Effects of Opiate Antagonists on Serotonin Turnover and on Luteinizing Hormone and Prolactin Secretion in Estrogen- or Morphine-Treated Rats

Johnson, Mahlon D.; Crowley, William R.

doi:10.1159/000123911

Cited by 34 publications

(8 citation statements)

References 24 publications

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“…The synaptic sequence in this model is consistent with previous studies reporting that opioids increase 5-HT turnover in the hypothalamus [27] and that opioid stimu lated prolactin release depends upon intact serotonergic neurotransmission [28][29][30], Several pieces of evidence support the proposition that the final mechanism of pro lactin release through this pathway does indeed involve dopaminergic inhibition. For examples, 5-HT [5] as well as morphine and (3-endorphin [31] decrease dopamine concentrations in pituitary stalk plasma.…”

Section: Discussionsupporting

confidence: 88%

Partial Characterization of a Neurotransmitter Pathway Regulating the in vivo Release of Prolactin

Flores¹,

Hulihan-Giblin²,

Hornby³

et al. 1992

Neuroendocrinology

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Nicotinic cholinergic, opiate and serotonergic agonists as well as dopaminer-gic antagonists induce the release of pituitary prolactin. The purposes of the present studies were to determine if nicotine, morphine and the serotonin _1A (5-HT_1A) agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) utilize a common synaptic pathway to release prolactin and, if so, to establish the serial order of the receptors involved. We also sought to determine whether the pathway under investigation leads to the secretion of prolactin via a mechanism involving dopamine, the prolactin inhibitory factor. Male rats with indwelling jugular catheters were pretreated with saline, mecamylamine, naltrexone, methysergide or bromocriptine. In the saline-treated animals, administration of nicotine, morphine, 8-OH-DPATand haloperidol resulted in significant increases in plasma prolactin levels. Mecamylamine pretreatment prevented the prolactin response to nicotine only. N-altrexone blocked the stimulation of prolactin release by morphine and by nicotine. Methysergide inhibited the effects of 8-OH-DPAT, morphine and nicotine but not haloperidol. Bromocriptine blocked the prolactin secretion induced by haloperidol as well as by each of the above agonists. Also, in dual-immunocytochemically stained sections, tyrosine hydroxylase-immunoreactive cells and serotonin-immunoreactive processes were detected in close anatomical proximity in the dorsomedial arcuate nucleus. These data indicate that nicotine, morphine and 8-OH-DPAT act to release prolactin via a common synaptic pathway expressing nicotinic cholinergic, opiate, and 5-HT_1A receptors at synapses arranged serially in that functional order. Furthermore, the data indicate that the in vivo secretion of prolactin via this pathway may ultimately occur through the inhibition of dopamine release.

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Section: Discussionsupporting

confidence: 88%

Partial Characterization of a Neurotransmitter Pathway Regulating the in vivo Release of Prolactin

Flores¹,

Hulihan-Giblin²,

Hornby³

et al. 1992

Neuroendocrinology

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“…This does not, however, exclude the possibility of opioid-5-HT interactions under other conditions. Previous results do show that the acute effects of estradiol on 5-HT activity appear to involve endogenous opioid neurons and that this seems more important for the control of PRL, rather than LH, secretion (51).…”

Section: Discussionmentioning

confidence: 90%

Role of Central Serotonin Systems in the Stimulatory Effects of Ovarian Hormones and Naloxone on Luteinizing Hormone Release in Female Rats*

1986

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The present experiments tested whether serotonergic neurons that innervate discrete areas of the hypothalamus are involved in the stimulation of LH release by ovarian hormones or the opiate antagonist naloxone in female rats. Ovariectomized rats received oil vehicle, estradiol benzoate (EB) alone, or EB followed by progesterone (P) 2 days later. Serotonin (5-HT) activity was assessed from the accumulation observed after the administration of the monoamine oxidase inhibitor pargyline. Two days after EB treatment, LH concentrations were reduced in the morning and rose by later afternoon. Administration of P to EB-primed rats stimulated a LH surge. This latter treatment also enhanced pargyline-induced 5-HT accumulation, suggesting increased 5-HT activity, in the medial preoptic nucleus and interstitial nucleus of the stria terminalis, but reduced 5-HT accumulation, suggesting decreased 5-HT activity, in the ventromedial nucleus. 5-HT activity was unaffected after EB alone, either in the morning or afternoon, or by the administration of naloxone to EB-primed rats. Specific depletion of 5-HT in the medial preoptic/stria terminalis area, achieved by microinjection of the neurotoxic indoleamine 5,7-dihydroxytryptamine resulted in a blockade of the LH surge induced by EB plus P. The present results suggest that central 5-HT neurons innervating the preoptic area are involved in the LH surge induced by progesterone, but not in the increases in LH occurring after treatment with estradiol alone or after blockade of opiate receptors.

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“…Selective lesioning of hypothalamic 5HT systems leads to alterations in both the timing and amplitude of cyclic LH surges [8,12]. The exact nature of the role played by hypothalamic 5HT in regulating GnRH release is not clearly understood.…”

Section: Discussionmentioning

confidence: 99%

Cocaine Disrupts Estrous Cyclicity and Alters the Reproductive Neuroendocrine Axis in the Rat

King¹,

Schenken²,

Kang³

et al. 1990

Neuroendocrinology

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Although a common drug of abuse, cocaine’s effects on cyclic reproductive functions and the neuroendocrine systems regulating these functions have not been studied. Here, we report the effects of cocaine on (1) estrous cyclicity and ovulation rates and (2) the stimulated in vitro release of hypothalamic GnRH and aminergic neurotransmitters directly involved in regulating or modulating GnRH release. Within 7 days of treatment with 10 mg kg^–1 day^–1 of cocaine HC1 subcutaneously, rats demonstrated significant estrous cycle irregularity including repetitive days of estrus and prolonged periods of diestrus. After 6 weeks of treatment, cocaine-treated rats exhibited a 44.3% decrease in ovulation rates. For the in vitro studies, bilaterally ovariectomized rats were injected with cocaine (10 mg kg^–1 day^–1) or with saline for 2 weeks. Each rat received estradiol benzoate (50 mg kg^–1 day^–1 s.c.) for 2 days before sacrifice. Hypothalamic slices were prepared, placed in 0.1 ml microchambers and perfused with modified Krebs buffer (pH 7.4) using a programmable perfusion system. Basal release of norepinephrine (NE) and serotonin (5HT) was significantly increased in the cocaine-treated group versus controls. Ten-minute pulses of 10^–7M progesterone (P4) increase NE and 5HT, but not dopamine (DA), release in the saline-treated group. In contrast, pulses of P4 increased NE, but not 5HT or DA, in the cocaine-treated rats. Ten-minute pulses of 0.1 µM NE increased GnRH release in both saline- and cocaine-treated rats. However, the response to pulsed NE was significantly attenuated in the cocaine-treated group. The results of this study demonstrate that cocaine disrupts estrous cyclicity by altering the hypothalamic amine activity necessary for pulsatile hypothalamic GnRH release. However, a direct effect of cocaine on the pituitary gland or ovaries cannot be excluded on the basis of these results.

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Effects of Opiate Antagonists on Serotonin Turnover and on Luteinizing Hormone and Prolactin Secretion in Estrogen- or Morphine-Treated Rats

Cited by 34 publications

References 24 publications

Partial Characterization of a Neurotransmitter Pathway Regulating the in vivo Release of Prolactin

Partial Characterization of a Neurotransmitter Pathway Regulating the in vivo Release of Prolactin

Role of Central Serotonin Systems in the Stimulatory Effects of Ovarian Hormones and Naloxone on Luteinizing Hormone Release in Female Rats*

Cocaine Disrupts Estrous Cyclicity and Alters the Reproductive Neuroendocrine Axis in the Rat

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