Lesioning of the hypothalamic paraventricular nucleus inhibits ether- induced ACTH but not prolactin release

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9 Citations (Scopus)

Abstract

Stress mediators, CRF-41 and vasopressin known to be synthesized in, and released from the parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVN) are essential to release adrenocorticotropin (ACTH) in response to stress. In addition, suckling-induced prolactin (PRL) release also depends on the integrity of the PVN. In the present study, ether stress-induced adrenocorticotrop hormone (ACTH) and prolactin (PRL) release was studied 2, 5 and 42 days after placing lesions in the hypothalamic paraventricular nucleus (PVN) of male rats. Ether-induced ACTH secretion was strongly inhibited 2 and 5 days after lesions whereas 6 weeks later the lesion induced inhibition was fading. In contrast, PVN lesion failed to inhibit ether-induced PRL release at any time studied. The results suggest that contrary to previous suggestions the peptidergic neurons essential for stress-induced PRL release are outside the PVN.

Original languageEnglish
Pages (from-to)403-411
Number of pages9
JournalNeurobiology
Volume5
Issue number3
Publication statusPublished - 1997

Fingerprint

Paraventricular Hypothalamic Nucleus
Prolactin
Ether
Hormones
Neurons
Corticotropin-Releasing Hormone
Vasopressins
Adrenocorticotropic Hormone

Keywords

  • ACTH
  • PRF
  • Prolactin
  • Prolactin releasing factor

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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abstract = "Stress mediators, CRF-41 and vasopressin known to be synthesized in, and released from the parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVN) are essential to release adrenocorticotropin (ACTH) in response to stress. In addition, suckling-induced prolactin (PRL) release also depends on the integrity of the PVN. In the present study, ether stress-induced adrenocorticotrop hormone (ACTH) and prolactin (PRL) release was studied 2, 5 and 42 days after placing lesions in the hypothalamic paraventricular nucleus (PVN) of male rats. Ether-induced ACTH secretion was strongly inhibited 2 and 5 days after lesions whereas 6 weeks later the lesion induced inhibition was fading. In contrast, PVN lesion failed to inhibit ether-induced PRL release at any time studied. The results suggest that contrary to previous suggestions the peptidergic neurons essential for stress-induced PRL release are outside the PVN.",
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AU - Makara, G.

AU - Kovács, K.

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N2 - Stress mediators, CRF-41 and vasopressin known to be synthesized in, and released from the parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVN) are essential to release adrenocorticotropin (ACTH) in response to stress. In addition, suckling-induced prolactin (PRL) release also depends on the integrity of the PVN. In the present study, ether stress-induced adrenocorticotrop hormone (ACTH) and prolactin (PRL) release was studied 2, 5 and 42 days after placing lesions in the hypothalamic paraventricular nucleus (PVN) of male rats. Ether-induced ACTH secretion was strongly inhibited 2 and 5 days after lesions whereas 6 weeks later the lesion induced inhibition was fading. In contrast, PVN lesion failed to inhibit ether-induced PRL release at any time studied. The results suggest that contrary to previous suggestions the peptidergic neurons essential for stress-induced PRL release are outside the PVN.

AB - Stress mediators, CRF-41 and vasopressin known to be synthesized in, and released from the parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVN) are essential to release adrenocorticotropin (ACTH) in response to stress. In addition, suckling-induced prolactin (PRL) release also depends on the integrity of the PVN. In the present study, ether stress-induced adrenocorticotrop hormone (ACTH) and prolactin (PRL) release was studied 2, 5 and 42 days after placing lesions in the hypothalamic paraventricular nucleus (PVN) of male rats. Ether-induced ACTH secretion was strongly inhibited 2 and 5 days after lesions whereas 6 weeks later the lesion induced inhibition was fading. In contrast, PVN lesion failed to inhibit ether-induced PRL release at any time studied. The results suggest that contrary to previous suggestions the peptidergic neurons essential for stress-induced PRL release are outside the PVN.

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