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Melatonin reverses pinealectomy-induced decrease of benzodiazepine binding in rat cerebral cortex.

P R Lowenstein1, R Rosenstein, D P Cardinali

  • 1Centro de Estudios Farmacológicos y de Principios Naturales (CEFAPRIN), Serrano 665, (1414)-Buenos Aires, Argentina.

Neurochemistry International
|May 25, 2010
PubMed
Summary
This summary is machine-generated.

Pinealectomy in rats reduced benzodiazepine receptors. Melatonin administration restored these receptors and, with daily treatment, altered receptor density or binding affinity in intact rats, suggesting a link between pineal function and brain benzodiazepine sites.

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Area of Science:

  • Neuroscience
  • Endocrinology

Background:

  • The pineal gland produces melatonin, a hormone influencing circadian rhythms.
  • Benzodiazepine receptors are crucial for neurotransmission and are targeted by anxiolytic drugs.

Purpose of the Study:

  • To investigate the effect of pinealectomy and melatonin on benzodiazepine receptor binding in rat cerebral cortex.
  • To explore the relationship between pineal gland activity and central nervous system benzodiazepine receptor regulation.

Main Methods:

  • Rats underwent pinealectomy, followed by assessment of benzodiazepine receptors using [(3)H]flunitrazepam binding.
  • Melatonin was administered via subcutaneous injection at various doses and schedules.
  • In vitro experiments assessed melatonin's direct effect on receptor binding.

Main Results:

  • Pinealectomy significantly decreased benzodiazepine receptor density in the cerebral cortex.
  • A single melatonin injection reversed the receptor density decrease post-pinealectomy.
  • Daily melatonin treatment in intact rats increased receptor density or altered binding affinity depending on administration time.

Conclusions:

  • Pineal activity is linked to the regulation of benzodiazepine receptors in the rat brain.
  • Pharmacological doses of melatonin can modulate benzodiazepine binding sites, indicating a functional interaction.