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Trophic Effect of Thyrotropin‐Releasing Hormone in Murine Ventral Horn Neuronal Cultures a

Thyrotropin-releasing hormone (TRH) has been localized in the ventral horn of mammalian spinal cord. By radioimmunoassay (RIA), the levels of TRH in the ventral horn are among the highest in the nervous system. TRH also induces choline acetyltransferase and creatine kinase in fetal rat ventral horn neuronal cultures. Furthermore, TRH was found to exert a protective effect on neuronal loss following peripheral nerve section especially in infant rats. This study was conducted to determine, in morphometric terms, the effects of TRH in murine ventral horn neuronal cultures. Dissociated fetal murine ventral horn neuronal cultures were established from 12-14-day-old mouse embryos using standard techniques. Nine groups of cultures were treated daily with increasing doses of TRH, achieving final concentrations of lo-'* to 10P4M, respectively. Two other groups were pulsed daily with TRH-OH (pGlu-His-Pro), a major metabolite of TRH in the nervous system, produced by way of the proline endopeptidase pathway, achieving final concentrations of and 10-4M, respectively. One group of cultures received vehicle only, and a final group remained untreated. At 21 days, all 13 groups were fixed and histologically stained with cresyl violet or immunohistochemically stained with an antibody to phosphorylated neurofilamentous protein. Neuronal perikaryal area, maximal diameter, and numbers and lengths of the primary, secondary, and tertiary processes were computed using a Leitz Dialux 22 microscope with camera lucida attachment and a Zeiss Videoplan semiautomatic image analyzer equipped with software, allowing statistical analysis. The results (TABLE 1 ) reveal that TRH treatment causes a statistically significant increase in neuronal perikaryal area and maximal diameter. This morphometric trophic effect follows a sigmoidal curve with a plateau at loP8 to 10P9M, concentrations not too distant from those observed by RIA in the ventral horns. At these same concentrations, TRH causes a statistically significant increase in the numbers of secondary and tertiary processes but not the primary processes (TABLE 2). TRH-OH, the deaminated metabolite, does not have any effect on somal area at similar concentrations. We conclude, therefore, that TRH has a neurotrophic effect on dissociated murine fetal ventral horn neurons in culture in terms of increased somal size and