Endogenous galanin (GAL) has emerged as a physiological regulator of the preovulatory surge of LH and prolactin. Early studies from our group have uncovered several sites where the peptide acts to control the secretion of some pituitary hormones. First, GAL acts at the hypothalamic level and, more specifically on LHRH neurons, to increase the release of the neuropeptide LHRH. In addition, GALergic neuronal systems, including LHRH, release GAL into the hypophyseal portal circulation so that, after reaching the anterior pituitary gland. it can modulate basal or stimulated release of adenohypophyseal hormones. Intrapituitary-synthesized GAL can participate in local modulation by paracrine mechanism. Since classical neurotransmitters, such as catecholamines and serotonin, are involved in the mechanisms involved in the genesis of the preovulatory release of gonadotropins and prolactin, we hypothesized that the effects of endogenous GAL previously observed on the proestrous surge of LH and PRL could be mediated, at least in part, by alterations in brain catecholamine and serotonin turnover rates. In initial studies, we have evaluated catecholamine and serotonin, as well as their primary metabolite levels in the median eminence (ME) in a passive immunization paradigm against GAL during proestrus. Using this model, we observed that blockade of endogenous GAL blunts the preovulatory surges of LH and PRL without altering the FSH surge. Under these conditions, norepinephrine (NE) and dopamine (DA) levels in the ME did not change at 1600 and 1900 h regardless of the treatment. In contrast, serotonin (5HT) levels were elevated in GAL antiserum (GAL-AS)- treated rats. Treatment with GAL-AS did not alter 3-methoxy-4- hydroxyphenylethyleneglycol (MHPG; the primary metabolite of NE) levels in the ME. The levels of 3,4-dihydroxyphenyl-acetic acid (DOPAC; the primary metabolite of DA) were reduced at 1900 h in control animals when compared to 1600 h. In contrast, GAL-AS administration reduced significantly (DOPAC) at 1600 h. This effect was also observed in 5- hydroxyindol-3-acetic acid levels (5HIAA; the primary metabolite of 5HT). The evaluation of amine metabolism ratio between metabolite and amine levels) revealed that GAL-AS administration reduced between DA and 5HT metabolism at 1600 h without altering the rate in NE. In summary. these data indicate that endogenous GAL controls the preovulatory surge of LH and PRL with a concomitant alteration in the metabolism of DA and 5HT.
