SEROTONIN DEPLETION BY 5,7-DIHYDROXYTRYPTAMINE ALTERS DEUTOCEREBRAL DEVELOPMENT IN THE LOBSTER, HOMARUS-AMERICANUS

Citation
J. Benton et al., SEROTONIN DEPLETION BY 5,7-DIHYDROXYTRYPTAMINE ALTERS DEUTOCEREBRAL DEVELOPMENT IN THE LOBSTER, HOMARUS-AMERICANUS, Journal of neurobiology, 33(4), 1997, pp. 357-373
Citations number
62
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00223034
Volume
33
Issue
4
Year of publication
1997
Pages
357 - 373
Database
ISI
SICI code
0022-3034(1997)33:4<357:SDB5AD>2.0.ZU;2-G
Abstract
The olfactory and accessory lobes constitute prominent histological st ructures within the larval and mature lobster deutocerebrum, and both are associated with a dense innervation from paired serotonergic nerve cells, the dorsal giant neurons (DGNs), During development, the cell bodies of the DGNs are the first central somata to express serotonin ( 5-HT), and the onset of their 5-HT immunoreactivity coincides with the beginning of accessory lobe formation, In contrast, the olfactory lob e anlagen emerge much earlier and grow in the apparent absence of sero tonin, The role of serotonergic input for the development of these bra in structures was investigated in lobster embryos after serotonin had been depleted pharmacologically with the neurotoxin 5,7-dihydroxytrypt amine. A similar to 90% reduction of serotonin was confirmed in eggs u sing high-performance liquid chromatography with electrochemical detec tion. Morphometric analyses suggested that serotonin depletion dramati cally slowed the growth of olfactory and accessory lobes, although glo meruli differentiated at the normal time in both areas. The toxin exhi bited a high degree of specificity for serotonergic neurons and associ ated target regions, and serotonin depletion persisted for at least 2 months following treatment. The goal of future experiments is to deter mine which of the cell types that innervate the olfactory and accessor y lobes are affected by toxin treatment, thereby resulting in the reta rded growth of these areas. (C) 1997 John Wiley & Sons, Inc.