The involvement of brain catecholamines (CAs) in the neuroendocrine mechanisms that control the release of LH has been studied in somatically mature quail with regressed and with recrudescing testes and in sexually mature quail. In quail with recrudescing testes, serum LH was markedly increased 3 days after the onset of photostimulation. Administration of an inhibitor of CA synthesis, α-methyltyrosine (MT), started on the day of photostimulation and continued for 3 days thereafter, decreased brain dopamine (DA), norepinephrine (NE), and epinephrine (E) content and blocked the photoperiodically induced rise in serum LH. Treatment with bis(4-methyl-1-homopiperazinil-thiocarbonil) disulfide (FLA63), an inhibitor of DA-β-hydroxylase, caused a marked reduction of brain NE and E levels and a significant increase in brain DA content, and like MT, blocked the photoperiodically induced rise in serum LH. In sexually mature quail, serum LH and testicular regression were effected differently by MT and FLA63. MT partially reduced LH levels, but FLA63 suppressed them completely (i.e., to those of nonphotostimulated birds). Testicular weights were reduced by both MT and FLA63, but as with LH, the FLA63 was more effectual than MT. Treatment with l-dihydroxyphenylalanine, a direct precursor of DA, augmented DA content in the brain, caused a reduction of LH levels, and induced gonadal regression. The results are consistent with the hypothesis that NE-containing neurons facilitate central mechanisms which release LH in response to neural inputs involved in the photoperiodic stimulus, and that activation of DA-containing neurons is capable of inhibiting this release and inducing testicular regression.