Adrenocortical hormone regulation of nicotine sensitivity in mice

Pauly, James R.; Ullman, Elizabeth A.; Collins, Allan C.

doi:10.1016/0031-9384(88)90353-8

Cited by 48 publications

(24 citation statements)

References 41 publications

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“…It is possible that different receptor systems were altered by the stress of isolation rearing. For example, high levels of circulating corticosterone, known to be elevated during stress (Gilad et al 1985), have been shown to reduce the numbers of hippocampal a 7 receptors in mice (Pauly et al 1988(Pauly et al , 1990Pauly and Collins 1993), which has functional consequences ). Other studies have demonstrated alterations in catecholaminergic and serotonergic response following isolation rearing (Jones et al 1990(Jones et al , 1992Smith et al 1997).…”

Section: Discussionmentioning

confidence: 96%

DMXB, an ?7 nicotinic agonist, normalizes auditory gating in isolation-reared rats

et al. 2003

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DMXB improved the auditory gating deficit seen in isolation-reared rats. As previously observed in another model, the change was produced through a decrease in the test amplitude in isolation-reared animals. Control animals had a significant reduction in conditioning amplitude at the high dose, which produced the loss of auditory gating. The results in the isolation-reared rats are in concert with previous studies which found similar improvement in auditory gating following administration of DMXB to DBA mice, the only differences being in the duration of the effect.

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Section: Discussionmentioning

confidence: 96%

DMXB, an ?7 nicotinic agonist, normalizes auditory gating in isolation-reared rats

et al. 2003

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“…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%

“…Since there is evidence that both non-pharmacological stress and nicotine stimulate HPA activity via nicotinic-cholinergic receptors (Marty et al 1985), it is not unreasonable to postulate that CORT may attenuate nicotine-induced activation of HPA activity by an action at these receptors. The possibility that these inhibitory actions of CORT could extend to other actions of nicotine by acting directly or indirectly to reduce nicotine's actions at nicotinic-cholinergic receptors has been raised (Pauly et al 1988;Collins et al 1990a;Pomerleau and Pomerleau 1990b).…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

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confidence: 92%

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

et al. 1993

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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)

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“…We have shown that nicotine elicits a dose-dependent increase in plasma corticosterone (CORT) levels [I]; the increase in CORT may have func tional consequences since alterations in glucocorticoid hormones affect sensitivity to nicotine. For example, ad renalectomy (ADX) increases the behavioral and physio logical sensitivity to systemically administered nicotine and CORT reverses this increase in sensitivity [2,3]. Sham-operated animals that are given CORTsupplemen-…”

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confidence: 99%

An Autoradiographic Analysis of Alterations in Nicotinic Cholinergic Receptors following 1 Week of Corticosterone Supplementation

Pauly

Collins²

1993

Neuroendocrinology

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Previous studies from our laboratory have established an interaction between central nervous system nicotinic cholinergic systems and glucocorticoid hormones. When mice are treated for 1 week with exogenous corticosterone (CORT) they become insensitive to the behavioral and physiological actions of nicotine and also have a reduction in brain α-bungarotoxin (BTX) receptor binding. In the present study, mice were treated with high stress levels of CORT and nicotinic receptor binding was measured using quantitative autoradiographic methods. L-[³H]-nicotine and α-[¹²⁵I]-bungarotoxin were used to label both high- and low-affinity nicotinic sites. Chronic CORT administration reduced BTX binding in 77 of 115 (67.0%) brain regions examined. In general, forebrain regions were more sensitive to this regulation than were more posterior brain regions. Hippocampal and hypothalamic regions were particularly susceptible, with binding in treated animals being reduced by up to 80% in some nuclei. L-[³H]-nicotine sites were not as sensitive to CORT regulation as binding was significantly reduced in only 7 of the 83 (8.4%) regions measured. Regions affected were restricted to the thalamus and septum. The mechanism by which CORT reduces brain nicotinic cholinergic receptor binding is unknown and may or may not be dependent on CNS glucocorticoid receptors.

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Adrenocortical hormone regulation of nicotine sensitivity in mice

Cited by 48 publications

References 41 publications

DMXB, an ?7 nicotinic agonist, normalizes auditory gating in isolation-reared rats

DMXB, an ?7 nicotinic agonist, normalizes auditory gating in isolation-reared rats

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

An Autoradiographic Analysis of Alterations in Nicotinic Cholinergic Receptors following 1 Week of Corticosterone Supplementation

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