Intravenous injections of nicotine induce very rapid and discrete reductions of hypothalamic catecholamine levels associated with increases of ACTH, vasopressin and prolactin secretion

Andersson, Kurt; Siegel, Richard A.; Fuxé, Kjell; Eneroth, P.

doi:10.1111/j.1748-1716.1983.tb07237.x

Cited by 75 publications

(22 citation statements)

References 15 publications

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“…Analogues of AVP such as desmopressin or lysine vasopressin have been used to treat nocturnal enuresis (bed wetting) in normal children (44) or to enhance learning and memory in mentally disabled children (45,46), respectively. Particularly disturbing is the fact that nicotine, a potent releaser of AVP (47)(48)(49)(50), can freely pass both the placental and blood-brain barriers of fetuses and their mothers alike (51,52). Given the recent rise in cigarette use among young girls and pregnant teenagers in the United States (53), it is important to understand the links among nicotine, vasopressin, and various conduct disorders observed in children of smoking mothers (54)(55)(56)(57)(58)(59).…”

Section: Discussionmentioning

confidence: 99%

Developmental exposure to vasopressin increases aggression in adult prairie voles

Stribley

Carter

1999

Proc. Natl. Acad. Sci. U.S.A.

111

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Although the biological roots of aggression have been the source of intense debate, the precise physiological mechanisms responsible for aggression remain poorly understood. In most species, aggression is more common in males than females; thus, gonadal hormones have been a focal point for research in this field. Although gonadal hormones have been shown to influence the expression of aggression, in many cases aggression can continue after castration, indicating that testicular steroids are not completely essential for the expression of aggression. Recently, the mammalian neuropeptide arginine vasopressin (AVP) has been implicated in aggression. AVP plays a particularly important role in social behavior in monogamous mammals, such as prairie voles (Microtus ochrogaster). In turn, the effects of social experiences may be mediated by neuropeptides, including AVP. For example, sexually naïve prairie voles are rarely aggressive. However, 24 h after the onset of mating, males of this species become significantly aggressive toward strangers. Likewise, in adult male prairie voles, central (intracerebroventricular) injections of AVP can significantly increase intermale aggression, suggesting a role for AVP in the expression of postcopulatory aggression in adult male prairie voles. In this paper, we demonstrate that early postnatal exposure to AVP can have long-lasting effects on the tendency to show aggression, producing levels of aggression in sexually naïve, adult male prairie voles that are comparable to those levels observed after mating. Females showed less aggression and were less responsive to exogenous AVP, but the capacity of an AVP V 1a receptor antagonist to block female aggression also implicates AVP in the development of female aggression.A rginine vasopressin (AVP) is a nonapeptide hormone primarily synthesized in the paraventricular nucleus and the supraoptic nucleus of the hypothalamus. In the brain, AVP predominantly binds to a G protein-coupled, V 1a receptor subtype having seven transmembrane domains. V 1 receptors depend on phosphatidyl inositol hydrolysis and intracellular calcium mobilization as part of the second messenger system for transcriptional activation and gene expression. In addition, there are numerous areas within the brain that receive AVP fiber projections from the paraventricular nucleus, including the amygdala, hippocampus, and posterior pituitary. Additional sites of AVP synthesis include the locus ceruleus and the bed nucleus of the stria terminalis, which sends neural projections to the lateral septum and the lateral habenular nucleus, among others (see refs. 1-4).AVP and related peptides have well documented effects on a variety of systems associated with the physiological and behavioral defense of homeostasis. For example, AVP is necessary for water retention and affects blood pressure and other aspects of cardiovascular function (5). In rats, AVP influences the regulation of the hypothalamic-pituitary-adrenal axis, and it is likely that the central release of AVP is sensitive ...

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Section: Discussionmentioning

confidence: 99%

Developmental exposure to vasopressin increases aggression in adult prairie voles

Stribley

Carter

1999

Proc. Natl. Acad. Sci. U.S.A.

111

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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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“…However, since nicotine is an extremely po tent secretagogue for ACTH [11][12][13][14], and since ACTH, too, produces an impressive re versal of the shock condition in the same experimental model [2][3][4][5][6]8], the possibility that a massive release of ACTH could partici pate in the nicotine-induced shock reversal seemed reasonably likely.…”

Section: Discussionmentioning

confidence: 99%

“…or 1-20 pg/rat intoacerebral ventricle (i.e.v.) causes within minutes an impressive release of ACTH [11][12][13][14] which, in the case of i.e.v. administration, can peak at about 9,000 pg/ml/min.…”

Section: Introductionmentioning

confidence: 99%

Adrenocorticotropin Release Is Not Involved in the Nicotine-Induced Reversal of Hemorrhagic Shock in Anesthetized Rats

Bazzani

Bertolini²,

L³

et al. 1995

Pharmacology

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In a model of volume-controlled hemorrhagic shock causing the death of all control animals within 30 min, the intravenous injection of nicotine produced a rapid, sustained and dose-dependent restoration of cardiovascular and respiratory functions, with 60 and 100% survival 2 h after the administration of 3 and 12 µg/kg, respectively. An effect similar to that of the highest dose of nicotine were obtained with the intravenous bolus injection of ACTH(l-24) at the dose of 160 µg/kg. However, the ACTH plasma levels of hemorrhage-shocked rats treated with nicotine was not different from that of hemorrhage-shocked rats treated with saline, thus excluding the possibility that nicotine-induced shock reversal may be due to the massive release of ACTH. Since in rats pretreated with cycloheximide at a dose (20 mg/kg intraperitoneally) causing an 82% inhibition of protein synthesis, and then bled to hemorrhagic shock, the effect of nicotine was greatly reduced (only the dose of 50 µg/kg producing 100% survival 2 h after treatment), protein synthesis, however, seems to be important for the effect of nicotine in hemorrhagic shock, at least at the lowest doses.

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Intravenous injections of nicotine induce very rapid and discrete reductions of hypothalamic catecholamine levels associated with increases of ACTH, vasopressin and prolactin secretion

Cited by 75 publications

References 15 publications

Developmental exposure to vasopressin increases aggression in adult prairie voles

Developmental exposure to vasopressin increases aggression in adult prairie voles

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

Adrenocorticotropin Release Is Not Involved in the Nicotine-Induced Reversal of Hemorrhagic Shock in Anesthetized Rats

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