Central epinergic inhibition of corticosterone release in rat

Roth, Kevin A.; Katz, Richard J.; Sibel, Michael; Mefford, Ivan N.; Barchas, Jack D.; Carroll, Bernard J.

doi:10.1016/0024-3205(81)90505-1

Cited by 56 publications

(4 citation statements)

References 14 publications

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“…The changes in these brain eatecholamines might be related to the increased secretion of ACTH and corticoids. Evidence sup, porting an inhibitory (Ganong, 1980;Mezey et al, 1984;Roth et al, 1981) or a stimulatory (Plotsky, 1987;Guillaume et al, 1987) role of norepinephrine or epinephrine in the secretion of ACTH has been reported. Further research is needed to clarify the role these central catecholamines play in the regulation of corticosterone secretion.…”

Section: Resultsmentioning

confidence: 96%

Endocrine and neurochemical effects of (+)-PHNO, a dopamine D2 agonist

Gust

Hemrick‐Luecke

Fuller

1989

J. Neural Transmission

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The naphthoxazine compound, (+)-PHNO, is a dopamine D2 receptor agonist which acts within the central nervous system. The effects of this drug on serum concentrations of corticosterone and prolactin and on brain concentrations of catecholamines and some of their metabolites were determined in male rats. Administration of (+)-PHNO in doses ranging from 3-300 micrograms/kg i.p. resulted in increased serum corticosterone, decreased serum prolactin and decreased concentrations of the dopamine metabolites, DOPAC and HVA, in the brain. At the higher doses of (+)-PHNO, concentrations of MHPG sulfate in the brain stem were increased and hypothalamic epinephrine concentrations were decreased. Pretreatment with centrally acting dopamine antagonists (spiperone or haloperidol) prevented the (+)-PHNO-induced changes in serum corticosterone, prolactin and brain catecholamines. In contrast, pretreatment with halopemide, a dopamine antagonist which penetrates poorly into the brain, was unable to block the effects of (+)-PHNO on serum corticosterone and brain catecholamines. These data show that (+)-PHNO, a dopamine agonist structurally unrelated to other dopamine agonists, acts centrally to affect serum corticosterone and brain catecholamines.

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Section: Resultsmentioning

confidence: 96%

Endocrine and neurochemical effects of (+)-PHNO, a dopamine D2 agonist

Gust

Hemrick‐Luecke

Fuller

1989

J. Neural Transmission

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“…The same group has also shown that NE-blocked the acetylcholine-induced increase in CRF release [19]. Moreover, hypothalamic E has been shown to inhibit corticosterone release in the rat [20] and an increased staining of CRF immunoreactivity in rat paraventricular neurons following depletion of hypothalamic E has been found [21].…”

Section: Discussionmentioning

confidence: 91%

Relationship between pituitary ACTH content and hypothalamic catecholamines in the rat

et al. 1989

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Hypothalamic concentrations of epinephrine and norepinephrine were determined in rats following 6-hydroxydopamine lesions of the locus coeruleus and subcoeruleus system and following sham-operation. These concentrations were correlated with pituitary ACTH content. While the lesion procedure did not have a major effect on hypothalamic monoamine levels, we were able to demonstrate a strong negative correlation between hypothalamic epinephrine and pituitary ACTH content independent of the experimental condition. Only a weak negative correlation was observed for hypothalamic norepinephrine and pituitary ACTH. Our recent and previous data suggest a tonic and phasic inhibition of ACTH release by hypothalamic monoamines.

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“…Also Sawchenko and Swanson [1981] postulated that noradrenergic cells in the ventrolateral medulla (A 1), dorsal vagal complex (A 2) and locus ceruleus (A 6) regions give rise to projections to the PVN and supraoptic nucleus. Jones and Hillhouse [1977] and Roth et al [1981], using pharmacological investigations in vitro or in vivo, reported that noradrenaline is an inhibitory neurotransmitter in CRF secretion. Mezey et al [1984] have shown by immunohistochemistry using antisera to PNMT and CRF that the depletion of adrenaline resulted in an increase of CFR immunoreactivity in the PVN.…”

Section: Discussionmentioning

confidence: 99%

Catecholaminergic Innervation of Neurons Containing Corticotropin-Releasing Factor in the Paraventricular Nucleus of the Rat Hypothalamus

Kitazawa

Shioda

Nakai³

1987

Cells Tissues Organs

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Catecholaminergic synaptic input to neurons containing corticotropin-releasing factor (CRF) in the parvocellular portion of the paraventricular nucleus (PVN) in the rat hypothalamus was observed. The experimental techniques used combine autoradiography after ³H-noradrenaline ( H-NA) injection or uptake of 5-hydroxy-dopamine (5-OHDA) with immunocytochemistry using CRF antiserum. CRF-like immunoreactive cell bodies and fibers in the PVN received synaptic inputs from the axon terminals in which a selective accumulation of ³H-NA or 5-OHDA was found. This finding suggests that the secretion of CRF neurons may be regulated via synapses by catecholaminergic neurons.

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Central epinergic inhibition of corticosterone release in rat

Cited by 56 publications

References 14 publications

Endocrine and neurochemical effects of (+)-PHNO, a dopamine D2 agonist

Endocrine and neurochemical effects of (+)-PHNO, a dopamine D2 agonist

Relationship between pituitary ACTH content and hypothalamic catecholamines in the rat

Catecholaminergic Innervation of Neurons Containing Corticotropin-Releasing Factor in the Paraventricular Nucleus of the Rat Hypothalamus

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