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The prenatal development of the serotonin transporter was analyzed in mouse brain and spinal cord by autoradiographic localization of [3H]citalopram binding. Transporter expression started at embryonic day (E) 12 in two discontinuous bands in the anterior and posterior brainstem. Labeling extended cranially and caudally, reaching the basal diencephalon at E 13, the septal complex at E 15, and the cerebral cortex at E 16. The caudal extension of the labeling descended at the ventrolateral margin of the spinal cord and reached lumbar levels at E 14. At E 17-E 18, [3H]citalopram binding emerged in the striatum, amygdaloid area, ventrobasal thalamus, paraventricular and periventricular hypothalamic nuclei, and substantia nigra. The overall spatiotemporal expression pattern of the serotonin transporter in the mouse agrees with data on the immunohistochemical localization of serotonin in the rat embryo. These results suggest that serotonergic fibers have the equipment to engage in transmitter reuptake long before synapse formation, and that transporter expression might represent a prerequesite for the developmental functions exerted by serotonin.

Nitric oxide (NO) is generated intracellularly from L-arginine by the action of the enzyme nitric oxide synthase (NOS). The present investigation demonstrates immunoreactivity against NOS and nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity in nerve cells and fibers of the reproductive system of the female mouse. The density of nerve fibers staining for NOS varied among different genital organs. The ovary and Fallopian tube were devoid of NOS-positive nerves. The uterine horns received sparse innervation by NOS-containing nerve fibers. The most abundant NOergic innervation was found in the uterine cervix and vagina, where the nerve fibers ran parallel to the smooth muscle bundles and beneath the epithelium; they also accompanied intramural blood vessels. The vaginal muscular wall contained single or groups of NOS-reactive nerve cells. Clusters of NOS-containing neurons were located in Frankenhäuser's ganglion at the cervico-vaginal junction. NO may therefore act as a transmitter in the nervous control of the female reproductive tract.

14C-5,6-DHT-Melanin was injected into the left lateral ventricle of adult rats and its fate followed by light and EM autoradiography and by TEM of structures identified as labeled in preceding light micrographs. Shortly after injection, melanin particles were seen ingested by supraependymal and epiplexus cells, by cells residing in the pia-arachnoid, i.e. free subarachnoidal cells and perivascular cells, and by subependymally located microglia-like cells with intraventricular processes. Up to day four, an increase in the number of labelled phagocytes in the CSF was noted which transformed into typical reactive macrophages. After this time, many intraventricular melanin-laden phagocytes formed rounded clusters; cells of such clusters were subsequently found to invade the brain parenchyma by penetrating the ependymal lining and to accumulate in the perivascular space of brain vessels. 14C-Melanin-storing macrophages were found in the marginal sinus of the deep jugular lymph nodes suggesting emigration of CNS-derived phagocytes via lymphatics or pre-lymphatics that contact the subarachnoidal space compartment. This does not exclude the possibility that some of the macrophages leave the brain via the systemic circulation by penetrating the vascular endothelium; these may be disposed of in peripheral organs other than the lymph nodes. The ability of supraependymal, epiplexus, free subarachnoidal and perivascular cells in the pia and of subependymal microglia cells to accumulate synthetic melanin by phagocytosis suggests that these cells are local variants of the same type of resting potential phagocytes of the mammalian brain. The present study shows that 14C-5,6-DHT-melanin is an ideal phagocytic stimulant and marker for phagocytosis.