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Noradrenaline-induced feeding responses in the rat do not depend on food characteristics

100%
Swiergiel A. H., Wieczorek M.
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issue 3
354-361
EN
The noradrenergic system of the hypothalamic paraventricular nuclei (PVN) has been associated with feeding, but whether it controls feeding in a way that is relevant to energy balance is still unclear. Rats were maintained on a high energy, carbohydrate-rich diet (HC), or a low energy, carbohydrate-free, protein-rich diet (LP), until their daily energy intakes equalized. When injected with noradrenaline (NA) into the PVN, they ingested the same amounts of both diets so that the animals on the LP diet consumed only half the total energy of those on the HC diet. Continuous delivery of NA into the PVN via a microdialysis probe induced chewing on non-nutritive pieces of corks. The same chewing pattern could again be elicited by the subsequent NA deliveries. It is concluded that the nutritional value of a diet is irrelevant to the NA feeding response. The failure of NA administration to increase rat feeding in terms of energy intake, combined with its ability to stimulate chewing, suggests that the primary role of the NA system of the PVN may not be controlling the carbohydrate and energy intake, but rather gating behavioral responses that under appropriate circumstances may lead to ingestion.
2
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The neurochemistry of the GnRH pulse generator

75%
Wuttke W., Jarry H., Felder C., Moguilevsky J., Leonhard S., Seong J. Y., Kim K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 3
707-713
EN
We review the crucial role of the two neurotransmitters norepinerine (NE) and GABA in eliciting GnRH pulses.NE acts via an alpha1-receptor mechanism and also GABA acts at the alpha-subtype of the GABA receptor.The function of NE appears to be induction of phasic activation of GnRH neurons and GABA inhibits GNRH neurons tonically until they are all ready for phasic activation.By an unknown mechanism preoptic GABA release is dramatically reduced which causes simultaneous desinhibition of the GnRH neurons.Hence they release their product into the portal vessels simultanously which is the appopriate signal for the pituitery ganodotrophs.THe action of norepinerphine and GABA is most likely exerted at the perikarya level of the GnRH neurons since the alpha-1-adreno receptor blocker doxazosin and GABA inhibit GnRH secretion only when applied into the medial preoptic/anterior hypothalmic area.Utilizing a quantitative reverse transcription polymerase chain reaction, we demonstrate furthermore that GnRH receptors are present in the mediobasal hypothalmus as well as in the preoptic area of rats.Their function appears to serve autoinhibitory puroses since Buserelin addet to medium significantly decreased GnRH release.Simultanoeusly, the release of GABA was increased and that of glutamate decreased.We conclude from these experiments that GABAergic and glutamatergic neurons in the hypothalmus may also be GnRH-receptive.
3
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Neural systems mediating the negative feedback actions of estradiol and progesterone in the ewe

63%
Goodman R. L.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 3
727-741
EN
The ewe shows a marked seasonal variation in the effect of ovarian steroids on pulsatile GnRH secretion.In the breeding season progesterone inhibits GnRH pulse frequency, while estradiol suppresses puilse amplitude.In anestrus, both steriods inhibit pulse frequency.The effects of progestrone in both seasons are mediated by endogenous opioid peptides (EOP) that act in the preoptic area (POA) and medial basal hypothalmus (MBH).However, knife cut studies indicate that actions in the MBH are most important.Moreover, blockade of EOP receptors activates GnRH perikarya in the MBH, but not those in the POA.Thus interactions between EOP and GnRH neurons within the MBH may be critical for progesterone negative feedback.The neural systems mediating estradiol suppression of GnRH pulse amplitude in the breeding season are largely unknown, although alpha-adrenergic neurons nay be involved.The seasonal variation in inhibition of GnRH pulse frequency by estradiol is postulated to be mediated by a group of dopaminergic (DA) neurons that have three important properties: (1)they inhibit GnRH pulse frequency; (2) their activity is stimulated by estradiol; and (3) they are functional in anestrus, but not the breeding season.Recent work examining the effects of lesions of DA neyrone and the ability of estradiol to induce Fos inDA cells srongly suggest that DA neurons in the retrochiasmatic area (A15) and POA (A14) have all three characteristics.We thus propose that these DA neurons are responsible for the seasonal variation in the ability of estradiol to inhibit GnRH pulse frequency.
4

Adrenomedullary and glycemic responses to ACTH, corticosterone, aldosterone, epinephrine and norepinephrine administrations in the soft-shelled turtle

63%
Ray P. P., Chaudhuri-Sengupta S., Maiti B. R.
Folia Biologica
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2004
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vol. 52
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issue 1-2
73-80
EN
The aim of the current investigation was to ascertain the role of ACTH and adrenal hormones on adrenomedullary and glycemic functions in soft-shelled turtles, Lissemys punctata punctata. All the experiments were carried out on sexually immature animals. Findings revealed that: (1) ACTH administration (0.5 IU/1.0 IU/2.0 IU per 100 g body wt. daily for 10 days) in all doses stimulated adrenomedullary function by increasing medullary cell nuclear diameter with elevations of norepinephrine, epinephrine and blood sugar levels. Only moderate and higher doses (50 mug/100 mug per 100 g body wt. daily for 10 days) of dexamethasone suppressed adrenomedullary activity and blood sugar level by reversing the changes to those of ACTH; the responses were dose-dependent. But these changes were no longer observed after ACTH treatment in dexamethasone (DMS) recipients (DMS: 100mug / 100 g body wt daily for the first 10 days and ACTH: 0.5 IU / 100 g body wt daily for the next 10 days); (2) Only moderate and higher doses (50 mug/100 mug per 100 g body wt daily for 10 days) of corticosterone increased adrenomedullary activity and blood sugar level and the responses were also dose-dependent. But aldosterone treatment in all doses (same as for corticosterone) had no significant effect on the adrenal medulla or blood sugar level; (3) Only moderate and higher doses of norepinephrine or epinephrine (same as for corticosterone) caused adrenomedullary atrophy with depletions of norepinephrine and epinephrine levels but elevated the glycemic level. The findings are briefly discussed.
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