Inhibition of Gonadotropin Secretion Induced by Cholecystokinin Implants in the Medial Preoptic Area by the Dopamine Receptor Blocker, Pimozide, in the Rat

Hashimoto, Ryuhei; Kimura, Fukuko

doi:10.1159/000124245

Cited by 28 publications

(16 citation statements)

References 22 publications

(27 reference statements)

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“…preop tic administration of dopamine also facilitated the circa dian rise in LH secretion in ovariectomized estrogenprimed rats [9,10]. Whether there is a certain functional in teraction between NT and dopamine in the preoptic area, similar to that observed between cholecystokinin and dopa mine [6], in controlling LH secretion will be studied soon.…”

Section: Discussionmentioning

confidence: 91%

Effects of Preoptic Microinjection of Neurotensin on Luteinizing Hormone Secretion in Unanesthetized Ovariectomized Rats with or without Estrogen Priming

Akema¹,

Praputpittaya²,

Kimura³

1987

Neuroendocrinology

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Effects of microinjection of neurotensin (NT) into the medial preoptic area on luteinizing hormone (LH) release were examined in unanesthetized ovariectomized rats with or without estrogen priming. Microinjection of NT (100 ng) into the medial preoptic area of ovariectomized estrogen-primed rats significantly facilitated the circadian afternoon rise of LH secretion as compared to the hormone values in control animals microinjected with physiological saline. The timing of the afternoon LH rise was not altered by the peptide. In ovariectomized estrogen-unprimed rats, on the other hand, NT did not affect the existing pulsatile LH secretion nor induced an afternoon rise of the hormone secretion. These results show that NT can stimulate the preoptic LH release mechanism which undergoes the circadian clock under the influence of estrogen.

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Section: Discussionmentioning

confidence: 91%

Effects of Preoptic Microinjection of Neurotensin on Luteinizing Hormone Secretion in Unanesthetized Ovariectomized Rats with or without Estrogen Priming

Akema¹,

Praputpittaya²,

Kimura³

1987

Neuroendocrinology

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“…The rapid restoration of pulsatile LH secretion in refed animals (18,20,23,67,168,214,217,254) could be due to the prandial release of CCK from the duodenum. It has been reported that CCK treatment stimulates LH secretion whether given directly into the brain (91,128) or systemically (169,215), but the significance of these findings for nutritional infertility is unclear. Refeeding food-restricted lambs did not affect hypothalamic levels of CCK peptide or mRNA (102).…”

Section: Peripheral Detectors With Humoral Transmission To the Cnsmentioning

confidence: 99%

Neuroendocrinology of nutritional infertility

Wade¹,

Jones²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

229

166

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Natural selection has linked the physiological controls of energy balance and fertility such that reproduction is deferred during lean times, particularly in female mammals. In this way, an energetically costly process is confined to periods when sufficient food is available to support pregnancy and lactation. Even in the face of abundance, nutritional infertility ensues if energy intake fails to keep pace with expenditure. A working hypothesis is proposed in which any activity or condition that limits the availability of oxidizable fuels (e.g., undereating, excessive energy expenditure, diabetes mellitus) can inhibit both gonadotropin-releasing hormone (GnRH)/luteinizing hormone secretion and female copulatory behaviors. Decreases in metabolic fuel availability appear to be detected by cells in the caudal hindbrain. Hindbrain neurons producing neuropeptide Y (NPY) and catecholamines (CA) then project to the forebrain where they contact GnRH neurons both directly and also indirectly via corticotropin-releasing hormone (CRH) neurons to inhibit GnRH secretion. In the case of estrous behavior, the best available evidence suggests that the inhibitory NPY/CA system acts primarily via CRH or urocortin projections to various forebrain loci that control sexual receptivity. Disruption of these signaling processes allows normal reproduction to proceed in the face of energetic deficits, indicating that the circuitry responds to energy deficits and that no signal is necessary to indicate that there is an adequate energy supply. While there is a large body of evidence to support this hypothesis, the data do not exclude nutritional inhibition of reproduction by other pathways and processes, and the full story will undoubtedly be more complex than this. luteinizing hormone; estrous behavior; corticotropin-releasing hormone; neuropeptide Y; hindbrain OF NECESSITY, the physiological controls of reproduction and energy balance are closely intertwined. Living creatures require a steady stream of oxidizable substrates to fuel their many energy-consuming activities, including reproduction. But in nature, energetic demands and opportunities for meal taking can be erratic and sometimes unpredictable, necessitating the existence of physiological and behavioral strategies to maximize chances of individual survival and permit propagation of the species (21,22,200,208).A need to eat constantly is obviated by the presence of internal caloric buffers that store glycogen and fatty acids and provide sustenance in between meals and during brief fasts. When food is abundant, animals adjust their intakes to meet all demands and keep their storage depots full (or overfull in an increasing number of cases). However, a more likely scenario in nature and during human evolution is that food can be scarce or have a very high acquisition cost. In that case, animals adjust their energetic priorities, i.e., how they partition and use the available metabolic fuels (Fig.

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“…In this area, the levels of proenkephalin mRNA increase %fold within one h after an estrogen injection into ovariectomized females and they decrease over the next day suggesting that estradiol stimulates metrelease by projections to the AVPv (75,76), which appears critical for the phasic release of LH (30). CCK injections into the AVPv stimulate LH release (79), possibly by acting on dopamine neurons, since dopamine antagonists block the effect of CCK on LH release (80). Hypothalamic dopamine neurons, in turn, form synapses on LHRH neurons (47).…”

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confidence: 99%