Effects of serotonin depletion on local interneurons in the developing olfactory pathway of lobsters.
During embryonic life, the growth of the olfactory and accessory lobes of the lobster brain is retarded by serotonin depletion using 5,7-dihydroxytryptamine (5,7-DHT) (Benton et al., 1997). The local and projection interneurons that synapse with chemosensory cells in the olfactory lobes are potential targets of this depletion. This study documents proliferation and survival in the local interneuron cell clusters, and examines the differentiation of a prominent local interneuron, the serotonergic dorsal giant neuron (DGN), following serotonin depletion. An increase in dye coupling between the DGN and nearby cells is seen after serotonin depletion. However, morphometric analyses of individual DGNs in normal, sham-injected, and 5,7-DHT-treated embryos show that the general morphology and size of the DGNs are not significantly altered by serotonin depletion. Thus, the DGN axonal arbor occupies a greater proportion of the reduced olfactory lobes in the 5,7-DHT-treated embryos than in normal and sham-injected groups. The paired olfactory globular tract neutrophils (OGTNs), where olfactory interneurons synapse onto the DGNs, are 75% smaller in volume than the comparable region in either sham-injected or normal embryos. In vivo experiments using bromodeoxyuridine (BrdU) show that proliferation in the local interneuron soma clusters is reduced by 5,7-DHT treatment and that survival of newly proliferated local interneurons is also compromised. Our data suggest that alterations in the growth of the DGNs do not contribute to the dramatic reduction in size of the olfactory neutrophils following serotonin depletion, but that cell proliferation and survival among the local interneurons are regulated by serotonin during development. Reduced numbers of local interneurons are therefore one likely reason for the growth reduction observed after serotonin depletion.
Benton
J
J
Department of Biological Sciences, Wellesley College, Wellesley, Massachusetts 02481, USA. jbenton@wellesley.edu
Beltz
B
B
D015116:5,7-Dihydroxytryptamine / Q000494:pharmacology; D000818:Animals; D001710:Biotin / Q000031:analogs & derivatives* / Q000494:pharmacology; D001973:Bromodeoxyuridine / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects / Q000502:physiology*; D048429:Cell Size / Q000187:drug effects / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology*; D004625:Embryo, Nonmammalian / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D007395:Interneurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008121:Nephropidae / Q000166:cytology / Q000196:embryology* / Q000378:metabolism; D009833:Olfactory Pathways / Q000166:cytology / Q000196:embryology* / Q000378:metabolism; D012701:Serotonin / Q000172:deficiency*; D016704:Synapsins / Q000378:metabolism
D016704:Synapsins; C070614:neurobiotin; D015116:5,7-Dihydroxytryptamine; D012701:Serotonin; D001710:Biotin; D001973:Bromodeoxyuridine