The participation of brain catecholamines (CA) in the neuroendocrine mechanism(s) that controls the release of LH following gonadectomy has been studied in prepuberal male and female rats of 1–28 days of age. Plasma concentrations of LH were considerably increased 3 days following gonadectomy in rats of both sexes at all ages studied, except in 7-day-old ovariectomized pups in which the post-castration LH rise was less evident. Administration of an inhibitor of both norepinephrine (NE) and dopamine (DA) synthesis, α-methyl-tyrosine (α-MT) 24 and 48 hr after castration was completely ineffective in counteracting the LH rise that follows gonadectomy in most of the age groups studied, except in 14-day-old male and 21-day-old female rats, in which a reduction in plasma LH levels was present. Acute administration of α-MT to 28-day-old female rats, castrated 24 hr before, did not induce significant changes in LH levels measured during the four hour post-injection period. Bis-(4-methyl-l-homopiperazinil- thiocarbonil) disulfide (FLA 63), a selective blocker of NE synthesis, administered twice a day × 2 days almost completely suppressed in all the animals studied, the rise in plasma LH taking place after gonadectomy. Biochemical determinations of NE and DA provided evidence on the effects of the drugs used on actual brain monoamine levels. Results obtained with FLA 63 indicate that NE is the neurotransmitter that triggers in prepuberal rats the increased release of LH occurring in the postcastration phase. In the light of the action of FLA 63, the ineffectiveness of α-MT implies that dopamine does not play a stimulatory role in the postcastration rise of plasma LH. (Endocrinology95: 1649, 1974)

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