Orexins, Orexigenic Hypothalamic Neuropeptides, Suppress the Pulsatile Secretion of Luteinizing Hormone in Ovariectomized Female Rats

Tamura, Takao; Irahara, Minoru; Tezuka, Michiko; Kiyokawa, Machiko; Aono, Toshihiro

doi:10.1006/bbrc.1999.1573

Cited by 143 publications

(107 citation statements)

References 16 publications

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“…On the other hand, the Hcrt projections to the NTS may function to modulate the activity of visceral afferents and/or to provide a general activation of the parasympathetic system during the digestive and absorptive phases of ingestion. However, it is now clear that orexin systems are not only involved in ingestive behaviors, but also exert an effect on a variety of physiological mechanisms involved in homeostasis (3,13,19,21,23,25,42,44,45,48). Therefore, it is possible that orexigenic pathways may function to adjust cardiovascular responses to activation of these different homeostatic mechanisms (10,12,15,33,42).…”

Section: Discussionmentioning

confidence: 99%

“…Although both Hcrt-1 and -2 have been shown to have similar physiological effects when administered centrally, Hcrt-1 appears to exert a more potent effect on most of these physiological variables (10,12,33,42,47). Hcrt-1 injections into the brain have been shown to increase feeding and drinking behaviors; produce sleep, wakefulness, and arousal disturbances; produce analgesia; activate the hypothalamic-pituitary axis; elicit gastric acid secretion; and alter temperature regulating mechanisms (3,14,19,21,23,25,42,44,45,48). Hcrt-1 neurons have been shown to contribute to an extensive innervation of forebrain, brain stem, and spinal cord structures (10,33,42,46,47), and receptors to Hcrt-1 have been demonstrated throughout the neuraxis (28).…”

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confidence: 99%

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Cardiovascular effects of hypocretin-1 in nucleus of the solitary tract

Oliveira

Rosas‐Arellano

Solano-Flores

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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lar effects of hypocretin-1 in nucleus of the solitary tract. Am J Physiol Heart Circ Physiol 284: H1369-H1377, 2003. First published December 12, 2002 10.1152/ajpheart.00877.2002Experiments were done in male Wistar rats to investigate the effects of microinjection of hypocretin-1 (Hcrt-1) into the nucleus of the solitary tract (NTS) on mean arterial pressure (MAP), heart rate (HR), and the baroreflex. In the first series, the distribution of Hcrt-1-like immunoreactivity (Ir) was mapped within the region of NTS. Hcrt-1 Ir was found throughout the NTS region, predominantly within the caudal dorsolateral (Slt), medial (Sm), and interstitial subnuclei of the NTS. In the second series, in ␣-chloralose or urethaneanesthetized rats, microinjection of Hcrt-1 (0.5-5 pmol) into the caudal NTS elicited a dose-dependent decrease in MAP and HR. A mapping of the caudal NTS region showed that the largest depressor and bradycardia responses elicited by Hcrt-1 were from sites in the Slt and Sm. In addition, doses Ͼ2.5 pmol at a small number of sites localized to the caudal commissural nucleus of NTS elicited pressor and tachycardia responses. Intravenous administration of the muscarinic receptor blocker atropine methyl bromide abolished the bradycardia response and attenuated the depressor response, whereas subsequent administration of the nicotinic receptor blocker hexamethonium bromide abolished the remaining MAP response. Finally, microinjection of Hcrt-1 into the NTS significantly potentiated the reflex bradycardia to activation of arterial baroreceptors as a result of increasing MAP by systemic injections of phenylephrine (2-4 g/kg). These results suggest that Hcrt-1 in the NTS activates neuronal circuits that increases vagal activity to the heart, inhibits sympathetic activity to the heart and vasculature, and alters the excitability of NTS neuronal circuits that reflexly control the circulation.orexin-A; blood pressure; baroreceptor reflex; brain stem; ingestive behavior HYPOCRETIN (Hcrt) neuropeptides have been recently shown to be almost exclusively expressed within neurons of the lateral and perifornical hypothalamic areas (30,33,35,47,49). These peptides, Hcrt-1, a 33 amino-acid peptide with an NH 2 -terminal pyrogutalmyl residue, and Hcrt-2, a 28 amino acid peptide with a COOH-terminal amide (35), are de-

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cardiovascular effects of hypocretin-1 in nucleus of the solitary tract

Oliveira

Rosas‐Arellano

Solano-Flores

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…The hypocretinergic system has been suggested to play a role in a variety of physiological processes, most of which involve activation of the somatomotor system (Pu et al, 1998;Chemelli et al, 1999;Haynes et al, 1999;Lin et al, 1999;Siegel, 1999;Tamura et al, 1999;Kilduff and Peyron, 2000;Sutcliffe and de Lecea, 2000;Lin et al, 2002;Wu et al, 2002). Hcrtcontaining neurons project to regions that are involved in the generation of somatomotor activity Zhang et al, 2002) that provides a foundation for the concept that Hcrt is involved in the control of motor processes.…”

Section: Considerations Of the Physiological Significance Of Hcrt Actmentioning

confidence: 99%

Hypocretinergic Control of Spinal Cord Motoneurons

Yamuy

Fung²,

Xi³

et al. 2004

Journal of Neuroscience

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Hypocretinergic (orexinergic) neurons in the lateral hypothalamus project to motor columns in the lumbar spinal cord. Consequently, we sought to determine whether the hypocretinergic system modulates the electrical activity of motoneurons. Using in vivo intracellular recording techniques, we examined the response of spinal motoneurons in the cat to electrical stimulation of the lateral hypothalamus. In addition, we examined the membrane potential response to orthodromic stimulation and intracellular current injection before and after both hypothalamic stimulation and the juxtacellular application of hypocretin-1. It was found that (1) hypothalamic stimulation produced a complex sequence of depolarizing-hyperpolarizing potentials in spinal motoneurons; (2) the depolarizing potentials decreased in amplitude after the application of SB-334867, a hypocretin type 1 receptor antagonist; (3) the EPSP induced by dorsal root stimulation was not affected by the application of SB-334867; (4) subthreshold stimulation of dorsal roots and intracellular depolarizing current steps produced spike potentials when applied in concert to stimulation of the hypothalamus or after the local application of hypocretin-1; (5) the juxtacellular application of hypocretin-1 induced motoneuron depolarization and, frequently, high-frequency discharge; (6) hypocretin-1 produced a significant decrease in rheobase (36%), membrane time constant (16.4%), and the equalizing time constant (23.3%); (7) in a small number of motoneurons, hypocretin-1 produced an increase in the synaptic noise; and (8) the input resistance was not affected after hypocretin-1. The juxtacellular application of vehicle (saline) and denatured hypocretin-1 did not produce changes in the preceding electrophysiological properties.We conclude that hypothalamic hypocretinergic neurons are capable of modulating the activity of lumbar motoneurons through presynaptic and postsynaptic mechanisms. The lack of hypocretin-induced facilitation of motoneurons may be a critical component of the pathophysiology of cataplexy.

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“…MCH or orexin. Melanin-concentrating hormone stimulates the secretion of LH in anaethetised rats (Gonzalez et al 1997, Murray et al 2000 but inhibits LH release in normal animals (Tsukamura et al 2000), whereas orexin inhibits LH secretion in ovariectomised rats (Pu et al 1998, Tamura et al 1999. It would seem unlikely that leptin would have a direct effect on GnRH neurons, since these cells express either low leptin receptor levels or no receptors in rodents (Hakansson et al 1998) and there is no co-localisation of GnRH and leptin receptor in monkeys (Finn et al 1998).…”

Section: Figurementioning

confidence: 99%

Intracerebroventricular infusion of leptin elevates the secretion of luteinising hormone without affecting food intake in long-term food-restricted sheep, but increases growth hormone irrespective of bodyweight

Henry

Goding

Tilbrook³

et al. 2001

Journal of Endocrinology

145

114

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Leptin can act as a satiety factor and exert neuroendocrine effects, but most studies have been performed in fasted animals. We aimed to determine the effect of chronic under-nutrition on the response to a 3-day intracerebroventricular infusion of leptin with regard to food intake and the secretion of pituitary hormones. Ovariectomised ewes (n=6) had a mean ( ...) bodyweight of 56 0·8 kg on a diet available ad libitum (ad lib) or 33·4 1 kg on a restricted diet. The differential bodyweight was achieved by dietary means over a period of 6 months prior to the commencement of the study. Leptin (4 µg/h) or vehicle (artificial cerebrospinal fluid (aCSF)) was infused into the third cerebral ventricle for 3 days. Blood samples were taken prior to commencement and on day 3 of infusion for the assay of plasma hormone levels. The experiment was repeated one week later in a crossover design. Food intake and metabolic status were monitored daily. The luteinising hormone (LH) pulse amplitude was lower (P<0·05) but plasma growth hormone (GH) levels were higher (P<0·05) in the food-restricted animals. Plasma levels of glucose, lactate, insulin, urea and triglycerides were similar in the two groups but nonesterified fatty acid levels were higher (P<0·01) in the animals on an ad lib diet. Leptin reduced (P<0·05) food intake only in the animals fed an ad lib diet. Leptin increased (P<0·05) the secretion of LH in the foodrestricted group only and increased (P<0·05) GH irrespective of bodyweight. In conclusion, leptin does not alter food intake in animals on a restricted diet but can increase the secretion of LH in the same animals. The treatment of leptin was not sufficient to reduce plasma GH levels in the food-restricted animals, suggesting that other factors or mechanisms must be involved in the regulation of this axis.

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Orexins, Orexigenic Hypothalamic Neuropeptides, Suppress the Pulsatile Secretion of Luteinizing Hormone in Ovariectomized Female Rats

Cited by 143 publications

References 16 publications

Cardiovascular effects of hypocretin-1 in nucleus of the solitary tract

Cardiovascular effects of hypocretin-1 in nucleus of the solitary tract

Hypocretinergic Control of Spinal Cord Motoneurons

Intracerebroventricular infusion of leptin elevates the secretion of luteinising hormone without affecting food intake in long-term food-restricted sheep, but increases growth hormone irrespective of bodyweight

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