Hallo Dr. Teut.
Ich habe eine Frage:
Ein Inhaltsstoff aus dem Cannabis, das Delta-9-Tetrahydrocannabinol ist auf BTM-Rezept bei entsprechender Indikation verschreibungsfähig (wie Dronabinol) so auch bei Depression.
Chemische Stoffe gegen Depression würden für mich in der Schwangerschaft als zu risikoreich ausscheiden.
Hypericum (Johanniskraut) ist wohl nicht hinreichend erforscht in bezug auf den Einsatz in der SS.
Außerdem ist es halt auch eine Frage der Wirksamkeit.
Nach vielem "Querlesen" im Internet haben meine eigenen Recherchen folgendes ergeben: Anandamide (körpereigene Cannabinoide) kommen in der GM-Schleimhaut bis zum Eisprung massiv vor, fallen dann aber drastisch ab.
Daher geht man davon aus das Cannabis die Einnistung hemmen könnte.
Zum Gebrauch in der SS habe ich aber nur Studien gefunden, die keine Beeinträchtigung des Föten / Kindes oder sogar einen "positiven" Einfluß aufzeigten.
(Vorausgesetzt die Cannabis-Exposition erfolgte nicht gemeinsam mit Tabak, dessen Nikotin ja durchaus schädlich ist)
Was ist ihre Meinung / Erfahrung ?
Kann man mit Delta-9-Tetrahydrocannabinol eine Depression in der SS behandeln ?
Wenn nicht - womit denn sonst ????
Vielen Dank für ihre Antwort.
Biggi
C. sativa
Hallo Biggi,
ich rate von Delta-9-Tetrahydrocannabinol ab, Cannabis hat keinen günstigen Einfluss (s.u.).
Die nebenwirkungsärmste und gesündeste Methode ist jeden Tag 30 min Ausdauertraining. Bei leichten und mittelschweren Depressionen ist das so gut wie konventionelle Antidepressiva.
Liebe Grüße,
M. Teut
Life Sci. 1999;65(6-7):695-701. Related Articles, Links
The effects of cannabinoids on the regulation of reproduction.
Wenger T, Toth BE, Juaneda C, Leonardelli J, Tramu G.
Department of Human Morphology and Developmental Biology, Semmelweis University of Medicine, Budapest, Hungary. wenger@ana2.sote.hu
It has been shown that the main psychoactive component of marihuana, delta9-tetrahydrocannabinol (THC) has mainly inhibitory effects on the regulation of reproduction. Recently, the purification and availability of the endogenous ligand of the cannabinoid receptor, arachidonyl ethanolamide, anandamide, (ANA) and its specific long lasting antagonist, the SR 141716 (SR) provided us the opportunity to compare the effects of THC and ANA on the neuroendocrine regulation of reproduction. ANA decreases serum luteinizing hormone (LH) and prolactin (PRL) levels in rats of both sexes. It has no action on serum follicle stimulating hormone (FSH) level. When ANA was administered to pregnant rats it resulted in an increase of the duration of pregnancy and in the frequency of stillbirths. The postnatal development of hypothalamo-pituitary axis in offspring was temporarily inhibited. In conclusion, we found that exogenous and endogenous cannabinoids have only slightly different effects on the reproductive parameters. These effects may occur via the central cannabinoid receptor. It is possible that the sites of action are at both hypothalamic and pituitary levels. The results further support the view that ANA may be a central neurotransmitter or neuromodulator.
Publication Types:
• Review
• Review, Tutorial
PMID: 10462070 [PubMed - indexed for MEDLINE]
________________________________________
Neurobiol Dis. 1998 Dec;5(6 Pt B):432-46. Related Articles, Links
Function of cannabinoid receptors in the neuroendocrine regulation of hormone secretion.
Murphy LL, Munoz RM, Adrian BA, Villanua MA.
Department of Physiology, School of Medicine, Southern Illinois University, Carbondale 62901, USA. lmurph@som.siu.edu
Marijuana and its cannabinoid constituents have profound effects on anterior pituitary hormone secretion. Exposure to delta 9-tetrahydrocannabinol inhibits gonadotropin, prolactin, growth hormone, and thyroid-stimulating hormone release and stimulates the release of corticotropin. Consequently, cannabinoid exposure could have profound effects on the function of the reproductive system, lactation, metabolism, and on the endocrine stress axis. The acute effects of cannabinoids on the endocrine system are consistent with its actions on brain neurotransmitter systems involved in the regulation of neuropeptides that modulate anterior pituitary hormone secretion. Although cannabinoid receptors appear to play a major role in the ability of cannabinoids to influence hormone release, much remains to be learned concerning their function in the neuroendocrine regulation of hormone secretion.
Publication Types:
• Review
PMID: 9974176 [PubMed - indexed for MEDLINE]
Med J Aust. 1992 Apr 6;156(7):495-7. Related Articles, Links
Comment in:
• Med J Aust. 1994 Sep 5;161(5):338-9.
• Med J Aust. 1995 Jan 2;162(1):54-5.
The human toxicity of marijuana.
Nahas G, Latour C.
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University.
The pathophysiological effects of marijuana smoke and its constituent cannabinoids were reported first from in-vitro and in-vivo experimental studies. Marijuana smoke is mutagenic in the Ames test and in tissue culture and cannabinoids inhibit biosynthesis of macromolecules. In animals, marijuana or delta 9-tetrahydrocannabinol (THC), the intoxicating material it contains, produces symptoms of neurobehavioural toxicity, disrupts all phases of gonadal or reproductive function, and is fetotoxic. Smoking marijuana can lead to symptoms of airway obstruction as well as squamous metaplasia. Clinical manifestations of pathophysiology due to marijuana smoking are now being reported. These include: long-term impairment of memory in adolescents; prolonged impairment of psychomotor performance; a sixfold increase in the incidence of schizophrenia; cancer of mouth, jaw, tongue and lung in 19-30 year olds; fetotoxicity; and non-lymphoblastic leukemia in children of marijuana-smoking mothers.
Publication Types:
• Review
• Review, Tutorial
Pharmacol Biochem Behav. 1984 Jan;20(1):115-23. Related Articles, Links
Early cannabinoid exposure influences neuroendocrine and reproductive functions in mice: II. Postnatal effects.
Dalterio S, Steger R, Mayfield D, Bartke A.
Maternal exposure to delta 9-tetrahydrocannabinol (THC), the major psychoactive component in marihuana, or to the non-psychoactive cannabinol (CBN) or cannabidiol (CBD) alters male reproductive functions and brain biogenic amines in male and female offspring. Postnatal exposure to THC or CBN reduced body weights, while testicular weights were lower in CBD-exposed mice. Testicular testosterone (T) levels were also lower in CBN- and CBD-exposed animals. Postnatal cannabinoid exposure reduced plasma luteinizing hormone (LH) levels in intact and castrated adults. Although basal T production in vitro was not affected by postnatal cannabinoid exposure, testes from CBD-exposed males were more responsive to gonadotropin stimulation. In contrast, in vivo responsiveness to intratesticular human chorionic gonadotropin (hCG) administration was significantly reduced in THC- and CBD-exposed males. Pituitary weights and their basal LH production in vitro was higher in THC- or CBN-exposed mice. Pituitaries from cannabinoid-exposed males were less responsive to LH releasing hormone (RH) stimulation, however, hypothalamic LHRH content was significantly higher in the THC-exposed males. Hypothalamic dopamine (DA) levels were significantly lower in CBN-exposed castrated mice, compared to castrated controls. The reduction in hypothalmic norepinephrine (NE) in THC- and CBN-exposed castrates after alpha-methylparatyrosine (alpha-MPT) was significantly less than that observed in control castrates. Hypothalamic DA levels were depleted to a greater extent in CBD-exposed males. Brain levels of serotonin (5-HT) and 5-HIAA were significantly higher in castrated, than in intact THC-exposed males. In ovariectomized CBN-exposed females, hypothalamic NE levels were lower, while the alpha-MPT-induced depletion of NE was less in CBD-exposed, compared to control females. Levels of 5-HT were lower only in THC-exposed females. Plasma levels of LH were significantly higher in CBN-exposed, while plasma levels of FSH were reduced in THC- and CBD females. Maternal exposure to psychoactive or non-psychoactive cannabinoids on the day of parturition results in long term alterations in neuroendocrine function in male and female offspring. It is possible that the observed alterations in biogenic amines may mediate the effects of cannabinoids on pituitary and gonadal function.
PMID: 6320228 [PubMed - indexed for MEDLINE]
Neurobehav Toxicol Teratol. 1986 Jul-Aug;8(4):391-7. Related Articles, Links
Perinatal cannabinoid exposure: demasculinization in male mice.
Dalterio SL, Michael SD, Thomford PJ.
Maternal exposure to psychoactive or non-psychoactive cannabinoids produces long-term changes in body weight regulation, pituitary-gonadal feedback, testicular function, and also affects adult sexual behavior in male offspring. Alterations in brain biogenic amine concentration and metabolism have also been observed in adult males perinatally-exposed to cannabinoids. The possibility that these effects are mediated by cannabinoid-induced suppression or interference with fetal and/or neonatal androgen production is discussed. In addition, data are presented showing that exposure to the major psychoactive component of marihuana, delta 9-tetrahydrocannabinol (THC), on day 12 of gestation significantly increased hepatic cytochromes P-450 levels. In contrast, cytochromes P-450 levels were significantly decreased in adult males exposed to these cannabinoids on day 1 post-partum. The response of these animals to the negative feedback effects of exogenous androgen was also influenced by perinatal cannabinoid exposure. One hr after injection of 20 micrograms testosterone (T), plasma levels of luteinizing hormone (LH), were markedly increased in castrated males exposed to CBD on day 12 of gestation, while the THC and control mice showed no response to T injection. In contrast to the reduced plasma LH levels in the controls, the levels of LH were significantly increased in postnatal THC-exposed males, while the CBN and CBD-exposed mice exhibited no reduction in plasma LH in response to exogenous androgen. Prenatal exposure to THC resulted in a greater suppression of plasma follicle-stimulating hormone (FSH) levels in mice receiving 20 micrograms T, compared to the effects in the castrated controls.(ABSTRACT TRUNCATED AT 250 WORDS)
J Toxicol Environ Health. 1980 Mar;6(2):297-313. Related Articles, Links
Cannabinoid-induced hormone changes in monkeys and rats.
Rosenkrantz H, Esber HJ.
Previous findings at various laboratories indicated that cannabinoids distribute to sexual behavior centers in the brain, and endocrine aberrations have consistently been observed in animals treated with cannabis constituents. Subacute and chronic studies were performed to monitor hormone changes in rats and monkeys exposed to marihuana smoke or pure cannabinoids. In oral studies, young Fischer rats of both sexes were given delta 9-tetrahydrocannabinol (delta 9-THC) doses of 2, 10, or 50 mg/kg for 14--180 d and pregnant rats received 1, 5 or 10 mg/kg during gestation and lactation. Other male rats were exposed to marihuana smoke at delta 9-THC doses of 2 or 4 mg/kg for 14 d. Rhesus monkeys of either sex were given oral cannabidiol doses of 30, 100, and 300 mg/kg for 90 d. Serum pituitary, steroid, and thyroid hormone levels were determined by radioimmunoassay. Marihuana smoke (and oral delta 9-THC) depressed testosterone 20--30% and triiodothyronine 17--29%. In pregnant rats, small doses of delta 9-THC suppressed luteinizing hormone, but larger doses elevated both follicle-stimulating hormone and estrogens (approximately 50--100%) without affecting progesterone levels. Prolonged oral administration of delta 9-THC to young rats tended to increase gonadotropins, to which tolerance developed in males. Cannabidiol-treated monkeys responded with slight elevations in luteinizing hormone and follicle-stimulating hormone in males, whereas steroid hormones were essentially unchanged for both sexes. Hormone imbalance may explain cannabinoid-induced embryotoxicity and impaired gonadal function.
PMID: 6248648 [PubMed - indexed for MEDLINE]
________________________________________
Biol Reprod. 1988 Oct;39(3):540-5. Related Articles, Links
The effect of chronic prepubertal administration of marihuana (delta-9-tetrahydrocannabinol) on the onset of puberty and the postpubertal reproductive functions in female rats.
Wenger T, Croix D, Tramu G.
2nd Department of Anatomy, Semmelweis University Medical School, Budapest, Hungary.
The effect of the main psychoactive component of marihuana, delta-9-tetrahydrocannabinol (THC) was investigated on the onset of puberty and on the reproductive function in female rats up to the seventy-fifth to eightieth day of life. The drug was administered i.p. at a dose of 1 microgram/kg/day between the twenty-second postnatal day and the day of vaginal opening (V.O.). The administration of THC caused a 2-day delay in V. O., and the number of ova on the day of first estrus was significantly lower in treated rats than in controls. No differences were observed in serum gonadotropin and prolactin (PRL) levels on the day of V. O. After puberty, alterations occurred in the neuroendocrine functions of animals receiving THC that persisted until adulthood: estrous cycles were irregular, the number of ova in animals killed 35-40 days after V. O. was reduced, and serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were decreased (diminution of serum FSH content was less expressed). An increase in serum PRL concentration could be demonstrated only in animals killed on the day of estrus. From these results, it might be concluded that THC administered to prepubertal rats--even in a very low dose--causes long-term irreversible alterations in reproductive functions. The importance of the fight against drug abuse is emphasized.
PMID: 2848595 [PubMed - indexed for MEDLINE]
ich rate von Delta-9-Tetrahydrocannabinol ab, Cannabis hat keinen günstigen Einfluss (s.u.).
Die nebenwirkungsärmste und gesündeste Methode ist jeden Tag 30 min Ausdauertraining. Bei leichten und mittelschweren Depressionen ist das so gut wie konventionelle Antidepressiva.
Liebe Grüße,
M. Teut
Life Sci. 1999;65(6-7):695-701. Related Articles, Links
The effects of cannabinoids on the regulation of reproduction.
Wenger T, Toth BE, Juaneda C, Leonardelli J, Tramu G.
Department of Human Morphology and Developmental Biology, Semmelweis University of Medicine, Budapest, Hungary. wenger@ana2.sote.hu
It has been shown that the main psychoactive component of marihuana, delta9-tetrahydrocannabinol (THC) has mainly inhibitory effects on the regulation of reproduction. Recently, the purification and availability of the endogenous ligand of the cannabinoid receptor, arachidonyl ethanolamide, anandamide, (ANA) and its specific long lasting antagonist, the SR 141716 (SR) provided us the opportunity to compare the effects of THC and ANA on the neuroendocrine regulation of reproduction. ANA decreases serum luteinizing hormone (LH) and prolactin (PRL) levels in rats of both sexes. It has no action on serum follicle stimulating hormone (FSH) level. When ANA was administered to pregnant rats it resulted in an increase of the duration of pregnancy and in the frequency of stillbirths. The postnatal development of hypothalamo-pituitary axis in offspring was temporarily inhibited. In conclusion, we found that exogenous and endogenous cannabinoids have only slightly different effects on the reproductive parameters. These effects may occur via the central cannabinoid receptor. It is possible that the sites of action are at both hypothalamic and pituitary levels. The results further support the view that ANA may be a central neurotransmitter or neuromodulator.
Publication Types:
• Review
• Review, Tutorial
PMID: 10462070 [PubMed - indexed for MEDLINE]
________________________________________
Neurobiol Dis. 1998 Dec;5(6 Pt B):432-46. Related Articles, Links
Function of cannabinoid receptors in the neuroendocrine regulation of hormone secretion.
Murphy LL, Munoz RM, Adrian BA, Villanua MA.
Department of Physiology, School of Medicine, Southern Illinois University, Carbondale 62901, USA. lmurph@som.siu.edu
Marijuana and its cannabinoid constituents have profound effects on anterior pituitary hormone secretion. Exposure to delta 9-tetrahydrocannabinol inhibits gonadotropin, prolactin, growth hormone, and thyroid-stimulating hormone release and stimulates the release of corticotropin. Consequently, cannabinoid exposure could have profound effects on the function of the reproductive system, lactation, metabolism, and on the endocrine stress axis. The acute effects of cannabinoids on the endocrine system are consistent with its actions on brain neurotransmitter systems involved in the regulation of neuropeptides that modulate anterior pituitary hormone secretion. Although cannabinoid receptors appear to play a major role in the ability of cannabinoids to influence hormone release, much remains to be learned concerning their function in the neuroendocrine regulation of hormone secretion.
Publication Types:
• Review
PMID: 9974176 [PubMed - indexed for MEDLINE]
Med J Aust. 1992 Apr 6;156(7):495-7. Related Articles, Links
Comment in:
• Med J Aust. 1994 Sep 5;161(5):338-9.
• Med J Aust. 1995 Jan 2;162(1):54-5.
The human toxicity of marijuana.
Nahas G, Latour C.
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University.
The pathophysiological effects of marijuana smoke and its constituent cannabinoids were reported first from in-vitro and in-vivo experimental studies. Marijuana smoke is mutagenic in the Ames test and in tissue culture and cannabinoids inhibit biosynthesis of macromolecules. In animals, marijuana or delta 9-tetrahydrocannabinol (THC), the intoxicating material it contains, produces symptoms of neurobehavioural toxicity, disrupts all phases of gonadal or reproductive function, and is fetotoxic. Smoking marijuana can lead to symptoms of airway obstruction as well as squamous metaplasia. Clinical manifestations of pathophysiology due to marijuana smoking are now being reported. These include: long-term impairment of memory in adolescents; prolonged impairment of psychomotor performance; a sixfold increase in the incidence of schizophrenia; cancer of mouth, jaw, tongue and lung in 19-30 year olds; fetotoxicity; and non-lymphoblastic leukemia in children of marijuana-smoking mothers.
Publication Types:
• Review
• Review, Tutorial
Pharmacol Biochem Behav. 1984 Jan;20(1):115-23. Related Articles, Links
Early cannabinoid exposure influences neuroendocrine and reproductive functions in mice: II. Postnatal effects.
Dalterio S, Steger R, Mayfield D, Bartke A.
Maternal exposure to delta 9-tetrahydrocannabinol (THC), the major psychoactive component in marihuana, or to the non-psychoactive cannabinol (CBN) or cannabidiol (CBD) alters male reproductive functions and brain biogenic amines in male and female offspring. Postnatal exposure to THC or CBN reduced body weights, while testicular weights were lower in CBD-exposed mice. Testicular testosterone (T) levels were also lower in CBN- and CBD-exposed animals. Postnatal cannabinoid exposure reduced plasma luteinizing hormone (LH) levels in intact and castrated adults. Although basal T production in vitro was not affected by postnatal cannabinoid exposure, testes from CBD-exposed males were more responsive to gonadotropin stimulation. In contrast, in vivo responsiveness to intratesticular human chorionic gonadotropin (hCG) administration was significantly reduced in THC- and CBD-exposed males. Pituitary weights and their basal LH production in vitro was higher in THC- or CBN-exposed mice. Pituitaries from cannabinoid-exposed males were less responsive to LH releasing hormone (RH) stimulation, however, hypothalamic LHRH content was significantly higher in the THC-exposed males. Hypothalamic dopamine (DA) levels were significantly lower in CBN-exposed castrated mice, compared to castrated controls. The reduction in hypothalmic norepinephrine (NE) in THC- and CBN-exposed castrates after alpha-methylparatyrosine (alpha-MPT) was significantly less than that observed in control castrates. Hypothalamic DA levels were depleted to a greater extent in CBD-exposed males. Brain levels of serotonin (5-HT) and 5-HIAA were significantly higher in castrated, than in intact THC-exposed males. In ovariectomized CBN-exposed females, hypothalamic NE levels were lower, while the alpha-MPT-induced depletion of NE was less in CBD-exposed, compared to control females. Levels of 5-HT were lower only in THC-exposed females. Plasma levels of LH were significantly higher in CBN-exposed, while plasma levels of FSH were reduced in THC- and CBD females. Maternal exposure to psychoactive or non-psychoactive cannabinoids on the day of parturition results in long term alterations in neuroendocrine function in male and female offspring. It is possible that the observed alterations in biogenic amines may mediate the effects of cannabinoids on pituitary and gonadal function.
PMID: 6320228 [PubMed - indexed for MEDLINE]
Neurobehav Toxicol Teratol. 1986 Jul-Aug;8(4):391-7. Related Articles, Links
Perinatal cannabinoid exposure: demasculinization in male mice.
Dalterio SL, Michael SD, Thomford PJ.
Maternal exposure to psychoactive or non-psychoactive cannabinoids produces long-term changes in body weight regulation, pituitary-gonadal feedback, testicular function, and also affects adult sexual behavior in male offspring. Alterations in brain biogenic amine concentration and metabolism have also been observed in adult males perinatally-exposed to cannabinoids. The possibility that these effects are mediated by cannabinoid-induced suppression or interference with fetal and/or neonatal androgen production is discussed. In addition, data are presented showing that exposure to the major psychoactive component of marihuana, delta 9-tetrahydrocannabinol (THC), on day 12 of gestation significantly increased hepatic cytochromes P-450 levels. In contrast, cytochromes P-450 levels were significantly decreased in adult males exposed to these cannabinoids on day 1 post-partum. The response of these animals to the negative feedback effects of exogenous androgen was also influenced by perinatal cannabinoid exposure. One hr after injection of 20 micrograms testosterone (T), plasma levels of luteinizing hormone (LH), were markedly increased in castrated males exposed to CBD on day 12 of gestation, while the THC and control mice showed no response to T injection. In contrast to the reduced plasma LH levels in the controls, the levels of LH were significantly increased in postnatal THC-exposed males, while the CBN and CBD-exposed mice exhibited no reduction in plasma LH in response to exogenous androgen. Prenatal exposure to THC resulted in a greater suppression of plasma follicle-stimulating hormone (FSH) levels in mice receiving 20 micrograms T, compared to the effects in the castrated controls.(ABSTRACT TRUNCATED AT 250 WORDS)
J Toxicol Environ Health. 1980 Mar;6(2):297-313. Related Articles, Links
Cannabinoid-induced hormone changes in monkeys and rats.
Rosenkrantz H, Esber HJ.
Previous findings at various laboratories indicated that cannabinoids distribute to sexual behavior centers in the brain, and endocrine aberrations have consistently been observed in animals treated with cannabis constituents. Subacute and chronic studies were performed to monitor hormone changes in rats and monkeys exposed to marihuana smoke or pure cannabinoids. In oral studies, young Fischer rats of both sexes were given delta 9-tetrahydrocannabinol (delta 9-THC) doses of 2, 10, or 50 mg/kg for 14--180 d and pregnant rats received 1, 5 or 10 mg/kg during gestation and lactation. Other male rats were exposed to marihuana smoke at delta 9-THC doses of 2 or 4 mg/kg for 14 d. Rhesus monkeys of either sex were given oral cannabidiol doses of 30, 100, and 300 mg/kg for 90 d. Serum pituitary, steroid, and thyroid hormone levels were determined by radioimmunoassay. Marihuana smoke (and oral delta 9-THC) depressed testosterone 20--30% and triiodothyronine 17--29%. In pregnant rats, small doses of delta 9-THC suppressed luteinizing hormone, but larger doses elevated both follicle-stimulating hormone and estrogens (approximately 50--100%) without affecting progesterone levels. Prolonged oral administration of delta 9-THC to young rats tended to increase gonadotropins, to which tolerance developed in males. Cannabidiol-treated monkeys responded with slight elevations in luteinizing hormone and follicle-stimulating hormone in males, whereas steroid hormones were essentially unchanged for both sexes. Hormone imbalance may explain cannabinoid-induced embryotoxicity and impaired gonadal function.
PMID: 6248648 [PubMed - indexed for MEDLINE]
________________________________________
Biol Reprod. 1988 Oct;39(3):540-5. Related Articles, Links
The effect of chronic prepubertal administration of marihuana (delta-9-tetrahydrocannabinol) on the onset of puberty and the postpubertal reproductive functions in female rats.
Wenger T, Croix D, Tramu G.
2nd Department of Anatomy, Semmelweis University Medical School, Budapest, Hungary.
The effect of the main psychoactive component of marihuana, delta-9-tetrahydrocannabinol (THC) was investigated on the onset of puberty and on the reproductive function in female rats up to the seventy-fifth to eightieth day of life. The drug was administered i.p. at a dose of 1 microgram/kg/day between the twenty-second postnatal day and the day of vaginal opening (V.O.). The administration of THC caused a 2-day delay in V. O., and the number of ova on the day of first estrus was significantly lower in treated rats than in controls. No differences were observed in serum gonadotropin and prolactin (PRL) levels on the day of V. O. After puberty, alterations occurred in the neuroendocrine functions of animals receiving THC that persisted until adulthood: estrous cycles were irregular, the number of ova in animals killed 35-40 days after V. O. was reduced, and serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were decreased (diminution of serum FSH content was less expressed). An increase in serum PRL concentration could be demonstrated only in animals killed on the day of estrus. From these results, it might be concluded that THC administered to prepubertal rats--even in a very low dose--causes long-term irreversible alterations in reproductive functions. The importance of the fight against drug abuse is emphasized.
PMID: 2848595 [PubMed - indexed for MEDLINE]
