Chronic injections of saline produce subsensitivity to nicotine

Flemmer, Duane D.; Dilsaver, Steven C.

doi:10.1016/0091-3057(89)90309-2

Cited by 26 publications

(14 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However the actions of MEC on NMDA receptors occur only at much higher doses than the 1 mg/kg used here McDonough and Shih 1995). Furthermore, there was no effect of multiple vehicle injections on antinociception in the present study, and other work indicates that stress decreases, rather than increases, the antinociceptive effects of NIC (Caggiula et al 1993; see also Flemmer and Dilsaver 1989).…”

Section: Discussioncontrasting

confidence: 66%

Mecamylamine prevents tolerance but enhances whole brain [ 3 H]epibatidine binding in response to repeated nicotine administration in rats

et al. 2000

View full text Add to dashboard Cite

show abstract

Section: Discussioncontrasting

confidence: 66%

Mecamylamine prevents tolerance but enhances whole brain [ 3 H]epibatidine binding in response to repeated nicotine administration in rats

et al. 2000

View full text Add to dashboard Cite

show abstract

“…Others have shown that stressful manipulations which should be capable of producing HPA activation in rats (Dilsaver t988;Flemmer and Dilsaver 1989;Peck et al 1991), or direct CORT administration in mice (Pauly et al 1988(Pauly et al , 1990, can reduce nicotine sensitivity across a wide array of measures, whereas adrenalectomy increases responsiveness to nicotine (Pauly et al 1988(Pauly et al , 1990. However, these studies involved chronic manipulations.…”

Section: Discussionmentioning

confidence: 96%

“…This is suggested by the recent finding of elevated, preinjection levels of CORT accompanying the development of tolerance to nicotine administration in mice (Pauly et al 1990). This hypothesis is further supported by the following: (1) endogenous CORT responses to at least some stimuli can be conditioned (Ader 1976;Hennessey et al 1977); (2) CORT has widespread regulatory effects on many physiological systems (Munk et al 1984); (3) exogenous CORT given chronically reduces a number of behavioral and physiological effects of nicotine in mice (Pauly et al 1988(Pauly et al , 1990; (4) chronic stress, which also would be expected to elevate CORT levels, reduces nicotine sensitivity in rats (Dilsaver 1988;Flemmer and Dilsaver 1989;Peck et al 1991).…”

mentioning

confidence: 97%

Acute stress or corticosterone administration reduces responsiveness to nicotine: implictions for a mechanism of conditioned tolerance

et al. 1993

View full text Add to dashboard Cite

We have shown that conditioned tolerance develops to some of the behavioral and endocrine effects of nicotine in rats. Other investigators have suggested that tolerance to multiple nicotine injections in mice may be due, in part, to elevated plasma corticosterone (CORT) levels, since repeated nicotine injections are associated with elevated CORT, chronically elevated CORT reduces nicotine responsiveness and adrenalectomy disrupts nicotine tolerance. Three experiments tested the feasibility of this hypothesis, as a mechanism for conditioned nicotine tolerance in rats, by determining whether acute administration of CORT or manipulations that increase adrenocortical activity reduce nicotine responsiveness. In experiment 1, male rats were injected IP with CORT (1 mg/kg), vehicle (ETOH + distilled water) or no injection 10 min before nicotine (0.75 mg/kg, SC) and tested for nicotine-induced analgesia every other day for 10 days. A significant reduction in withdrawal latencies was obtained for CORT pretreated rats compared to animals given only nicotine. A similar reduction was produced by the vehicle pretreatment, which itself induced an elevation of endogenous CORT. Experiments 2 and 3 established that similar effects could be produced by doses of CORT as low as 0.125 mg/kg or by exposure to a novel environment which also elevated CORT levels. Results also suggest that a conditioned release of endogenous CORT was triggered by stimuli associated with nicotine delivery. These data are consistent with the hypothesis that a conditioned release of CORT could contribute to the development of tolerance to some of nicotine's effects.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…CORT, in turn, can modulate the physiological and behavioral effects of nicotine in rodents. Administration of CORT or exposure to a stressor antagonizes the analgesic [101] and hypothermic [102] effects of nicotine. Conversely, adrenalectomy results in an increase in nicotine-dependent decreases in locomotor activity, heart rate and body temperature and an enhancement of the effect of nicotine on the startle response [103,104], that is reversed following administration of CORT [103,105].…”

Section: Neurochemical Mechanisms Underlying Nicotine's Effects On Emmentioning

confidence: 98%

Effect of nicotine and nicotinic receptors on anxiety and depression

Picciotto

Brunzell²,

Caldarone³

2002

Neuroreport

412

291

View full text Add to dashboard Cite

Nicotine has been shown to have effects on anxiety and depression in both human and animal studies. These studies suggest that nicotinic acetylcholine receptors (nAChRs) can modulate the function of pathways involved in stress response, anxiety and depression in the normal brain, and that smoking can result in alterations of anxiety level and mood. The effects of nicotine are complex however, and nicotine treatment can be either anxiolytic or anxiogenic depending on the anxiety model tested, the route of nicotine administration and the time course of administration. The paradoxical effects of nicotine on emotionality are likely due to the broad expression of nAChRs throughout the brain, the large number of nAChR subtypes that have been identified and the ability of nicotine treatment to both activate and desensitize nAChRs. Activation of nAChRs has been shown to modulate many systems associated with stress response including stress hormone pathways, monoaminergic transmission and release of classical neurotransmitters throughout the brain. Local administration studies in animals have identified brain areas that may be involved in the anxiogenic and anxiolytic actions of nicotine including the lateral septum, the dorsal raphe nuclei, the mesolimbic dopamine system and the hippocampus. The ensemble of studies to date suggest that under certain conditions nicotine can act as an anxiolytic and an antidepressant, but that following chronic use, adaptations to nicotine can occur resulting in increased anxiety and depression following withdrawal.

show abstract

Chronic injections of saline produce subsensitivity to nicotine

Cited by 26 publications

References 17 publications

Mecamylamine prevents tolerance but enhances whole brain [ 3 H]epibatidine binding in response to repeated nicotine administration in rats

Mecamylamine prevents tolerance but enhances whole brain [ 3 H]epibatidine binding in response to repeated nicotine administration in rats

Acute stress or corticosterone administration reduces responsiveness to nicotine: implictions for a mechanism of conditioned tolerance

Effect of nicotine and nicotinic receptors on anxiety and depression

Contact Info

Product

Resources

About