Ultrastructural Changes in the Neuropil of the Anterior Thalamic Nucleus following the Lesion in the Mamillary Body

유두체 손상이 시상전핵 조직상의 미세구조에 미치는 영향

Degeneration of the axon terminals of mamillo-thalamic tract following the electrical coagulation of mamillary body is well known. In this study, the author investigated the ultrastructural alterations of neuropil components, initiated by terminal degenerations. Rats weighing approximately 250 gm were fixed on the stereotaxic instrument(David Kopf Inc., Heavy duty model), and NE 300 active electrode(Rhodes Med. Instr. Inc.) was introduced to the mamillary position of anterior 3.8 mm, lateral 0.5 mm, height 3.8 mm and lateral angle of $23^{\circ}$ according to De Groot's Atlas. Electric current of 20 mA was applied during 1 minute between active and inactive electrodes with Radio Frequency Lesion Generator(RFG 4, Radionics Inc.). Two hours, 2 days, 1 week and 2 weeks following the electrical coagulation of mamillary body, ipsilateral anterior thalamic nucleus was fixed in 1% glutaraldehyde-l% paraformaldehyde and 2% osmium tetroxide, embedded in Araldite mixture, cutted with LKB ultra tome V, stained with uranyl acetate-lead citrate and observed with JEOL 100 CX electron microscope. Observed results were as follows; 1. Degenerated mamillo-thalamic synapses were observed to form asymmetric axospinous or axo-dendritic types. 2. Terminal degeneration was not easily discernible at 2 hours interval after mamillary lesion, but following 2 days the terminal degeneration was apparent. 3. Postsynaptic spines, dendrites and even their cell bodies show edematic changes caused by the degeneration of postsynaptic counterpart. 4. Astrocytic territories, including perivascular processes forming glial limitans of blood-brain barrier, exhibit remarkable expansion. 5. Oligoglia and astroglia are actively engaged in the removal of degenerated elements. 6. Active forms of microglia were increased. 7. The observed results may represent typical ultrastructural alteration pattern within neuropil following the degeneration of certain input axon terminals.