PubMed · 710015
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R L DeSaussure. 1978. Causalgia.. https://doi.org/10.1093/neurosurgery%2F25.cn_suppl_1.626
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We examined monoamine oxidase (MAO) activity in the intermediolateral nucleus (IML) of the rat thoracic spinal cord by histochemistry with tyramine as a common substrate for both MAO types A and B. Light microscopy showed MAO activity in neuronal cell bodies, processes, and varicosities. Electron microscopic examination showed both MAO-positive and -negative neuronal cell bodies. In the stained cell bodies, histochemical reaction products were localized in the cytoplasm showing a selective association with mitochondrial outer membranes. MAO-positive axon terminals were often found in contact with MAO-negative neurons but only occasionally with MAO-positive neurons. MAO histochemistry in the IML was also performed using serotonin (a MAO type A preferential substrate) and beta-phenylethylamine (a MAO type B preferential substrate). Light microscopy identified MAO activity for serotonin in a plexus of varicosities but not in any neuronal cell bodies. The activity for beta-phenylethylamine was detected frequently in neuronal cell bodies but rarely in varicosities. Our findings indicate that two groups of IML neurons can be chemically distinguished, one contains MAO type B while the other lacks both MAO types A and B. In addition, many axon terminals contain MAO type A but only a few fibers include MAO type B in the IML.
Sympathetic noradrenergic (NA) neuronal activities in the thymus, spleen and mesenteric lymph nodes (MLN) and immune responses in the spleen were examined in young male F344 rats treated daily with 0, 0.25 mg, or 2.5 mg/kg body weight of L-deprenyl, an irreversible monoamine oxidase-B (MAO-B) inhibitor. Rats were treated daily for 1, 15, or 30 days, and sacrificed 7 days after the last deprenyl treatment. Deprenyl treatment increased norepinephrine (NE) content in the spleen without modifying the pattern and density of NA innervation in the splenic white pulp. The concentration of NE was unaltered in the thymus, but it was increased in the MLN of deprenyl-treated rats. One day of treatment with deprenyl decreased splenic NK cell activity while 15 days of deprenyl treatment enhanced splenic NK cell activity. Deprenyl elevated Con A-induced T lymphocyte proliferation following 30 days of treatment, but did not alter spleen cell Con A-induced IL-2 production or the percentage of CD5 + T cells in the spleen. A moderate decrease in the percentage of sIgM + B cells was observed in the spleens of 15- and 30-day deprenyl-treated rats. These results suggest that deprenyl has sympathomimetic action on sympathetic NA nerve fibers in the spleen; the enhancement of NA neuronal activity may contribute to the modulation of immune responses in the spleen.
Nigrostriatal dopaminergic neurons undergo sprouting around the margins of a striatal wound. The mechanism of this periwound sprouting has been unclear. In this study, we have examined the role played by the macrophage and microglial response that follows striatal injury. Macrophages and activated microglia quickly accumulate after injury and reach their greatest numbers in the first week. Subsequently, the number of both cell types declines rapidly in the first month and thereafter more slowly. Macrophage numbers eventually cease to decline, and a sizable group of these cells remains at the wound site and forms a long-term, highly activated resident population. This population of macrophages expresses increasing amounts of glial cell line-derived neurotrophic factor mRNA with time. Brain-derived neurotrophic factor mRNA is also expressed in and around the wound site. Production of this factor is by both activated microglia and, to a lesser extent, macrophages. The production of these potent dopaminergic neurotrophic factors occurs in a similar spatial distribution to sprouting dopaminergic fibers. Moreover, dopamine transporter-positive dopaminergic neurites can be seen growing toward and embracing hemosiderin-filled wound macrophages. The dopaminergic sprouting that accompanies striatal injury thus appears to result from neurotrophic factor secretion by activated macrophages and microglia at the wound site.