Pinealectomy but not Melatonin Supplementation Affects the Diurnal Variations in 125I-Melatonin Binding Sites in the Rat Brain

Oaknin-Bendahan, Sol; Anis, Yossi; Nir, I.; Zisapel, Nava

doi:10.1515/jbcpp.1992.3.3.253

Cited by 11 publications

(12 citation statements)

References 34 publications

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“…Only a partial overlap existed between the timing of peaks or troughs of melatonin binding sites and crests or nadirs in tissue melatonin content. In pinealectomized rats, the densities of 125 I-melatonin binding sites in the medulla-ports, hippocampus and hypothalamus also varied diurnally (Oaknin-Bendahan et al, 1992), as is also confirmed in the present report. However, the densities of binding sites in these brain areas at 18.00 h, were lower in the pinealectomized animals, but higher in the sham-operated rats than at the other times of day tested.…”

Section: Introductionsupporting

confidence: 91%

Modification by oxazepam of the diurnal variations in brain125I-melatonin binding sites in sham-operated and pinealectomized rats

Anis

Nir²,

Schmidt³

et al. 1992

J. Neural Transmission

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Summary. Sham-operated and pinealectomized male rats were maintained at 14h light: 10 h dark cycles (lights-on 5.00h) and injected daily, for 14 days, with o• or vehicle. 125 I-melatonin binding was recorded in synaptosomes prepared at 10.00, 18.00, and 24.00h from the hypothalamus, hippocampus and medulla-pons of the rats. In the sham-operated, vehicle treated rats, specific 125 I-melatonin binding in all brain areas studied was higher at 18.00 h, whereas in the oxazepam-treated animals, binding was higher at 24.00h than at the other times tested. In the pinealectomized, vehicle-treated rats, the binding recorded at 18.00 h in all three brain areas, was lower than at the other times of day tested. Oxazepam treatment decreased 125 I-melatonin binding at 24.00 h in the hippocampus and medulla-pons of the pinealectomized rats and did not significantly affect the binding in the hypothalamus. These results indicate the ability of oxazepam, pinealectomy and their combination, to manipulate the diurnal variations in 125 I-melatonin binding sites in the rat brain.

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Section: Introductionsupporting

confidence: 91%

Modification by oxazepam of the diurnal variations in brain125I-melatonin binding sites in sham-operated and pinealectomized rats

Anis

Nir²,

Schmidt³

et al. 1992

J. Neural Transmission

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“…This dose-dependent inhibition was noticeable at the lowest concentration of melatonin tested, 10 nM, i.e. within the range of the circulating levels of melatonin in rodents (Oaknin-Bendahan et al, 1992) and, therefore, could be a physiologically relevant process. Moreover, the ectopic production of melatonin by a variety of tissues is a well characterized phenomenon (Ozaki and Lynch, 1976;Kvetnoy and Yuzhakov, 1993) and may lead to local concentrations of the hormone at least one order of magnitude higher than the circulating levels (Shaw et al, 1989).…”

Section: Discussionmentioning

confidence: 82%

Melatonin Antagonizes α‐Melanocyte‐Stimulating Hormone Enhancement of Melanogenesis in Mouse Melanoma Cells by Blocking the Hormone‐Induced Accumulation of the C Locus Tyrosinase

Valverde

Benedito

Solano

et al. 1995

European Journal of Biochemistry

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Melatonin was found to have a small inhibitory effect on tyrosinase activity and a slight stimulatory action on dopachrome tautomerase activity in B16 mouse melanoma cells. These effects were time and dose dependent, with the maximal response being observed after 24-48 h treatment and at concentrations of melatonin higher than the physiologic levels of the circulating hormone. Although these effects on the melanogenic activities were modest, incubation of melanocytes with melatonin prior to the addition of the melanotropin mediated a dramatic inhibition of a-melanocyte-stimulating-hormone-(a-MSH)-induced melanogenesis. This inhibitory effect was evident at melatonin concentrations as low as 10 nM. Inhibition was nearly total at 0.1 mM melatonin, even at high concentrations of a-MSH (1 pM).The inhibitory effect of melatonin on a-MSH stimulation of melanogenesis was investigated. Melatonin appeared to act at least at two stages. Pharmacological concentrations of melatonin diminished the number of a-MSH receptors to about 75% of the control values without an apparent effect on receptor affinity, as determined by receptor-binding studies using '251-[N-Leu4-~-Phe7]a-MSH as a probe. Physiological concentrations of melatonin also appeared to interfere with the intracellular events coupling increased CAMP levels and induction of the c locus tyrosinase, since it strongly inhibited the theophyllinemediated stimulation of melanogenesis. The inhibiton of tyrosinase stimulation was higher in the microsoma1 than in the melanosomal fractions of cells which were treated with melatonin, then exposed to either a-MSH (1 pM) or theophylline (1 mM), suggesting that one of the main effects of melatonin might be inhibition of the induction of tyrosinase de novo synthesis.Keywords : melatonin ; a-melanocyte-stimulating hormone ; tyrosinase ; tyrosinase-related proteins ; melanogenesis.Mammalian pigmentation is the result of melanin production by the epidermal melanocytes. Within melanocytes, melanin synthesis proceeds in specialized organelles, the melanosomes, through a series of coupled enzymic and chemical reactions (reviewed in Prota, 1992). The two initial steps of the pathway, rate-limiting hydroxylation of tyrosine to yield ~-3P-dihydroxyphenylalanine (L-Dopa) and L-Dopa oxidation to L-dopaquinone, are catalyzed by tyrosinase. These two reactions can also be catalyzed, although with lower efficiency, by the tyrosinaserelated protein-1 (TRP1; Jimenez et al., 1991 ; JimCnez-Cervantes et al., 1994) a protein encoded by the b Locus (Jackson, 1988). At least one other enzymic protein, dopachrome tautomerase (Aroca et al., 1990), has been shown to be involved in regulation of the pathway. This enzyme catalyzes the tautomerization of L-dopachrome, the product of spontaneous evolution

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“…In light of evidence that GABA A receptor-mediated 402 nature neuroscience • volume 2 no 5 • may 1999 currents in CA1 neurons in hippocampal slices (Fig. 1d), as previous studies have revealed the presence of melatonin-binding sites in these neurons 11 . To our surprise, potentiation of GABA A receptor-mediated currents by melatonin was not observed in any neurons tested in this region.…”

mentioning

confidence: 99%

Differential modulation of GABAA receptor function by Mel1a and Mel1b receptors

et al. 1999

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Correspondence should be addressed to Y. T.W. (y.t.wang@utoronto.ca) Melatonin, a hormone principally produced and released by the pineal gland, has been shown to regulate a variety of biological functions including circadian rhythms, sleep-wake cycles and reproduction 1 , presumably through activating high-affinity G-protein-coupled receptors 2-5 . We report here that these subtypes can differentially modulate the function of type-A g-aminobutyric acid (GABA A ) receptor, the principal neurotransmitter receptor mediating synaptic inhibition in the CNS 6,7 . This work demonstrates that melatonin, through activation of different receptor subtypes, can exert opposite effects on the same substrate, suggesting that receptor subtype is the primary molecular basis for the diversity of melatonin effects.Two mammalian melatonin receptor subtypes, Mel 1a and Mel 1b , have been cloned 2-4 , but, because of a lack of subtype-specific agonists and antagonists, it has proven difficult to assign specific roles to each subtype 2,5 . Probably the best-characterized actions of melatonin in

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Pinealectomy but not Melatonin Supplementation Affects the Diurnal Variations in 125I-Melatonin Binding Sites in the Rat Brain

Cited by 11 publications

References 34 publications

Modification by oxazepam of the diurnal variations in brain125I-melatonin binding sites in sham-operated and pinealectomized rats

Modification by oxazepam of the diurnal variations in brain125I-melatonin binding sites in sham-operated and pinealectomized rats

Melatonin Antagonizes α‐Melanocyte‐Stimulating Hormone Enhancement of Melanogenesis in Mouse Melanoma Cells by Blocking the Hormone‐Induced Accumulation of the C Locus Tyrosinase

Differential modulation of GABAA receptor function by Mel1a and Mel1b receptors

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