Norepinephrine Is a Possible Neurotransmitter Stimulating Pulsatile Release of Luteinizing Hormone-Releasing Hormone in the Rhesus Monkey*

Terasawa, Ei; Krook, C.; Hei, D. L.; Gearing, Marla; Schultz, N; Davis, Gary A.

doi:10.1210/endo-123-4-1808

Cited by 146 publications

(96 citation statements)

References 39 publications

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“…Before the push-pull perfusion, monkeys were implanted with a cranial chamber under halothane anesthesia (22)(23)(24) above the infundibular recess of the third ventricle, which was visualized with x-ray ventriculograms. The animals were allowed to recover for at least 1 mo and were well adapted to the primate chair, the experimental environment, and the investigators before experimentation was initiated (22). The method for push-pull perfusion ofthe stalk-median eminence (S-ME) in conscious monkeys was similar to that described previously (22)(23)(24).…”

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“…The animals were allowed to recover for at least 1 mo and were well adapted to the primate chair, the experimental environment, and the investigators before experimentation was initiated (22). The method for push-pull perfusion ofthe stalk-median eminence (S-ME) in conscious monkeys was similar to that described previously (22)(23)(24). Three days before the push-pull perfusion, an outer cannula (20 gauge) with a inner stylet (28 gauge) was inserted stereotaxically into the S-ME with a micromanipulator unit (Narishige, Tokyo) under ketamine (10 mg/kg ofbody weight) plus xylazine (2 mg) anesthesia.…”

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gamma-Aminobutyric acid is an inhibitory neurotransmitter restricting the release of luteinizing hormone-releasing hormone before the onset of puberty.

Mitsushima

Hei

Terasawa

1994

Proc. Natl. Acad. Sci. U.S.A.

236

147

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To test the hypothesis that the pubertal increase in luteinizing hormone-releasing hormone (LHRH) re-lease is withheld by a dominant inhibitory neuronal system, the role of -aminobutyric acid (GABA), a known inhibitory neurotransmitter, in the control of LHRH release was examined in conscious female monkeys at the prepubertal and pubertal stages using a push-pull perfusion method. GABA, bicuculline (a GABAA receptor blocker), and 2-hydroxysaclofen (a GABAB receptor blocker) were directly infused into the stalk-median eminence while perfusates were collected for LHRH determination. Bicuculline, but not saclofen, induced a large and prompt increase in LHRH release in prepubertal monkeys, whereas it stimulated LHRH release slightly in pubertal monkeys. In contrast, GABA suppressed LHRH release in pubertal, but not prepubertal, monkeys. These differential effects of GABA and the GABA antagonist on LHRH release in the two developmental stages were due to an age factor rather than to the steroid hormonal background. Moreover, GABA release in the stalk-median eminence of prepubertal monkeys was much higher than that in pubertal monkeys. Thus, the results suggest that in the prepubertal period there is a powerful GABA inhibition of the LHRH neurosecretory system: infusions of GABAA, but not GABAB, antagonists stimulate LHRH release by removal of the endogenous GABA inhibition, whereas exogenous GABA is ineffective because of high endogenous GABA levels. The decrease of this tonic inhibition may be a key factor for the onset of puberty in non-human primates.Two lines of evidence support the hypothesis that an increase in pulsatile luteinizing hormone-releasing hormone (LHRH) release is the critical factor for the onset of puberty in primates: An increase in pulsatile LHRH release occurs at the onset of puberty in female rhesus monkeys (1-3), and pulsatile infusion of LHRH into sexually immature monkeys with a pump induces precocious puberty (4). However, the mechanism by which LHRH release increases at puberty in primates is still unknown. The pubertal increase in LHRH release is probably not due to the developmental changes in properties of LHRH neurons themselves, since (i) the expression of LHRH mRNA is similar in monkeys during the prepubertal period and in adulthood (5) and (ii) prior to puberty, LHRH release can be induced by electrical stimulation of the medial basal hypothalamus (MBH) (2) or by neurochemical stimulation with N-methyl-D-aspartate (6). In fact, these studies further indicate that releasable LHRH is present in the hypothalamus of prepubertal monkeys but that the control mechanisms for pulsatile LHRH release are immature before the onset of puberty.The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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confidence: 99%

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confidence: 99%

gamma-Aminobutyric acid is an inhibitory neurotransmitter restricting the release of luteinizing hormone-releasing hormone before the onset of puberty.

Mitsushima

Hei

Terasawa

1994

Proc. Natl. Acad. Sci. U.S.A.

236

147

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“…The inhibition of norepinephrine (NE) synthesis or depletion of NE stores suppresses Gn-RH release from the median eminence and this effect can be reversed by administration of an a2-adrenergic receptor agonist (for review see reference 17). In addition, NE is involved in the pulsatile release of Gn-RH, as shown by investigations that documented that NE release in the median eminence-pituitary stalk of ovariectomized monkeys is pulsatile and synchronous with Gn-RH release [27]. The stimulatory effects of NE on the Gn-RH system appear to be exerted in the median eminence where noradrenergic nerve terminals, whose cell bodies are located in the A1 and A2 medullary nuclei and in A5 and A7 midbrain cell groups [14, 231, are in close juxtaposition to Gn-RH containing axon terminals [ 131.…”

Section: Discussionmentioning

confidence: 99%

Luteinizing Hormone Pulsatility is Altered in Essential Hypertension

Santiemma¹,

Garufi²,

Magnanti³

et al. 1997

Archives of Andrology

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“…These compounds may affect amplitude or frequency of GnRH release, but also may affect GnRH gene expression. Furthermore, some neurotransmitters like norepinephrine have been assigned as 'pacemakers' driving episodic GnRH release (Terasawa et al 1988). However, recent evidence with immortalized GnRH neurons (GT1 cells) indicate that the pulsatile release of GnRH is due to an intrinsic episodic activity of these immortalized GnRH neurons (Escalera et al 1992).…”

Section: MD Brown School Of Sport and Exercise Sciences University Omentioning

confidence: 99%

Symposium Proceedings

1995

The Journal of Physiology

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Starting with the earliest in vivo studies of the microcirculation, observers have been impressed with the variability and heterogeneity of microcirculation blood flow. The question I should like to address is how heterogeneity of microvascular perfusion influences transport of diffusible solutes, and how control of heterogeneity may contribute to regulation of blood-tissue exchange. Available exchange vessel surface area and inter-exchange vessel distances are controlled at the arteriolar level by the number of vessels open to the supply of arterial blood. When metabolic requirements are low, only a fraction of the exchange vessels in a vascular network are perfused; as metabolic activity increases, more exchange vessels are recruited. However, the efficiency with which available exchange vessel surface is utilized for diffusion of a given solute depends on the distribution of individual blood flow/permeability surface area ratios (Q/PS) in the network. Maximum efficiency (full utilization of available PS) is achieved when Q/PS is uniform.In vivo observations of red blood cell velocities show wide variation among individual exchange vessels of the same class (capillaries, postcapillary venules); presumably the same is true of plasma velocities. Flow velocity is only one of the factors that determines local transport; the critical parameter is the product of velocity and vessel radius divided by vessel length times solute permeability (v. r/ 1 P). The impression I get from published intra-vital microscope data is that this ratio may vary even more widely than velocity alone. Physiological measurements of solute transport in whole organs provide indirect support for broad heterogeneity of perfusion, at least in low metabolic states. In resting skeletal muscles the apparent (measured) PS products for 86Rb and 51Cr EDTA increase with increasing perfusion rate, approaching limiting values at high flow rates, as predicted for a heterogeneity perfused assemblage of exchange vessels. Estimated coefficients of variation (cv = S.D./mean) of Q/PS or v. r/ 1 P lie in the range 07-09.In heterogeneously perfused organs and tissues, the degree of heterogeneity (cv of Q/PS) and the total blood flow are potentially important secondary regulators of capillary transport, because they determine the efficiency with which the primary controlling factors, total blood flow and available exchange vessel surface area, are utilized (note that blood flow acts both directly and indirectly). Efficiency, defined as the ratio of apparent PS to the maximum PS at uniform perfusion, is inversely related to the degree of heterogeneity and directly related to the mean flow velocity. There is conflicting evidence in the literature concerning the degree to which alteration of Q/PS heterogeneity is involved in adaptive control of diffusion exchange. However, even with constant total PS and fixed heterogeneity, an increase in total blood flow can decrease the influence of heterogeneity on transport and thus contribute substantially to Berlin 33, Ger...

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Norepinephrine Is a Possible Neurotransmitter Stimulating Pulsatile Release of Luteinizing Hormone-Releasing Hormone in the Rhesus Monkey*

Cited by 146 publications

References 39 publications

gamma-Aminobutyric acid is an inhibitory neurotransmitter restricting the release of luteinizing hormone-releasing hormone before the onset of puberty.

gamma-Aminobutyric acid is an inhibitory neurotransmitter restricting the release of luteinizing hormone-releasing hormone before the onset of puberty.

Luteinizing Hormone Pulsatility is Altered in Essential Hypertension

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