Retrograde axonal transport following injection of [ 3H]-serotonin into the olfactory bulb. II. Radioautographic study

Abstract

Radioautography was used to study the intraneuronal distribution of [ 3H]-serotonin (5-HT) and/or its derivatives selectively taken up by the olfactory bulb (OB) serotonergic terminals and subsequently transported to their parent cell bodies in the midbrain raphe nuclei. This was done 24 h after injection of [ 3H]5-HT into the main OB of rats either pretreated or not with monoamine oxidase (MAO) inhibitor. A prior mechanical obstruction of the rostral ventricular cavities prevented diffusion of the tracer towards cerebrospinal fluid. Heavily labelled nerve cell bodies were found mainly in the ipsilateral raphe dorsalis nucleus (RDN) and to a lesser extent in the raphe centralis nucleus. The radio-autographic reaction often extended to dendritic processes while sparing the nucleus. A diffuse reaction was also observed but limited to the raphe area. The supraependymal 5-HT fibers were found to be free of labelling. Neither local destruction of catecholaminergic terminals with 6-OHDA, nor absence of MAO inhibition, impaired this radioautographic pattern, while destruction of serotonergic terminals with 5,6-dihydroxytryptamine in OB resulted in the disappearance of labelled axonal varicosities and neurons in the OB and the RDN respectively. At the electron microscope level, labelled cell bodies in the RDN were medium-sized (12–15 μm). Silver grains were localized mainly on mitochondria and, to a lesser extent, on lysosomes and endoplasmic reticulum but spared the nucleus and the nucleolus. Silver grains were also found near the nuclear membran and outside the neuronal membrane. The observation of heavy metal impregnated thich sections confirmed the preferential localization of silver grains on mitochondria with or without inhibition of MAO. These resuls could account for the subcellular compartments involved in the retrograde axonal transport of [ 3H]-5-HT and its subsequent degradation and/or dendritic release.