PubMed HealthSearch

Biomedical subjects

F J Lopez

Publications and source records attributed to F J Lopez.

4 recordsLinked to original sources

Colocalization of galanin and luteinizing hormone-releasing hormone in a subset of preoptic hypothalamic neurons: anatomical and functional correlates.

Colocalization of neurotransmitters, including neuropeptides and amines, in the same neuron of certain areas or well-defined nuclei of the central and peripheral nervous systems appears to be the rule rather than the exception. The coexistent neurotransmitters can be coreleased and interact at pre- and postsynaptic levels in a synergistic or antagonistic manner. Galanin is a recently isolated and characterized "gut-brain" peptide. It is colocalized with many neurotransmitters in both the central and the peripheral nervous systems. Among other regions in the central nervous system, galanin is present in neuronal perikarya of the septum and the hypothalamus. The dense accumulation of nerve terminals in the external zone of the median eminence suggests that galanin is an important peptide regulating neuroendocrine functions. Although most galanin and luteinizing hormone-releasing hormone (LHRH) neurons have a distinctly different morphology, a subset of galanin-immunoreactive perikarya in the diagonal band of Broca and the medial preoptic area, near the organum vasculosum of the lamina terminalis, have morphological features similar to those of LHRH neurons. By using double-labeling immunocytochemistry, we have found that in the preoptic region of the male rat brain approximately 15-20% of these "LHRH-like" galanin-immunoreactive neurons are also immunopositive for LHRH. Moreover, in the medial preoptic area and the diagonal band of Broca, some of the single-labeled LHRH cells are surrounded with galanin-immunoreactive nerve terminals, suggesting that LHRH perikarya have synaptic contacts with galanin-immunoreactive terminals. Additional studies indicated that galanin can readily enhance in vitro release of LHRH from nerve terminals in the median eminence. The observations that (i) galanin is coexpressed with LHRH, (ii) galanin seems to innervate LHRH-producing neurons, and (iii) galanin acts as a putative neurotransmitter to enhance the release of LHRH suggest that galanin should be considered an important regulator of LHRH-containing neurons and, therefore, of reproductive functions.

Animals

Galanin stimulates luteinizing hormone-releasing hormone secretion from arcuate nucleus-median eminence fragments in vitro: involvement of an alpha-adrenergic mechanism.

Galanin (GAL), a 29-amino acid peptide originally isolated from porcine intestine, has been shown to be widely distributed not only in the gut, but also in the central nervous system. Several studies have shown that GAL participates in the hypothalamic regulation of PRL, GH, and LH secretion. In this study, we evaluate the effects of rat GAL (rGAL) on LHRH and prostaglandin (PG) E2 release from arcuate nucleus-median eminence fragments in vitro. Fragments were incubated for 30-min periods in Krebs-Ringer bicarbonate buffer containing the different test substances. The addition to the medium of rGAL in concentrations ranging from 5-1000 nM increased the release of both LHRH and PGE2 in a concentration-dependent manner. The ED50 values were approximately 55 and 80 nM for LHRH and PGE2, respectively. rGAL-induced LHRH and PGE2 release were related, as suggested by the finding that the addition to the medium of indomethacin (10 microM), a PG synthesis blocker, completely blocked rGAL-induced LHRH release. In addition, an active catecholaminergic system appears to be necessary for obtaining the stimulatory effect of rGAL. The addition to the medium of the alpha-adrenergic blocker phentolamine or prazosin impaired the ability of rGAL to release both LHRH and PGE2. rGAL-induced stimulation of LHRH and PGE2 release was blocked by phentolamine at doses of 1-10 microM, while prazosin was able to block it at doses as low as 0.1 microM. In summary, rGAL stimulates LHRH and PGE2 release from arcuate nucleus-median eminence fragments in vitro in a dose-dependent fashion. Such an effect is blocked by both indomethacin and alpha-adrenergic blockers, indicating that rGAL-induced stimulation of LHRH secretion is exerted through alpha-adrenergic receptors and requires PGE2 as an intracellular mediator.

Adrenergic alpha-Antagonists