Central dopamine receptors mediating pergolide-induced elevation of serum corticosterone in rats

Fuller, Ray W.; Snoddy, Harold D.

doi:10.1016/0028-3908(84)90078-9

Cited by 28 publications

(12 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, APO-CORT responses were not correlated with cortisol responses to serotonergic agonists (e.g. L-5-hydroxytryptophan, MK-212, a 5-HT 2A / 2C agonists, or ipsapirone, a 5-HT 1A agonist) in normal controls (Meltzer and Lee, unpublished observation), which is consistent with a rodent study reported by Fuller and Snoddy (1984). In addition, cortisol response to 5-HT 2A / 2C agonists (MK-212 and MCPP) were not different between patients with SCH and normals (Ranjan et al 1995;Maes and Meltzer 1996).…”

Section: The Dopaminergic Mechanism Mediating the Blunted Cortisol Ansupporting

confidence: 89%

“…Furthermore, the D 1 antagonist, SCH 23390, and the D 2 antagonist, sulpiride, blocked the ACTH and corticosterone increases induced by the corresponding D 1 and D 2 agonists respectively. Fuller and Snoddy (1984) have reported that the ED 50 values of 14 DA antagonists for inhibition of the stimulation of corticosterone by pergolide, a DA agonist with a high affinity for D 2 and D 3 receptors (Sokoloff et al 1990) and a moderate affinity for D 1 receptors correlated well with its affinity for the D 2 receptor, but not with its affinity for the D 1 receptor. In addition, the pergolide-stimulated corticosterone response was blocked by centrally acting antagonists (e.g.…”

Section: Da Receptors Mediating Hormone Responses To Apomentioning

confidence: 99%

“…Animal studies have reported that DA agonist-stimulated HPA axis responses are mediated via D 1 and/or D 2 receptor stimulation (Borowsky and Kuhn 1992;Fuller and Snoddy 1984). In addition, ventral striatum, which is one of anatomical regions related to pathophysiology of SCH, has been reported to be involved in the corticosterone secretion induced by the combined administration of D 1 /D 2 agonists (SKF 38393/quinpirole) in rats (Ikemoto and Goeders 1998).…”

mentioning

confidence: 99%

See 2 more Smart Citations

The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia

Meltzer

Lee

Jayathilake

2001

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

Section: The Dopaminergic Mechanism Mediating the Blunted Cortisol Ansupporting

confidence: 89%

Section: Da Receptors Mediating Hormone Responses To Apomentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia

Meltzer

Lee

Jayathilake

2001

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…First, neurotensin increased serum corticosterone concentration at doses much less than those required to increase the activity of tuberoinfundibular dopamine neurons. Secondly, the neurotensin-induced in crease in serum corticosterone concentrations was not dimini shed by haloperidol which was given in a dose shown by Fuller and Snoddy [7] to be sufficient to antagonize dopamine ago nist-induced corticosterone secretion. Thus, the increase in serum corticosterone concentrations produced by neurotensin does not appear to depend upon the concomitant activation of • tuberoinfundibular dopamine neurons.…”

Section: Discussionmentioning

confidence: 99%

Neurotensin Activates Tuberoinfundibular Dopamine Neurons and Increases Serum Corticosterone Concentrations in the Rat

1989

View full text Add to dashboard Cite

The activity of tuberoinfundibular dopamine neurons, as estimated from the amount of dihydroxyphenylalanine (DOPA) formed in the median eminence after the inhibition of DOPA decarboxylase and the concentration of dihydroxyphenyl-acetic acid (DOPAC) in this brain region, was significantly increased 1–8 h following the intracerebroventricular (i.c.v.) administration of neurotensin (20 µg). Neurotensin (5 and 20 µg i.c.v.) also significantly increased DOPAC concentrations in the n. accumbens but had no effect in the striatum. Serum concentrations of corticosterone in rats treated with neurotensin (1–20 µg i.c.v.) were 5–7 times those in vehicle-treated animals. [D-Trp¹¹]-neurotensin (0.5 µg i.v.c.) also significantly increased DOPAC concentrations in the median eminence and serum corticosterone concentrations. It is concluded that neurotensin acutely increases the activity of tuberoinfundibular and mesolimbic dopamine neurons and the secretion of ACTH.

show abstract

“…It is well documented that stimulation of the HPA axis in rats may also result from activation of the central 5-HT or dopamine (DA) system, this effect being mediated by 5-HT~ A and 5-HT 2 receptors (Koenig et al, 1987;Przegaliflski et al, 1989) or D 2 receptors (Fuller and Snoddy, 1984;Przegaliflski et al, 1990), respectively. Since the OXA enantiomers have been reported to activate the central DA system (Delini-Stula and Mogilnicka, 1988;Maj etal., 1990), but not the 5-HT system (Maj et al, 1989), we examined the effect of the selective D2 receptor antagonist sulpiride and the non-selective 5-HT receptor blocker metergoline on the (+)-and (-)-OXA-induced corticosterone secretion.…”

Section: E Przegalifiski Et Almentioning

confidence: 99%

Oxaprotiline enantiomers stimulate ACTH and corticosterone secretion in the rat

Przegaliński

Budziszewska

Grochmal

1991

J. Neural Transmission

View full text Add to dashboard Cite

The effect of oxaprotiline (OXA) enantiomers--of which (+)-OXA inhibits noradrenaline (NA) uptake, whereas (-)-OXA does not--on the secretion of adrenocorticotropin hormone (ACTH) and corticosterone was studied in rats. Both enantiomers dose-dependently and with a similar potency increased the plasma level of ACTH and corticosterone, the effect of (-)-OXA on corticosterone being of a longer duration. The stimulation of ACTH secretion and the inability of (+)- and (-)-OXA to increase the plasma corticosterone concentration in animals pretreated with dexamethasone indicate that secretion of the latter hormone results from the action of the enantiomers at a level superior to the adrenal cortex, i.e. the hypothalamus/pituitary. The corticosterone response to (+)- or (-)-OXA was not modified in rats with a selective lesion of NA nerve endings induced by the neurotoxin DSP-4, nor was it affected by the selective alpha 1-antagonist prazosin, the selective alpha 2-antagonist yohimbine, the mixed alpha 1/alpha 2-antagonist phentolamine, the selective dopamine (D2) receptor antagonist sulpiride and the non-selective 5-hydroxytryptamine (5-HT) receptor antagonist metergoline. These results indicate that neither the NA system nor D2 and 5-HT receptors are involved in the hormonal response to the OXA enantiomers. Although the (+)- and (-)-OXA-induced stimulation of corticosterone secretion was not antagonized by diazepam, ipsapirone, naloxone, or propranolol, it cannot be excluded that both these enantiomers act as non-specific stressors.

show abstract

Central dopamine receptors mediating pergolide-induced elevation of serum corticosterone in rats

Cited by 28 publications

References 11 publications

The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia

The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia

Neurotensin Activates Tuberoinfundibular Dopamine Neurons and Increases Serum Corticosterone Concentrations in the Rat

Oxaprotiline enantiomers stimulate ACTH and corticosterone secretion in the rat

Contact Info

Product

Resources

About