Neural Regulation of Luteinizing Hormone Secretion in the Rat*

Kalra, Satya P.; Kalra, Pushpa S.

doi:10.1210/edrv-4-4-311

Cited by 662 publications

(338 citation statements)

References 108 publications

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“…Taken together, these results suggest that the MPO + PAG + RVM projection constitutes a functional pathway. This circuit may coordinately regulate neuroendocrine, motor, and autonomic adjustments necessary for the elaboration of sexual behaviors.Key words: reproduction; antinociception; cardiovascular regulation; brainstem; sexual behavior; immunohistochemistryThe medial preoptic area (h/[PO) is a sexually dimorphic structure Simerly et al, 1984;Bloch and Gorski, 1988) that plays a pivotal role in sexual behavior and neuroendocrine function (Lisk, 1966;Powers and Valenstein, 1972;Pfaff and Sakuma, 1979;Hansen et al, 1982;Arendash and Gorski, 1983;Kalra and Kalra, 1983;Docke et al, 1984;Sachs and Meisel, 1988;Simerly et al, 1990;DonCarlos et al, 1991;Takeo et al, 1993;Hoshina et al, 1994). We recently reported that MPO robustly innervates the midbrain periaqueductal gray (PAG) (Rizvi et al, 1992) and terminates in discrete, longitudinally organized columns running through the rostrocaudal axis of PAG.…”

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confidence: 99%

Medial preoptic area afferents to periaqueductal gray medullo-output neurons: a combined Fos and tract tracing study

et al. 1996

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We have shown recently that the medial preoptic area (MPO) robustly innervates discrete columns along the rostrocaudal axis of the midbrain periaqueductal gray (PAG). However, the location of PAG neurons responsive to MPO activation is not known. Anterograde tract tracing was used in combination with Fos immunohistochemistry to characterize the MPO -+ PAG pathway anatomically and ,functionally within the same animal. Focal electrical or chemical stimulation of MPO in anesthetized rats induced extensive Fos expression within the PAG compared with sham controls. Fos-positive neurons were organized as 2-3 longitudinal columns. The organization and location of these columns overlapped remarkably well with the distribution of fibers and terminals in PAG labeled by Phaseolus vulgaris leucoagglutinin (PHA-L) injected into the same MPO stimulation site. This indicates that MPO inputs may terminate on the soma or proximal dendrites of neurons exhibiting elevated Fos. A second series of experiments investigated whether MPO stimulation excited PAG neurons with descending projections to the medulla. Retrograde labeling of PAG neurons projecting to the medial and lateral regions of the rostroventral medulla (RVM) was combined with MPO-induced Fos expression. The results showed that a substantial population (3743%)of Fos-positive PAG neurons projected to the ventral medulla. This indicates that MPO stimulation engages PAG-medullary output neurons. Taken together, these results suggest that the MPO + PAG + RVM projection constitutes a functional pathway. This circuit may coordinately regulate neuroendocrine, motor, and autonomic adjustments necessary for the elaboration of sexual behaviors.Key words: reproduction; antinociception; cardiovascular regulation; brainstem; sexual behavior; immunohistochemistryThe medial preoptic area (h/[PO) is a sexually dimorphic structure Simerly et al., 1984;Bloch and Gorski, 1988) that plays a pivotal role in sexual behavior and neuroendocrine function (Lisk, 1966;Powers and Valenstein, 1972;Pfaff and Sakuma, 1979;Hansen et al., 1982;Arendash and Gorski, 1983;Kalra and Kalra, 1983;Docke et al., 1984;Sachs and Meisel, 1988;Simerly et al., 1990;DonCarlos et al., 1991;Takeo et al., 1993;Hoshina et al., 1994). We recently reported that MPO robustly innervates the midbrain periaqueductal gray (PAG) (Rizvi et al., 1992) and terminates in discrete, longitudinally organized columns running through the rostrocaudal axis of PAG.PAG plays a key role in antinociception (Reynolds, 1969;Liebeskind et al., 1973;Oliveras et al., 1974;Behbehani and Fields, 1979; Lovick, 3985;Morgan and Liebeskind, 1987;Reichling et al., 1988;Lovick, 1990), cardiovascular control (Lovick, 1985;Carrive et al., 1987;Carrive et al., 1988;Carrive et al., 1989a;Lovick, 1990;Verberne and Guyenet, 1992;Murphy et al., 1994a;Murphy et al., 1995), and many of the same neuroendocrine and reproductive functions as MPO (Pfaff and SchwartzGiblin, 1988;Ogawa et al., 1991;Shipley et al., 1995). PAG neurons involved in these functions also are ...

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Medial preoptic area afferents to periaqueductal gray medullo-output neurons: a combined Fos and tract tracing study

et al. 1996

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“…One of the bestcharacterized physiological functions of this neuropeptide is the control of the hypothalamic-pituitary-gonadal (HPG) axis. This axis is controlled by a long-loop negative feedback in which gonadally produced estrogen inhibits its own production through a decrease in pituitary gonadotropin release (see Kalra and Kalra, 1983;Ferin et al, 1984). This negative feedback is mediated by increasing the opioidergic tone ofthe hypothalamus, resulting in a decreased hypothalamic LHRH release, with a subsequent reduction in LH release from the pituitary (Van Vugt et al, 1982;Kalra and Kalra, 1983;Ferin et al, 1984;Millan and Herz, 1985).…”

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confidence: 99%

“…This axis is controlled by a long-loop negative feedback in which gonadally produced estrogen inhibits its own production through a decrease in pituitary gonadotropin release (see Kalra and Kalra, 1983;Ferin et al, 1984). This negative feedback is mediated by increasing the opioidergic tone ofthe hypothalamus, resulting in a decreased hypothalamic LHRH release, with a subsequent reduction in LH release from the pituitary (Van Vugt et al, 1982;Kalra and Kalra, 1983;Ferin et al, 1984;Millan and Herz, 1985). When estrogen levels are high, injection of the p-endorphin antagonist naloxone increases serum LH levels and can even advance the LH surge in women by an average of 2 d (Rossmanith et al, 1988).…”

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confidence: 99%

The potency of mu-opioid hyperpolarization of hypothalamic arcuate neurons is rapidly attenuated by 17 beta-estradiol

1994

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The mu-opioid agonist DAMGO (Tyr-D-Ala-Gly-MePhe-Gly-ol) hyperpolarizes the majority of arcuate hypothalamic (ARC) neurons by opening an inwardly rectifying potassium conductance. The EC50 for the DAMGO- induced hyperpolarization was 60 +/- 3 nM in ARC neurons from ovariectomized guinea pigs. Superfusion of 17 beta-estradiol (E2; 100 nM) for 20 min in vitro resulted in a significant decrease in DAMGO potency (EC50 = 212 +/- 16 nM) in 40% of the neurons that were tested. This rapid effect of E2 on the mu-opioid response was not mimicked by the biologically inactive isomer 17 alpha-estradiol. Multiple concentrations of E2 were used to generate an E2 concentration-response curve, with an EC50 of 9 nM and a maximal increase in the DAMGO EX50 of 411% of controls. The membrane properties and firing rate of E2- sensitive and E2-insensitive neurons were not different. Streptavidin- FITC labeling did not reveal any significant morphological differences between the groups, but a higher number of E2-sensitive cells was found in the lateral ARC and cell-poor zone. Moreover, immunocytochemical staining of the recorded cells revealed that beta-endorphin neurons were among those sensitive to E2. Therefore, E2 could increase beta- endorphin release by decreasing the potency of beta-endorphinergic autoinhibition, thus increasing the tonic opioid inhibition of E2- insensitive cells. Furthermore, the diffuse projections of hypothalamic beta-endorphin neurons would allow E2 to alter processes throughout the brain, as well as having local effects in the hypothalamus.

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“…DL-Propranolol did not reduce andro¬ gen secretion in sham-operated animals but caused a small, but significant, increase in testicular vein androgen concentrations. The reason for this increase is not known but intramuscular administration of the ß2-antagonist butoxamine has been reported to increase peripheral testosterone concentrations (Collu, Gibb & Ducharme, 1984 (Kalra & Kalra, 1983).…”

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confidence: 99%

Propranolol inhibits the compensatory increase in androgen secretion after unilateral orchidectomy in rats

Moger¹,

Anakwe²

1986

Reproduction

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Summary. Adrenergic antagonists were administered to rats by intratesticular injection at the time of unilateral orchidectomy and 5 h before autopsy, 24 h after surgery. Injections of the \g=b\-receptorantagonist DL-propranolol (0\m=.\5 or 1\ m=. \ 0mg/injection) significantly inhibited the increase in the concentration of androgens in testicular vein plasma or interstitial fluid that occurred in unilaterally orchidectomized animals injected with vehicle. DL-Propranolol injections in animals with both testes did not reduce testicular or peripheral androgen concentrations or their increase after hCG administration. Injections of the less potent isomer (+)-propranolol or the \g=a\-receptorantagonist phentolamine did not inhibit the response to unilateral orchidectomy. It is concluded that the compensatory increase in androgen secretion induced by unilateral orchidectomy is, at least in part, the result of \g=b\-adrenergic stimulation of steroidogenesis.

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Neural Regulation of Luteinizing Hormone Secretion in the Rat*

Cited by 662 publications

References 108 publications

Medial preoptic area afferents to periaqueductal gray medullo-output neurons: a combined Fos and tract tracing study

Medial preoptic area afferents to periaqueductal gray medullo-output neurons: a combined Fos and tract tracing study

The potency of mu-opioid hyperpolarization of hypothalamic arcuate neurons is rapidly attenuated by 17 beta-estradiol

Propranolol inhibits the compensatory increase in androgen secretion after unilateral orchidectomy in rats

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