Effect of β-endorphin on pulsatile luteinizing hormone release in conscious castrated rats

Kinoshita, Fumiko; Nakai, Yoshikatsu; Katakami, Hideki; Kato, Yuzuru; Yajima, Haruaki; Imura, Hiroo

doi:10.1016/0024-3205(80)90078-8

Cited by 95 publications

(33 citation statements)

References 7 publications

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“…However, the evidence obtained from the La Trobe rats suggests that endogenous opioids are involved in the stress blockage of ovulation, and that prevention of their binding to endogenous opiate receptors via the use of naloxone blocks the inhibitory effect of stress upon ovulation. This is consistent with the recent findings that opioid peptides, administered exogenously, inhibit plasma LH release (Bruni et al, 1977;Kinoshita et al, 1980), while naloxone administration results in large increments in LH release (Bruni et al, 1977;Ieiri et al, 1980;. If the immature PMSG-primed rat is a valid model for the adult, a similar mechanism can be assumed to exist in adult rats.…”

Section: Methodssupporting

confidence: 91%

Reversal of the anti-ovulatory action of stress in rats by prior administration of naloxone hydrochloride

Hulse¹,

Coleman²,

Nicholas³

et al. 1982

Reproduction

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Summary. Immature, 32-day-old rats were treated with PMSG. Stress consisting of 180 min immobilization administered during the period of the preovulatory LH surge resulted in the blockage of ovulation. The anti-ovulatory action of stress was effectively antagonized by the administration of naloxone hydrochloride shortly before the application of the stress, suggesting that the ovulation block by stress is mediated by endogenous opioids known to be elevated during stress. Blockage of ovulation by 180 min immobilization stress occurred only in rats from one of the two laboratory strains tested, suggesting that stress resistance is, at least in part, genetically determined.

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Section: Methodssupporting

confidence: 91%

Reversal of the anti-ovulatory action of stress in rats by prior administration of naloxone hydrochloride

Hulse¹,

Coleman²,

Nicholas³

et al. 1982

Reproduction

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“…It has been known for a number of years that morphine inhibits gonadotropin secretion in the mammal (Barraclough and Sawyer, 1955;Kinoshita et al, 1980;Sylvester et al, 1982;Gabriel et al, 1983). Moreover, opioid peptides attenuate the preovulatory increase of LH and prevent ovulation (Ieiri et al, 1980;Kalra, 1981), and naloxone potentiates the duration and magnitude of the ovulatory surge of LH in the rat (Ieiri et al, 1980;Kalra, 1981) elevates portal blood levels of gonadotrophinreleasing hormone in the rhesus monkey (Ferin et al, 1984) and advances ovulation in the human female (Rossmanith et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Estrogen suppresses mu-opioid- and GABAB-mediated hyperpolarization of hypothalamic arcuate neurons

1992

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The effects of estrogen on the response of hypothalamic arcuate neurons to mu-opioid and GABAB agonists were investigated. Intracellular recordings were made from arcuate neurons in slices prepared from ovariectomized guinea pigs that were pretreated with estrogen or vehicle. Estrogen shifted the dose-response curve to the mu-opioid agonist DAMGO (Tyr-D-Ala-Gly-MePhe-Gly-ol) by 3.4-fold; the EC50 for DAMGO was 240 +/- 25 nM in estrogen-treated females versus 70 +/- 12 nM in the controls. The maximal hyperpolarization induced by DAMGO was equivalent in neurons from both groups. The Ke for the naloxone antagonism of the DAMGO response was similar in both groups, which would indicate that the affinity of the mu-receptor was unchanged. To explore where in the receptor/G-protein/K+ channel cascade estrogen may be acting to attenuate the mu-opioid-mediated hyperpolarization, the response to the GABAB agonist baclofen was also tested. Estrogen treatment also shifted the dose-response curve for the baclofen-induced hyperpolarization by 3.3-fold without altering the maximum hyperpolarization; the EC50 shifted from 11.0 +/- 4.0 microM to 36.0 +/- 5.0 microM. All of the neurons were identified after linking the intracellular biocytin with streptavidin-FITC, and a subpopulation of cells in both groups were immunoreactive for beta-endorphin. We conclude that estrogen decreases the functional coupling of the mu- opioid and GABAB receptors to the inwardly rectifying K+ channel possibly through an action on the G-protein.

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“…As mentioned above, others have shown that a 3-min swim in 32ºC water produces a mixed opioid/nonopioid analgesia when animals were submitted to the hot-plate test (7). Opiates are likely to play a role in the decreased gonadotropin secretion observed during both acute and chronic stress, having a major impact on the regulation of amplitude and frequency of the pulsatile pattern of LH secretion (11,12). Testosterone released from the Leydig cells under the influence of LH and follicle-stimulating hormone are the key regulators of the spermatogenic function of the testis and it is clear that both hormones are needed to initiate and maintain the process of spermatogenesis (1).…”

mentioning

confidence: 99%

Fertility of male adult rats submitted to forced swimming stress

Mingoti

Pereira

Monteiro

2003

Braz J Med Biol Res

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We investigated whether stress interferes with fertility during adulthood. Male Wistar rats (weighing 220 g in the beginning of the experiment) were forced to swim for 3 min in water at 32ºC daily for 15 days. Stress was assessed by the hot-plate test after the last stressing session. To assess fertility, control and stressed males (N = 15 per group) were mated with sexually mature normal females. Males were sacrificed after copulation. Stress caused by forced swimming was demonstrated by a significant increase in the latency of the pain response in the hot-plate test (14.6 ± 1.25 s for control males vs 26.0 ± 1.53 s for stressed males, P = 0.0004). No changes were observed in body weight, testicular weight, seminal vesicle weight, ventral prostate weight or gross histological features of the testes of stressed males. Similarly, no changes were observed in fertility rate, measured by counting live fetuses in the uterus of normal females mated with control and stressed males; no dead or incompletely developed fetuses were observed in the uterus of either group. In contrast, there was a statistically significant decrease in spermatid production demonstrated by histometric evaluation (154.96 ± 5.41 vs 127.02 ± 3.95 spermatids per tubular section for control and stressed rats, respectively, P = 0.001). These data demonstrate that 15 days of forced swimming stress applied to adult male rats did not impair fertility, but significantly decreased spermatid production. This suggests that the effect of stress on fertility should not be assessed before at least the time required for one cycle of spermatogenesis.

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Effect of β-endorphin on pulsatile luteinizing hormone release in conscious castrated rats

Cited by 95 publications

References 7 publications

Reversal of the anti-ovulatory action of stress in rats by prior administration of naloxone hydrochloride

Reversal of the anti-ovulatory action of stress in rats by prior administration of naloxone hydrochloride

Estrogen suppresses mu-opioid- and GABAB-mediated hyperpolarization of hypothalamic arcuate neurons

Fertility of male adult rats submitted to forced swimming stress

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