Various putative neurotransmitters affect growth hormone (GH) release in rats with anterolateral hypothalamic deafferentiation of the medial basal hypothalamus: Evidence for mediation by a GH-releasing factor

I. Kakucska, G. Makara

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Anterolateral deafferentation of the rat medial basal hypothalamus was used to eliminate most of the somatostatinergic innervation of the stalk-median eminence while leaving a functional system producing GH-releasing factor (GHRF) in the partially deafferented hypothalamus. One week after the operation, the rats were anesthetized, the third ventricle was cannulated, and various putative neurotransmitters were infused for 5 min. Plasma GH levels were measured between 10 and 25 min after infusion. When infused into the third ventricle, acetylcholine (50 μg), substance (5 μg), dopamine (5 μg), and norepinephrine (2.5 μg) increased plasma GH levels in the deafferented rats but not in the controls, while 5-hydroxytryptamine (5 μg) caused a rise of plasma GH levels in both groups. Histamine (5 μg) failed to alter GH in any of the groups. We suggest that acetylcholine, substance P, norepinephrine and dopamine, but not histamine, may increase the secretion of GHRF acting either directly upon the GHRF cells or on neural circuits impinging upon them.

Original languageEnglish
Pages (from-to)318-323
Number of pages6
JournalEndocrinology
Volume113
Issue number1
Publication statusPublished - 1983

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Middle Hypothalamus
Growth Hormone-Releasing Hormone
Growth Hormone
Neurotransmitter Agents
Third Ventricle
Histamine
Acetylcholine
Dopamine
Norepinephrine
Median Eminence
Substance P
Hypothalamus
Serotonin

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Various putative neurotransmitters affect growth hormone (GH) release in rats with anterolateral hypothalamic deafferentiation of the medial basal hypothalamus: Evidence for mediation by a GH-releasing factor",
abstract = "Anterolateral deafferentation of the rat medial basal hypothalamus was used to eliminate most of the somatostatinergic innervation of the stalk-median eminence while leaving a functional system producing GH-releasing factor (GHRF) in the partially deafferented hypothalamus. One week after the operation, the rats were anesthetized, the third ventricle was cannulated, and various putative neurotransmitters were infused for 5 min. Plasma GH levels were measured between 10 and 25 min after infusion. When infused into the third ventricle, acetylcholine (50 μg), substance (5 μg), dopamine (5 μg), and norepinephrine (2.5 μg) increased plasma GH levels in the deafferented rats but not in the controls, while 5-hydroxytryptamine (5 μg) caused a rise of plasma GH levels in both groups. Histamine (5 μg) failed to alter GH in any of the groups. We suggest that acetylcholine, substance P, norepinephrine and dopamine, but not histamine, may increase the secretion of GHRF acting either directly upon the GHRF cells or on neural circuits impinging upon them.",
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N2 - Anterolateral deafferentation of the rat medial basal hypothalamus was used to eliminate most of the somatostatinergic innervation of the stalk-median eminence while leaving a functional system producing GH-releasing factor (GHRF) in the partially deafferented hypothalamus. One week after the operation, the rats were anesthetized, the third ventricle was cannulated, and various putative neurotransmitters were infused for 5 min. Plasma GH levels were measured between 10 and 25 min after infusion. When infused into the third ventricle, acetylcholine (50 μg), substance (5 μg), dopamine (5 μg), and norepinephrine (2.5 μg) increased plasma GH levels in the deafferented rats but not in the controls, while 5-hydroxytryptamine (5 μg) caused a rise of plasma GH levels in both groups. Histamine (5 μg) failed to alter GH in any of the groups. We suggest that acetylcholine, substance P, norepinephrine and dopamine, but not histamine, may increase the secretion of GHRF acting either directly upon the GHRF cells or on neural circuits impinging upon them.

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