Effect of Intracerebroventricular Clonidine on Serum Corticosterone Levels in Rats

Zacny, Elżbieta; Bugajski, J

doi:10.1159/000179983

Cited by 12 publications

(5 citation statements)

References 17 publications

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“…However, no clear conclusions can be found in the scanty literature on icv administration of catecholamines. It has been reported that icv injections of the « 2 -agonist clonidine lead to increased corticosterone release, and that the effect is reversed by the a 2 -blocker yohimbine, but not by the preferential «i-blocker phenoxybenzamine (23). These results were taken as favoring the theory that catecholamines inhibit ACTH release via presynaptic a 2 -receptors, in agreement with hypotheses based on findings in the dog (1, 2).…”

Section: Discussionsupporting

confidence: 88%

Further Evidence for a Central Stimulatory Action of Catecholamines on Adrenocorticotropin Release in the Rat

et al. 1987

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Catecholamines may stimulate ACTH secretion during stress. To investigate the nature and site of such an action, plasma ACTH was measured in four groups of unanesthetized adult female rats with an indwelling carotid cannula. Sequential 300-microliter blood samples were taken 60 min, 30 min, and immediately before an intracerebroventricular (icv) infusion of 2.5 microliter adrenaline or noradrenaline and 5, 15, 45, 60, and 120 min after the infusion. The four groups were: 1) intact rats; 2) rats infused 7 days after undergoing a discrete bilateral lesion of the ventral noradrenergic ascending bundle caused by 6-hydroxydopamine, which depleted their hypothalamic adrenaline and noradrenaline levels by 90% and 80%, respectively; 3) rats infused 30 min after pretreatment via the icv route with either prazosin or propranolol; and 4) rats infused 16 and 2 h after two successive intracarotid injections of an anti-rCRH-41 serum. In another group, the effects of icv catecholamine administration were compared with those of an intracerebral (ic) microinfusion close to a single paraventricular nucleus (PVN). Finally, in two additional groups blood was sampled at the above-mentioned times before and after a 2-min ether inhalation by intact rats or prazosin- and/or propranolol-pretreated rats. In the intact rats (group 1), a stress-like stimulatory dose response was noted after both adrenaline and noradrenaline infusions, with a half-maximal effect at concentrations of about 0.6 nmol and a maximal effect at 2.7 nmol or more. At maximally effective doses, adrenaline was significantly more active than noradrenaline. In the rats with ventral noradrenergic ascending bundle lesions (group 2), 2.7 nM adrenaline or noradrenaline stimulated ACTH release as in the controls without lesions. In group 3, prazosin blocked the ACTH responses to both adrenaline and noradrenaline, whereas propranolol only blocked the response to adrenaline. In group 4, i.e. rats pretreated with an anti-rCRH-41 serum, the amplitude of the ACTH surge after icv adrenaline or noradrenaline infusion was halved. A unilateral ic catecholamine microinfusion next to the PVN (half the icv dose given in group 1) led to a rapid ACTH release that peaked at half the response measured in the icv infused rats. Ether stress-induced ACTH release was decreased by 50-60% after icv pretreatment with 1 or 10 micrograms prazosin, 1 or 6.5 micrograms propranolol, or a combined dose comprising 1 microgram of both. The following conclusions were reached.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Discussionsupporting

confidence: 88%

Further Evidence for a Central Stimulatory Action of Catecholamines on Adrenocorticotropin Release in the Rat

et al. 1987

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“…The injection of clonidine resulted in a significant stimulation of corticosterone secretion which agrees with the findings of others (37,(39)(40)(41). Previously we could not show any clonidine-mediated stimulation of corticosterone release, possibly because the basal corticosterone levels of the control rats were relatively increased as a result of suboptimal experimental conditions (18).…”

Section: Discussionsupporting

confidence: 92%

“…Current evidence strongly favours a stimulatory action for noradrenaline (12,13,35), although inhibitory effects have also been reported (36)(37)(38). Most of the discrepancies appear to result from differences in methodological approaches eg.…”

Section: Discussionmentioning

confidence: 99%

?2 and ?-adrenergic stimulation of corticosterone secretion in rats

et al. 1993

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Bilateral injection of 6-hydroxydopamine into the medial forebrain bundle (MFB) significantly decreased monoamine concentrations in the hypothalamus. The noradrenaline and serotonin content of the paraventricular nucleus (PVN) was also significantly reduced. These drastic decreases in neurotransmitter concentration did not alter basal secretion of corticosterone. Isoproterenol, a beta-adrenoceptor agonist (1 mg/kg, i.p.), significantly stimulated corticosterone release in saline and MFB lesioned rats. This stimulation did not differ significantly between the two groups. Clonidine, an alpha 2-adrenoceptor agonist, injected either intraperitoneally or intracerebrally just dorsal to the PVN, caused a dose-dependent increase in corticosterone secretion. The stimulation of corticosterone release by clonidine (250 micrograms/kg, i.p.) was antagonised by the selective alpha 2-adrenoceptor antagonist, yohimbine (1 mg/kg, i.p.) and significantly reduced by the MFB lesion. These results suggest that corticosterone secretion is stimulated by activation of alpha 2-adrenoceptors which occur on noradrenergic nerve terminals in the PVN.

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“…This is supported by the facts that clonidine, another (x2-adrenoceptor agonist, increases both plasma glucagon (Gotoh et al 1988) and corticosterone (Zacny and Bugajski 1984) concentrations in rats. Since the secretion of catecholamines is negatively controlled by c~2-adrenoceptors (Sakurai et al 1983), they probably did not contribute to the hyperglycemia in our studies with amitraz.…”

Section: Discussionmentioning

confidence: 80%

Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin

1990

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Amitraz (N'-[2,4-dimethylphenyl]-N-[(2,4-dimethylphenyl)imino]-N- methylmethanimidamide) is a formamidine insecticide/acaricide that increases plasma glucose and decreases plasma insulin concentrations in dogs when applied topically. Because amitraz activates alpha 2-adrenoceptors in numerous tissues, in this study we used rats as a model to determine whether these effects of amitraz are mediated by alpha 2-adrenoceptors. The i.v. injection of amitraz (0.1, 0.3, and 1 mg/kg) followed by i.v. glucose injection (1 g/kg) induced a dose-dependent glucose intolerance characterized by hypoinsulinemia. At 1 mg/kg, amitraz completely blocked the insulin release induced by i.v. glucose administration. The alpha 2-adrenoceptor antagonist yohimbine (1 mg/kg, i.v.) prevented the effects of amitraz, but the alpha 1-adrenoceptor antagonist prazosin (0.3 mg/kg, i.v.) did not. The results suggested that one mechanism by which amitraz prolongs glucose-induced hyperglycemia is via inhibition of insulin release and this effect is mediated by alpha 2-adrenoceptors.

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Effect of Intracerebroventricular Clonidine on Serum Corticosterone Levels in Rats

Cited by 12 publications

References 17 publications

Further Evidence for a Central Stimulatory Action of Catecholamines on Adrenocorticotropin Release in the Rat

Further Evidence for a Central Stimulatory Action of Catecholamines on Adrenocorticotropin Release in the Rat

?2 and ?-adrenergic stimulation of corticosterone secretion in rats

Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin

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