Influence of propranolol, phenoxybenzamine or phentolamine on the nocturnal rise of pineal melatonin levels in the syrian hamster

Lipton, J.Stuart; Petterborg, Larry J.; Reíter, Russel J.

doi:10.1016/0024-3205(81)90503-8

Cited by 47 publications

(26 citation statements)

References 12 publications

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“…Endogenous melatonin was reduced by maintaining animals for 2 days in constant light (LL; Carneiro et al, 1991) or injecting propranolol (5, 10, or 20 mg/kg body weight; Lipton et al, 1981) 1 h before lights off during two consecutive days. Vehicle (saline, 0.9%)-injected rats, at the same hour of the day, were taken as control.…”

Section: Methodsmentioning

confidence: 99%

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Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [³H]Glutamate Release in Rat Cerebellum Slices

Markus

Santos²,

Zago³

et al. 2003

J Pharmacol Exp Ther

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Section: Methodsmentioning

confidence: 99%

“…Stimulation of ␤ 1 -adrenoceptors is a required step for induction of the rate-limiting enzyme, Nacetyltransferase, transcription (Klein et al, 1981). Therefore, ␤ antagonists inhibit pineal melatonin production (Lipton et al, 1981).…”

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confidence: 99%

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [³H]Glutamate Release in Rat Cerebellum Slices

Markus

Santos²,

Zago³

et al. 2003

J Pharmacol Exp Ther

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“…Craft et al [ 1985] found beta-receptors in the Syrian hamster pineal that (unlike in the rat) did not rise in density after prolonged light exposure or SCGX and noted that hamster pineal NE synthesis (evaluated from L-dopa accumulation after decarboxylase inhibition) normally rose at night. The nocturnal pineal melatonin rise in this species is prevented by beta-blockade [Lipton et al, 1981] and SCGX [Panke et al, 1979;Vaughan and Reiter, 19851. In the light of such findings, the nocturnal appearance of a pineal melatonin response to NE and protection from humoral-route activation by a neuronal uptake system in Syrian hamsters (a) indicate that NE is likely the pineal neurotransmitter responsible for the nocturnal melatonin surge, (b) explain previous negative results with NE, and (c) provide possible mechanisms to eliminate noise in the 24-h rhythmic melatonin signal by preventing untimely rises in melatonin synthesis due to general sympathetic stimuli. Indeed, such partitioning of sympathetic function for independent and specific control of the pineal may help explain the observed lack of evidence for augmented melatonin production after general sympathetic stimuli in Syrian hamsters and humans [see Vaughan, 1984;Gupta et al, 1983;Champney et al, 1985;Vaughan et al, 1985].…”

Section: Hw-ister Melatonin Response To Norepinephrine 247mentioning

confidence: 99%

“…Both beta-blockade and sympathetic neuronal lesions interrupt or prevent the normal nocturnal surge of pineal melatonin synthesis or of circulating or excreted melatonin in rats, Syrian hamsters, and humans [Eichler and Moore, 1971;Deguchi and Axelrod, 1972;Reiter and Sorrentino, 1972;Reiter, 1972;Kneisley et al, 1978;Klein and Moore, 1979;Panke et al, 1979;Tetsuo et al, 1981;Lipton et al, 1981;Cowan et al, 1983;Vaughan, 1984;Arendt et al, 1985;Vaughan and Reiter, 19851. Taken together, these findings indicate similarity of these three species with regard to sympathetic control of melatonin production as revealed by neural lesions and beta-blockade.…”

Section: Introductionmentioning

confidence: 99%

Rhythmic Melatonin Response of the Syrian Hamster Pineal Gland to Norepinephrine In Vitro and In Vivo

Vaughan

Lasko

Coggins

et al. 1986

Journal of Pineal Research

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Norepinephrine (NE, 10−6 M) stimulated melatonin accumulation in the incubation medium of rat (but not Syrian hamster) pineals taken at the end of the light phase. However, NE elevated melatonin accumulation in the medium of pineals taken after 20 min of light exposure of animals of either species at 6 h into the 10‐h dark phase. A dose response to 10−7−10−5 M NE was observed in both the medium and pineals upon incubation of pineals taken from rats at 4 h into the light phase and from hamsters after 20 min light exposure at 6 h into the dark phase. Approximately 95% of the melatonin present was in the medium. The incubation time was 4 h in all cases. Subcutaneous injection of 1 μg/g NE (either at the end of the light phase or after 30 min of light at 6 h into the dark phase) did not stimulate in vivo Syrian hamster pineal melatonin content determined 1 or 2 h after injection, whether the hamsters were placed in light or darkness after the injection. However, after 30 min of light beginning at 6 h into dark, injection of 5 μg/g desipramine (DMI, a blocker of catecholamine uptake into nerve endings) allowed a dramatic hamster pineal melatonin response to additional injection of 1 μg/g NE, observed at 1 and 2 h in light after injection. A small effect of DMI alone was seen. DMI also potentiated the effect of NE (each 10−6 M) on melatonin accumulation in the medium of incubated hamster pineals taken after a short light exposure at night. No significant stimulatory effect of NE and/ or DMI was seen in vivo or in vitro near the middle of the light phase. Measurement of melatonin in the incubation medium is a useful method for studying pineal function. The Syrian hamster pineal has rhythm of sensitivity to NE (sensitivity evident at night) and even at night is protected by neuronal uptake from circulating NE‐induced stimulation of melatonin production. NE appears to be the neurotransmitter for stimulation of pineal melatonin production in the Syrian hamster. The sensitivity rhythm and uptake protection might provide specificity of control of the nightly melatonin signal by reducing the chance of a melatonin response during the day or a response to circulating catecholamines from general sympathetic stimuli.

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“…Experiments involving NE and its agonists have failed to stimulate levels of hamster pineal melatonin, the most thoroughly studied antigonadotrophic indole in the pineal gland [6,7]. On the other hand, propran olol, a fl-adrenergic antagonist, completely blocks the night time rise in melatonin in the hamster pineal gland.…”

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24-Hour Changes in Catecholamine Synthesis in Rat and Hamster Pineal Glands

Craft

Morgan

Reíter³

1984

Neuroendocrinology

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The purpose of this study was to examine the 24-hour variation in endogenous tyrosine hydroxylase (TH) activity and thus catecholamine (CA) synthesis in the hamster and rat pineal gland. To determine CA synthesis a time course of the accumulation of dihydroxyphenylalanine (DOPA) after DOPA decarboxylase inhibition with m-hydroxybenzylhydrazine (NSD-1015) was measured at 0, 15 and 30 min by liquid chromatography with electrochemical detection. Animals were under long photoperiods (LD 14:10; lights on at 06.00 h). In the hamster pineal gland, CA synthesis was greater in the dark (24.00 h) (0.017 ng/pineal/min) than in the light (12.00 h) (0.008 ng/pineal/min). Similarly, CA synthesis in the rat pineal was 0.037 ng/pineal/min (dark) and 0.005 ng/pineal/min (light). In a 24-hour study, animals were injected with NSD-1015,30 min prior to killing to determine if 24-hour changes were present in CA synthesis. In the hamster, DOPA in the dark (p < 0.001) was significantly greater than in the light (1.33 ± 0.42 ng/pineal at 06.00 h; 0.33 ± 0.07 at 13.00 h) in this study. No significant difference was measured in norepinephrine (NE) concentration during this 24-hour period. In the rat, DOPA accumulation was significantly different (p < 0.001) in the dark as compared to the light (0.86 ± 0.09 ng/pineal at 03.00 h; 0.21 ± 0.08 at 12.30 h). Within this 24-hour period, NE concentration fluctuated significantly between 2.28 ± 0.33 ng/pineal (15.30 h) to 4.65 ± 0.59 (05.30 h). These results indicate for the first time a definite 24-hour rhythm in endogenous TH activity and NE synthesis in the hamster pineal gland even though NE content does not change. In addition, a 24-hour change in CA synthesis and content is present in the rat pineal gland.

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Influence of propranolol, phenoxybenzamine or phentolamine on the nocturnal rise of pineal melatonin levels in the syrian hamster

Cited by 47 publications

References 12 publications

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [³H]Glutamate Release in Rat Cerebellum Slices

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [³H]Glutamate Release in Rat Cerebellum Slices

Rhythmic Melatonin Response of the Syrian Hamster Pineal Gland to Norepinephrine In Vitro and In Vivo

24-Hour Changes in Catecholamine Synthesis in Rat and Hamster Pineal Glands

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Influence of propranolol, phenoxybenzamine or phentolamine on the nocturnal rise of pineal melatonin levels in the syrian hamster

Cited by 47 publications

References 12 publications

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [3H]Glutamate Release in Rat Cerebellum Slices

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [3H]Glutamate Release in Rat Cerebellum Slices

Rhythmic Melatonin Response of the Syrian Hamster Pineal Gland to Norepinephrine In Vitro and In Vivo

24-Hour Changes in Catecholamine Synthesis in Rat and Hamster Pineal Glands

Contact Info

Product

Resources

About

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [³H]Glutamate Release in Rat Cerebellum Slices

Melatonin Nocturnal Surge Modulates Nicotinic Receptors and Nicotine-Induced [³H]Glutamate Release in Rat Cerebellum Slices