Effects of amphetamine, methylphenidate and cocaine on serum prolactin concentrations in the male rat

Ravitz, Alan; Moore, Kenneth E.

doi:10.1016/0024-3205(77)90311-3

Cited by 44 publications

(10 citation statements)

References 7 publications

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“…The presence of an inefficient recapture mechanism would permit the majority of released dopamine to enter the portal capillaries. This is consistent with the observation that spe cific inhibitors of dopamine uptake only produce slight re ductions in prolactin secretion [26]. On the other hand, the impaired DA uptake process in the terminals of the median eminence clarifies the early report of Lichtensteiger and Langemann [19].…”

Section: Discussionsupporting

confidence: 80%

Differences in the Kinetics of Dopamine Uptake in Synaptosome Preparations of the Median Eminence Relative to Other Dopaminergically Inervated Brain Regions

et al. 1980

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A comparison of the kinetics of dopamine uptake was made in synaptosomal preparations of the median eminence, striatum and olfactory tubercle. Double reciprocal Lineweaver-Burk plots of the initial velocity versus the concentration of dopamine yielded a single straight line in all three areas. The Michaelis constant (K_m) in the median eminence (1.8 ± 0.9 × 10^–6M) was significantly higher (p<0.05) than in the striatum (4.2 ± 0.8 × 10^–8M) or olfactory tubercle (6.3 ± 1.9 × 10^–8M). Uptake in the median eminence appeared to be predominantly into dopaminergic terminals since preincubation with desipramine did not affect the maximum velocity (V_max) of dopamine uptake. Observed uptake was predominantly due to transport across the neuronal membrane and not into storage granules, since reserpine only caused a small decrease in uptake. The low affinity of dopamine uptake in median eminence synaptosomes is consistent with the neurose-cretory nature of these terminals, whereas, in the striatum and olfactory tubercle, high affinity reuptake is consistent with the role of dopamine as a neurotransmitter.

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Section: Discussionsupporting

confidence: 80%

Differences in the Kinetics of Dopamine Uptake in Synaptosome Preparations of the Median Eminence Relative to Other Dopaminergically Inervated Brain Regions

et al. 1980

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“…We did not, however, observe any significant increase in prolactin levels in cocaine-treated rats. In other studies, cocaine has either had no demonstrable effect on PRL levels [25] or has decreased PRL levels [29]. In view of the re ported absence of a high-affinity DA reuptake mechanism within the median eminence (i.e.…”

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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“…Ldopa has also been found to lower prolactin although this effect is less consistent (Lal, Martin, de la Vega & Friesen, 1975). Amphetamines, however, have weak and inconsistent effects upon PRL in both animal (Ravitz & Moore, 1977) and human studies (Wells, Silverstone & Rees, 1978;Slater, de la Vega, Shyler & Murphy, 1978). Dopamine infusions reduce PRL secretion from pituitary cell cultures (Birge, Jacobs, Hammer & Daughaday, 1970) animals, including stalk-sectioned monkeys (Diefenbach, Carmel, Frantz & Ferin, 1976) and from human subjects (Leblanc, Lachein, Abu-Fadel & Yen, 1976;Leebaw, Lee & Woolf, 1978).…”

Section: Anxiolyticsmentioning

confidence: 99%

“…Van Thiel (1978) Loosen et al (1979) to produce a slight reduction in serum prolactin in rats (Ravitz & Moore, 1977).…”

Section: (C) Cocainementioning

confidence: 99%

Neuroendocrine markers of CNS drug effects.

Johnstone¹,

Ferrier²

1980

Brit J Clinical Pharma

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Effects of amphetamine, methylphenidate and cocaine on serum prolactin concentrations in the male rat

Cited by 44 publications

References 7 publications

Differences in the Kinetics of Dopamine Uptake in Synaptosome Preparations of the Median Eminence Relative to Other Dopaminergically Inervated Brain Regions

Differences in the Kinetics of Dopamine Uptake in Synaptosome Preparations of the Median Eminence Relative to Other Dopaminergically Inervated Brain Regions

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

Neuroendocrine markers of CNS drug effects.

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