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Prenatal Protein Malnutrition in Rats Enhances Serotonin Release from Hippocampus¹

Jin-Chung Chen, John Tonkiss^*, Janina R. Galler^* and Ladislav Volicer

Department of Pharmacology, University of Massachusetts Medical School, Worcester, MA 91655 ^* Center for Behavioral Development and Mental Retardation Department of Pharmacology, Boston University Medical Center, Boston, MA 02118

The effect of prenatal protein malnutrition on central serotonin metabolism was assessed in 220- to 240-d-old male rats. The malnourished rats (denoted 6,25 group) were males born to dams fed a 6% casein diet during pregnancy and fostered at birth to dams fed a control (25% casein) diet. They were compared with males born to dams fed 25% casein diet. Tissue concentrations of serotonin, 5-hydroxyindoleacetic acid, 5-hydroxytryptophan, L-tryptophan and catecholamines in the hippocampal formation in the 6,25 group were similar to those of well-fed controls (25,25 group). However, a twofold greater basal serotonin efflux from hippocampal slices of 6,25 rats compared with slices from 25,25 rats was observed during a 20-min incubation period. Hippocampal [³H]paroxetine binding indicated that there was no alteration of apparent maximal binding and affinity of the serotonin transporter in the 6,25 rats. In addition, there was no difference in serotonin receptor binding in hippocampal membranes from 6,25 and 25,25 rats. The results indicate that prenatal protein malnutrition causes selective changes in central serotonin metabolism.

KEY WORDS: • protein malnutrition • serotonin • hippocampal formation • rats

¹ Supported by University Hospital BRS grant to J.-C.C. and J.R.G., by U.S. Public Health Service grant NICHD PO1-HD22539 and by the U.S. Department of Veterans Affairs.

Manuscript received 27 May 1992. Revision accepted 9 July 1992.