Details

Autor(en) / Beteiligte

• Arismendi-Morillo, G J
• Castejón, O J
• Castellano-Ramírez, A

Titel

Ultrastructural features of the synaptic plasticity in peritumoral cerebral oedema in humans

Ist Teil von

• Revista de neurologiá, 2007-11, Vol.45 (10), p.587-593

Ort / Verlag

Spain

Erscheinungsjahr

2007

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• To provide an ultrastructural characterisation of the synaptic plasticity phenomena in peritumoral brain tissue in humans. Sixteen peritumoral tissue biopsy samples were processed using conventional transmission electron microscope techniques. Clinical data and post-surgical follow-up were reviewed and analysed. In the peritumoral brain tissue there was a predominance of cellular or oncotic cerebral oedema. A large number of synapses were seen to be perforated with both convex and, although less frequently, irregular curvatures. Generally, the presynaptic terminals had an oedematous appearance, with oedematous mitochondria with cristolysis and electron-dense deposits in the mitochondrial matrix. The presynaptic terminals showed numerous synaptic vesicles of different sizes and which were sometimes arranged in small accumulations. Observations also confirmed the presence of endocytosis vesicles, which suggest high neurotransmitter reuptake. Some presynaptic terminals displayed degenerative changes. The postsynaptic terminals were seen to be oedematous and the dendritic spines displayed different shapes and spiny processes that were degenerated to varying degrees. Perisynaptic astrocytic prolongations were seen to be oedematous, with a variable number of glycogen granules. We propose a possible sequence of structural changes in the process of forming perforated synapses in peritumoral brain tissue. The ultrastructural findings observed in the synapses and their microenvironment can be considered to be significant with respect to the clinical manifestations and the sequelae in the patients who were studied. Moreover, they are linked to functional alterations in injured tissue, degenerative changes and neuronal death.