Elevation of Serum Corticosterone in Rats by Dopamine Agonists Related in Structure to Pergolide

Fuller, Ray W.; Snoddy, Harold D.; Mason, Norman R.; Clemens, James A.; Bemis, Kerry G.

doi:10.1159/000123469

Cited by 41 publications

(11 citation statements)

References 16 publications

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“…The refore, the D-2 stimulation in vivo probably involves the se cretion of hypothalamic CRF [32]. In support of a central D-2 mechanism are previous findings that the peripherally acting D-2 antagonist, domperidone, did not block the in crease in serum corticosterone evoked by LY141865 [9], In the present study, central administration of sulpiride inhi bited LY141865-evoked ip-END release ( fig. 5), whereas pe ripherally administered sulpiride did not [Farah and Mueller, unpubl.…”

Section: Discussionsupporting

confidence: 82%

“…Holland et al [12] observed that both the dopa mine receptor agonist, apomorphine, and the dopamine pre cursor, L-dihydroxyphenylalanine, stimulated the release of adrenal glucocorticoids in conscious dogs. More recently, Fuller et al [8,9] reported that dopaminergic agonists elevate serum corticosterone levels in rats. These findings have been extended by the observations that the dopamine agonist, ap omorphine, increases circulating levels of ACTH and (1-LPH in rats [6,15].…”

mentioning

confidence: 99%

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A D-2 Dopaminergic Agonist Stimulates Secretion of Anterior Pituitary Immunoreactive β-Endorphin in Rats

Farah

Mueller²

1989

Neuroendocrinology

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Hypothalamic dopamine neurons are known to control circulating levels of immunoreactive β-endorphin (iβ-END) by inhibiting hormone secretion by the intermediate lobe (IL) of the pituitary gland. We examined the ability of the D-2 selective dopaminergic agonist, LY141865, to influence circulating levels of iβ-END in rats and found that in contrast to inhibiting IL secretion, LY141865 increased release of iβ-END from the anterior lobe (AL). Intraperitoneal injection of 1 mg/kg LY141865 transiently increased plasma levels of iβ-END by 7–30 min after drug treatment; plasma prolactin levels were maximally reduced within 15 min and throughout the remaining 2-hour time course of treatment. Doses of 0.3 and 1.0 mg/kg of LY141865 increased circulating iβ-END to 440 and 690%, respectively, of control levels (0.38 ± 0.12 ng/ml, mean ± SEM, n = 6). Lower doses of the D-2 agonist (0.01–0.1 mg/kg) failed to significantly affect plasma iβ-END. Sephadex G-50 chromatography of plasma pools revealed that virtually all of the increase due to LY141865 treatment was immunoreactivity resembling β-lipotropin in molecular size, the principal component of AL secretion of iβ-END. Furthermore, LY141865-evoked release was blocked by pretreatment of rats with dexamethasone (50 µg/kg i.p., 4 h) which inhibits AL but not IL secretion of pro-opiomelanocortin-derived peptides. Stimulation of iβ-END release by LY141865 was also inhibited by the general dopamine antagonist, haloperidol, (0.1–3.0 mg/kg i.p., 2 h) and by the D-2 selective antagonist, sulphide (100 µg/rat i.c.v., 4 h). These results indicate that the effects of LY141865 treatment on pituitary release of iβ-END are mediated by dopaminergic receptor activation, probably of the D-2 type, within the central nervous system. Since neither dopamine nor LY141865 directly influences AL secretion of iβ-END, the effects of D-2 receptor stimulation in vivo are probably mediated by actions of LY141865 on secretion of hypothalamic corticotropin-releasing factor, the principal physiologic stimulator of hormone secretion from pituitary corticotrophs.

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

A D-2 Dopaminergic Agonist Stimulates Secretion of Anterior Pituitary Immunoreactive β-Endorphin in Rats

Farah

Mueller²

1989

Neuroendocrinology

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“…Reduced D2-receptor sensitivity was also observed with regard to corticosterone secretion. Both systemic and intraventricular administration of quinpirole stimulates plasma corticosterone secretion (Borowsky and Kuhn, 1992;Foreman et al, 1989;Fuller et al, 1983). More recent work has demonstrated that the stimulatory effects of dopamine agonists on corticosterone secretion are mediated by activation within the ventral striatum (Ikemoto and Goeders, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…The current study also measured plasma corticosterone immediately after the completion of behavioral testing to determine whether any of the effects on PPI observed in the postpartum females were due to alterations in corticosterone secretion in response to the testing conditions as lactating females have been found to be stress hyporesponsive under some conditions (Lightman and Young, 1989). Moreover, as D2-agonists have been found to stimulate corticosterone secretion (Borowsky and Kuhn, 1992;Foreman et al, 1989;Fuller et al, 1983) via their effects within the ventral striatum (Ikemoto and Goeders, 1998), quinpirole-stimulated corticosterone secretion served as yet another measure of D2 receptor sensitivity within the forebrain dopamine system. Finally, plasma estradiol and progesterone levels were determined in all subjects in an attempt to correlate behavioral and neurochemical changes with postpartum shifts in hormone levels.…”

Section: Introductionmentioning

confidence: 88%

Sensorimotor Gating and Dopamine Function in Postpartum Rats

Byrnes

Bridges

Scanlan

et al. 2006

Neuropsychopharmacol

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There is much speculation regarding the effects of estrogen withdrawal at the end of pregnancy on forebrain dopamine, however, few studies have directly examine changes in this system postpartum. The present work sought to determine what changes in forebrain dopamine function occur in the postpartum rat. Specifically, prepulse inhibition of the acoustic startle response (PPI) was measured in primiparous female rats on postpartum day 2 (PPD2) or 14 (PPD14) following treatment with saline or the dopamine D2 agonist, quinpirole. Diestrus (DI) females served as controls. Dopamine content and turnover as well as cyclic AMP (cAMP) accumulation were determined within the nucleus accumbens and dorsal striatum in these same females. In addition, circulating levels of plasma corticosterone, estradiol and progesterone were measured. PPI was significantly disrupted in both postpartum groups. This effect was associated with decreased cAMP content within the nucleus accumbens. Quinpirole treatment (0.1 and 0.5 mg/kg) dose-dependently disrupted PPI in DI controls while PPD2 and PPD14 animals demonstrated reduced sensitivity to the D2 agonist. PPD14 animals demonstrated increased startle amplitude, an effect that was attenuated by quinpirole treatment. PPD14 females were also less sensitive to quinpirole-mediated reductions in DA turnover within the nucleus accumbens and both PPD2 and PPD14 females had an attenuated response to the stimulatory effects of quinpirole on corticosterone secretion. Collectively these findings suggest that the postpartum period is associated with reduced sensorimotor gating and altered forebrain DA systems, which may be related to shifts in circulating hormones.

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“…This was finally achieved using administration of protamine sulfate, a heparin antagonist. We decided to study ACTH release as the importance of the pituitary-adrenocortical axis for the control of BBB func tion had been demonstrated [25] and as there are still man\ doubts on ACTH regulation by peripheral substances known stimulatory role of central, but not peripheral, dopa mine receptors in the control of ACTH release [9,10,17] was used to show that otherwise ineffective circulating substances can modify neuroendocrine regulations if a tran sient, reversible increase in BBB permeability occurs.…”

mentioning

confidence: 99%

Changes in Blood-Brain Barrier Function Modify the Neuroendocrine Response to Circulating Substances

Ježová

Bb²,

Oprsalová³

et al. 1989

Neuroendocrinology

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It is known that various experimental, pathological and even physiological situations may be accompanied by transient increases in blood-brain barrier (BBB) permeability. The hypothesis that under such conditions the blood-borne substances can reach the active sites in the brain in concentrations high enough to influence central control of hormone release was verified in these studies. A suitable experimental model of BBB opening by protamine sulfate administration in conscious rats was introduced. Using this model it was shown that the dopaminergic blocker domperidone inhibited apomorphine-induced ACTH release if permeability of the BBB was increased, but not under normal conditions. It is suggested that the changes in BBB function can modify the neuroendocrine response also to other circulating substances and this may be an important, until now unconsidered phenomenon in neuroendocrine research.

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Elevation of Serum Corticosterone in Rats by Dopamine Agonists Related in Structure to Pergolide

Cited by 41 publications

References 16 publications

A D-2 Dopaminergic Agonist Stimulates Secretion of Anterior Pituitary Immunoreactive β-Endorphin in Rats

A D-2 Dopaminergic Agonist Stimulates Secretion of Anterior Pituitary Immunoreactive β-Endorphin in Rats

Sensorimotor Gating and Dopamine Function in Postpartum Rats

Changes in Blood-Brain Barrier Function Modify the Neuroendocrine Response to Circulating Substances

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