Effect of nicotine on in vivo secretion of melanocorticotropic hormones in the rat

Conte-Devolx, B.; Oliver, Charles; Giraud, Pierre; Gillioz, P.; Castanas, Elias; Lissitzky, Jean‐Claude; Boudouresque, Françoise; Millet, Yves

doi:10.1016/0024-3205(81)90755-4

Cited by 71 publications

(29 citation statements)

References 17 publications

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“…However, whether smoking itself affects the response to stressors is controversial, because both reductions and increases in stress levels have been reported in smokers (Parrott, 1995;Koval et al, 2004;Croghan et al, 2006;Finkelstein et al, 2006). In animals, acute injection of nicotine, the principal psychoactive component of tobacco smoke, is a potent stimulus for secretion of the stress-responsive hypothalamo-pituitary-adrenal (HPA) axis hormones ACTH (Conte-Devolx et al, 1981;Cam and Bassett, 1983;Matta et al, 1987) and corticosterone (Balfour et al, 1975;Cam and Bassett, 1983). Acutely injected nicotine increased glutamate release and enhanced NMDA receptor activity in noradrenergic regions of the nucleus tractus solitarius projecting to the hypothalamic paraventricular nucleus (PVN) (Zhao et al, 2007), projections shown to stimulate norepinephrine release and activate corticotropin-releasing factor (CRF) neurons in PVN (Valentine et al, 1996;Matta et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Nicotine Self-Administration Differentially Regulates Hypothalamic Corticotropin-Releasing Factor and Arginine Vasopressin mRNAs and Facilitates Stress-Induced Neuronal Activation

Yu¹,

Chen²,

Zhao³

et al. 2008

J. Neurosci.

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Acute nicotine is a potent stimulus for activation of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis, while chronic nicotine self-administration (SA) desensitizes the ACTH response to self-administered nicotine but cross-sensitizes to mild footshock stress (mFSS). To identify underlying mechanisms, we investigated (1) the effects of chronic nicotine SA on the coexpression of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) mRNAs, the primary hypothalamic neuropeptides regulating ACTH release, in the parvocellular division of paraventricular nucleus (pcPVN), and (2) /AVP ϩ population was activated by this heterotypic stressor. These phenotypic neuronal alterations may provide the pivotal mechanism underlying the capacity of chronically selfadministered nicotine to cross-sensitize the HPA response to specific stressors, suggesting that nicotine may augment HPA responsiveness to specific stressors in human smokers.

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Section: Introductionmentioning

confidence: 99%

Nicotine Self-Administration Differentially Regulates Hypothalamic Corticotropin-Releasing Factor and Arginine Vasopressin mRNAs and Facilitates Stress-Induced Neuronal Activation

Yu¹,

Chen²,

Zhao³

et al. 2008

J. Neurosci.

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“…In animal studies, many laboratories, including ours, have reported that nicotine, the main psychoactive component of cigarettes, is a potent stimulus for the secretion of stressresponsive hormones, such as adrenocorticotropic hormone (ACTH) (Cam and Bassett, 1983b;Conte-Devolx et al, 1981;Matta et al, 1987), prolactin (Andersson et al, 1983;Sharp and Beyer, 1986), and corticosterone (CORT) (Balfour et al, 1975;Cam and Bassett, 1983a). We further demonstrated that nicotine indirectly induces ACTH secretion from the anterior pituitary by directly activating noradrenergic areas of the nucleus tractus solitarius (Matta et al, 1998;Zhao et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chen

Sharp

2007

Neuropsychopharmacol

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We investigated the effect of chronic nicotine self-administration (SA) on hypothalamic-pituitary-adrenal (HPA) hormonal responses to acute stressors. Adult male Sprague-Dawley rats were given access to nicotine (0.03 mg/kg) for 23 h per day for 20 days. On day 1 of acquisition of nicotine SA, plasma levels of both adrenocorticotropin and corticosterone were significantly increased 15-30 min after the first dose of nicotine. These hormonal changes were no longer significant on day 3, when adrenocorticotropin levels were o60 pg/ml and corticosterone levels were o110 ng/ml during the hour after the first dose of nicotine. Chronic nicotine SA (20 days) significantly augmented (2-3-fold) both hormonal responses to mild foot shock stress (0.6 mA, 0.5 s per shock, 5 shocks per 5 min), but did not affect hormonal responses to moderate shock (1.2 mA, 0.5 s per shock, 5 shocks per 5 min), lipopolysaccharide or immobilization. Similar data were obtained in Lewis rats. These results provide further support for the concept that chronic nicotine SA is a stressor. In alignment with the effects of other stressors, nicotine activated the HPA axis on the first day of SA, but desensitization occurred with repeated exposure. Furthermore, chronic nicotine SA selectively cross-sensitized the HPA response to a novel stressor. These observations suggest that nicotine may selectively increase the HPA response to stressors in human smokers.

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“…To demonstrate the age related changes in sensitivity to nicotine, we investi gated nicotine-induced convulsive movements and the pharmacokinetics of nicotine in old rats. Moreover, several studies on animals have demonstrated that the acute systemic injection of nicotine induces dose-depend ent increases in blood corticosterone (CS) levels (7,8). The nicotine-induced elevations of blood CS levels are regulated through nAChRs in the brain (8).…”

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confidence: 99%

“…Laurence and Stacey (12) observed that nicotine-induced convulsions were potentiated by the systemic pretreatment with adrenaline or noradrenaline, and they are suppressed by adrenalectomy. In addition, it has been shown that acute administration of nicotine stimulates the release of adrenocorticotropic hormone from the pituitary gland, resulting in the elevation of blood glucocorticoid level (7). Thus, the decreases in convulsive and CS responses induced by nicotine in old rats may also be related to the age-related decrease in sensitivity of the adrenal gland.…”

mentioning

confidence: 99%

Effects of Acute Administration of Nicotine on Convulsive Movements and Blood Levels of Corticosterone in Old Rats

Okamoto

Kita

Okuda

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-The convulsive movements, blood levels of corticosterone and pharmacokinetics of nico tine after an acute intraperitoneal injection of nicotine (5 mg/kg) were examined in young (6-week-old) and old (2-year-old) rats. In pharmacokinetic study, blood nicotine levels during the elimination phase were significantly higher in old rats than in young rats. However, the duration of convulsions and the elevation of corticosterone levels after the nicotine injection showed significant decreases in old rats compared with those in young rats. These differences of nicotine-induced responses between young and old rats may be involved in the decrease in nicotine sensitivity.

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Effect of nicotine on in vivo secretion of melanocorticotropic hormones in the rat

Cited by 71 publications

References 17 publications

Nicotine Self-Administration Differentially Regulates Hypothalamic Corticotropin-Releasing Factor and Arginine Vasopressin mRNAs and Facilitates Stress-Induced Neuronal Activation

Nicotine Self-Administration Differentially Regulates Hypothalamic Corticotropin-Releasing Factor and Arginine Vasopressin mRNAs and Facilitates Stress-Induced Neuronal Activation

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Effects of Acute Administration of Nicotine on Convulsive Movements and Blood Levels of Corticosterone in Old Rats

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