Induction of Luteinizing Hormone Release by Electrochemical Stimulation of the Medial Preoptic Area in Δ&lt;sup&gt;9&lt;/sup&gt;-Tetrahydrocannabinol-Blocked Proestrous Rats

Murphy, Laura; Tyrey, Lee

doi:10.1159/000124569

Cited by 11 publications

(2 citation statements)

References 15 publications

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“…Second, peripherally administered GnRH restores LH secretion in CB-treated animals (8,13,14). Third, electrical stimulation of the medial preoptic area alleviates the THC-induced blockade of the preovulatory LH surge (61). Finally, ANA is reported to depress GnRH release from the medial basal hypothalamus in vitro (62).…”

Section: Discussionmentioning

confidence: 98%

Regulation of Gonadotropin-Releasing Hormone Secretion by Cannabinoids

et al. 2005

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Cannabinoids (CBs) exert untoward effects on reproduction by reducing LH secretion and suppressing gonadal function. Recent evidence suggests these effects are due primarily to hypothalamic dysfunction; however, the mechanism is obscure. Using immortalized hypothalamic GnRH neurons, we find these cells produce and secrete at least two different endocannabinoids. After release, 2-arachidonyl monoacylglycerol and anandamide are rapidly transported into GnRH neurons and are degraded to other lipids by fatty-acid amide hydrolase. The immortalized GnRH neurons also possess CB1 and CB2 receptors that are coupled to Gi/Go proteins whose activation leads to inhibition of GnRH secretion. In perifusion experiments, CBs block pulsatile release of GnRH. When a CB receptor agonist is delivered into the third ventricle of adult female mice, estrous cycles are prolonged by at least 2 d. Although in situ hybridization experiments suggest either that GnRH neurons in vivo do not possess CB1 receptors or that they are very low, transcripts are localized in close proximity to these neurons. Inasmuch as GnRH neurons in vivo possess G protein receptors that are coupled to phospholipase C and increased intracellular Ca2+, these same neurons should also be able to synthesize endocannabinoids. These lipids, in turn, could bind to CB receptors on neighboring cells, and perhaps GnRH neurons, to exert feedback control over GnRH function. This network could serve as a novel mechanism for regulating GnRH secretion where reproductive functions as diverse as the onset of puberty, timing of ovulation, duration of lactational infertility, and initiation/persistence of menopause may be affected.

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Section: Discussionmentioning

confidence: 98%

Regulation of Gonadotropin-Releasing Hormone Secretion by Cannabinoids

et al. 2005

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“…In the rat, THC administration reduces LH release in intact [1] and castrated males [2] and recently, was shown to suppress the pulsatile pat tern of LH secretion in castrated testosterone-treated animals [3], Moreover, the tonic circulating level of PRL in the intact male is acutely suppressed following THC administration [4,5], The inhibitory effects ofTHC on LH and PRL secretion appear to result from a central drug action since THC is ineffective in suppressing basal or stimulated LH and PRL release from pitu itary cells in vitro [6][7][8], and since LH-releasing hormone (LHRH) stimulation or administration of exogenous thyrotro pin-releasing hormone readily provokes LH or PRL secretion, respectively, during THC-induced suppression of hormone re lease [9][10][11]. The recent findings that intracerebroventricular THC administration suppresses LH and PRL secretion in the male rat further substantiate a central nervous system site of Received: August 18, 1989 Accepted after revision: March 6, 1990 THC action [12,13].…”

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confidence: 99%

Effects of Delta-9-Tetrahydrocannabinol, Cannabinol and Cannabidiol, Alone and in Combinations, on Luteinizing Hormone and Prolactin Release and on Hypothalamic Neurotransmitters in the Male Rat

et al. 1990

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The acute effects of low oral doses of Δ⁹-tetrahydrocannabinol (THC), cannabinol (CBN) and cannabidiol (CBD) administered alone or in combinations on LH and prolactin (PRL) secretion and on hypothalamic norepinephrine (NE), dopamine (DA) and serotonin (5-HI) dynamics were examined in adult male rats. Plasma LH levels were significantly reduced 60 min after administration of 0.5 mgTHC/kg body weight and 30, 60 and 120 min after administration of THC + CBN or THC + CBD. There were no changes in plasma PRL in response to cannabinoid treatments. The turnover of NE in both the median eminence (ME) and medial basal hypothalamus (MBH) was dramatically affected by all the cannabinoid treatments. Complete suppression of NE turnover occurred 30 min post-THC and 120 min post-THC + CBN in the ME and 120 min post-THC + CBD in the MBH. Cannabinoids did not significantly affect DA turnover in the MBH or the content of NE, DA, 5-HT or 5-hydroxyindole-3-acetic acid in either the ME or MBH. These data demonstrate that treatment of adult male rats with a low dose of THC suppresses LH secretion and that CBN and CBD potentiate this action of THC. Although the mechanisms responsible for the inhibition of LH release by cannabinoids cannot be positively identified from these experiments, the results suggest that alterations in hypothalamic noradrenergic activity may be involved in this effect.

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