Abstract

The distribution and synaptic organization of GABAergic elements in the mammillary nuclei of rats have been examined by the immunocytochemical localization of GABA at the light and electron microscope levels. The distribution of GABA-immunoreactive fibres and terminals in the mammillary body is non-homogeneous. By light microscopy, small scattered immunoreactive terminals are observed in the pars medianus, pars posterior and ventral region of the pars medialis of the medial mammillary nucleus. Larger labelled terminals are found in the pars lateralis, the dorsal region of the pars medialis of the medial mammillary nucleus and the lateral mammillary nucleus. At the ultrastructural level, GABA-immunoreactive synaptic endings in the different subdivisions of the medial mammillary nucleus exhibit a widespread somadendritic distribution. By contrast, GABA-immunoreactive terminals within the lateral mammillary nucleus are located predominantly in the neuropil and less frequently on neuronal somata. GABA-immunoreactive synaptic endings contain pleiomorphic synaptic vesicles and have symmetrical synaptic contact zones with the somata and dendrites in the lateral and medial mammillary nuclei. After in vivo inhibition of GABA metabolism with amino-oxyacetic acid, light microscopic examination of the mammillary nuclei reveals numerous small GABA-immunoreactive cells in various subdivisions of the medial mammillary nucleus. No immunoreactive cells are observed, however, in the lateral mammillary nucleus. Electron microscopic examination demonstrates that the GABA-immunoreactive cells are astrocytes. In the labelled astrocytes, immunohistochemical reaction product is localized throughout the nucleus and cytoplasm of the cells, in thin sheet-like processes surrounding neuronal elements and in end-feet lining the basal lamina of capillaries. The results indicate that the mammillary nuclei in the rat receive a strong GABAergic innervation. Most if not all, of the GABA-immunoreactive synaptic endings in the mammillary nuclei probably arise from extrinsic inhibitory sources. The possible sources of the GABA-immunoreactive input to the mammillary complex are discussed.

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