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Identification of MSH release-inhibiting elements in the neurointermediate lobe of the rat
Abstract:
Neurointermediate lobes of rats comprise elements which, when excited in vitro, bring about an inhibition of the release of melanocyte stimulating hormone (MSH). Superfusion of neurointermediate lobes of intact donor rats with medium containing 45 mM K+ induced a stimulation of the release of oxytocin, arginine-vasopressin and dopamine (DA) and inhibited the release of MSH. Fluorescence histochemical observations and the results of release studies indicate that electrothermic lesions in the mediobasal hypothalamus induced a more rapid degeneration of dopaminergic than of peptidergic terminals in the neurointermediate lobe. Dopaminergic nerve terminals and the stimulated release of DA had vanished completely on the second day after these lesions, which coincided with the disappearance of K+-induced inhibition of MSH release. Frontal hypothalamic deafferentations resulted in disappearance of peptidergic nerve terminals as evidenced by the development of diabetes insipidus and the strong decline of depolarization-induced release of oxytocin and vasopressin from neurointermediate lobes in vitro. In contrast, the dopaminergic plexus was left intact, as was the K+-induced stimulation of DA release and inhibition of MSH release. We conclude that the K+-induced inhibition of MSH release is mediated by DA rather than by neuropeptides from terminals in the neurointermediate lobe. The results are in agreement with the proposed MSH release-inhibiting role of the dopaminergic tuberoinfundibular neurones.
Insights
Dopamine (DA) from hypothalamic neurons inhibits the release of melanocyte-stimulating hormone (MSH) from the neurointermediate lobe. This study confirms DA
Area of Science:
- Neuroendocrinology
- Neurobiology
- Hormone Regulation
Background:
- The neurointermediate lobe releases melanocyte-stimulating hormone (MSH).
- The regulation of MSH release involves hypothalamic inputs.
- Dopaminergic and peptidergic pathways innervate the neurointermediate lobe.
Purpose of the Study:
- To investigate the role of dopaminergic (DA) and peptidergic nerve terminals in the neurointermediate lobe.
- To determine the mechanism by which K+-induced stimulation affects MSH release.
- To elucidate the neurotransmitter mediating the inhibition of MSH release.
Main Methods:
- In vitro superfusion of rat neurointermediate lobes.
- High potassium (K+) stimulation to induce neurotransmitter release.
- Fluorescence histochemistry to assess nerve terminal integrity.
- Lesion studies (mediobasal hypothalamus and frontal deafferentation) to selectively damage nerve terminals.
Main Results:
- K+-induced stimulation released oxytocin, arginine-vasopressin, and DA, while inhibiting MSH release.
- Mediobasal hypothalamic lesions rapidly degenerated dopaminergic terminals, abolishing DA release and K+-induced MSH inhibition.
- Frontal deafferentations damaged peptidergic terminals, reducing peptide release but sparing DA release and MSH inhibition.
- Dopaminergic nerve terminals mediate the inhibition of MSH release.
Conclusions:
- K+-induced inhibition of MSH release is mediated by dopamine (DA), not neuropeptides.
- Dopaminergic tuberoinfundibular neurons play a role in inhibiting MSH release.
- The findings support the inhibitory role of dopaminergic pathways on MSH secretion.