6533b7d4fe1ef96bd126348b

RESEARCH PRODUCT

Day/night serotonin levels in the pineal gland of male BALB/c mice with melatonin deficiency

Bernhard ManzLutz VollrathKunhard PollowA. Huesgen

subject

Acetylserotonin O-MethyltransferaseMaleAgonistSerotoninendocrine systemmedicine.medical_specialtyArylamine N-Acetyltransferasemedicine.drug_classEndocrinology Diabetes and MetabolismPineal GlandBALB/cMelatoninMicePineal glandEndocrinologyInternal medicinemedicineAnimalsMelatonin synthesisCircadian rhythmMelatoninchemistry.chemical_classificationMice Inbred BALB CbiologyIsoproterenolGeneral Medicinebiology.organism_classificationCircadian RhythmEnzymeEndocrinologymedicine.anatomical_structurechemistrySerotoninhormones hormone substitutes and hormone antagonistsmedicine.drug

description

Abstract. Studies from another laboratory have shown that several strains of laboratory mice have a genetic defect for melatonin synthesis. In non-deficient species, melatonin synthesis undergoes a typical, β-adrenergically regulated day/night rhythm with low melatonin levels during daytime and high levels at night, the precursor serotonin showing an inverse behaviour. This study examines whether a day/night rhythm of pineal serotonin levels exists in melatonin-deficient male BALB/c mice. Mice kept under a lighting schedule of 12 h light (lights on at 07.00 h) and 12 h dark were killed at 13.00 and 01.00 h, respectively. Serotonin amounted to 12-15 ng/pineal and did not show regular day/night differences. Administration of the β-adrenergic agonist, isoproterenol, which is known to affect melatonin synthesis in a number of species, was without effect on pineal serotonin levels. Melatonin and two of the melatonin-forming enzymes, serotonin N-acetyltransferase (NAT) and hydroxyindole-O-methyltransferase (HIOMT) were below the detection limit in the pineal. It is concluded that in melatonin-deficient BALB/c mice, pineal serotonin synthesis is apparently intact. In BALB/c mice, serotonin synthesis and release do not appear to be directly or indirectly regulated by β-adrenergic mechanisms.

https://doi.org/10.1530/acta.0.1170093