its anxiogenic, rather than its anxiolytic properties.…”

Chronic nicotine exposure augments gustatory plasticity inCaenorhabditis elegans:involvement of dopamine signaling

“…1) In experiments using rats and mice, acute administration of nicotine evoked changes in locomotor activity, grooming, and feeding, 2,3) and could improve attention, mental flexibility, and working memory function. 3,4) Chronic nicotine administration enhances the affective, anxiogenic, and neurochemical effects, 5) although there is no consistent result of learning behavior in rodents.…”

Common effects of fat, ethanol, and nicotine on enkephalin in discrete areas of the brain

“…While some reports show these substances to induce psychological stress (Scheufele et al, 2000; Walker et al, 2010; Can et al, 2012), which itself may stimulate ENK and c-Fos (Shoji and Mizoguchi, 2010; Christiansen et al, 2011; Noh et al, 2012), there are others using low doses or short-term administration showing no such effects (Pohorecky, 1990; Villegier et al, 2010; Morganstern et al, 2012). These three substances also have reinforcing properties in common (Corrigall et al, 1994; Czachowski and Samson, 1999; Ackroff and Sclafani, 2014).…”

“…The final goal was to take steps towards determining whether fat, ethanol, and nicotine have specific behavioral and physiological effects in common, which may be related to their similar actions in the brain. These analyses involved measurements of stress-related behaviors and blood levels of the stress hormone corticosterone (CORT) and also the lipids, triglycerides (TG), which under some conditions are increased by these substances (Balfour et al, 1975; Widmaier et al, 1992; Scheufele et al, 2000; Chattopadhyay and Chattopadhyay, 2008; Barson et al, 2009; Cippitelli et al, 2014) and can themselves stimulate expression of ENK (Ahima et al, 1992; Chang et al, 2004) and c-Fos (Chang et al, 2004; Herring et al, 2004; Loughlin et al, 2006). A 5-day exposure was used in order to examine animals beyond their first encounter with the substances, which generally stimulates c-Fos expression in the brain (Ryabinin et al, 1997; Salminen et al, 2000; Chang et al, 2004), but before they become dependent or obese, which can decrease basal levels of ENK (McLaughlin et al, 1986) and greatly reduce a c-Fos response (Ryabinin et al, 1997; Salminen et al, 2000; Chang et al, 2004), therefore masking direct effects of the substances themselves.…”