Effect of early and late postnatal hypoxia on subcellular synaptosomal fractions from cerebral cortex of rats. I. An electron-microscopical and biochemical study.
Synaptosomal fractions of brain cortex of rats exposed to moderate intermittent hypobaric hypoxic conditions during the first or second decade of the postnatal life were investigated electron microscopically one day or up to one week after the hypoxia experiment. Mitochondria and synaptosomes with impaired morphology were observed to occur more frequently in fractions obtained from hypoxic animals. Synaptosomes showed lesions of the outer membrane and loss of the synaptoplasmatic content, or condensation of the synaptosomal content with increasing electron density, deformation of the synaptosomes in size and shape, disappearance of structural details, degeneration of intrasynaptosomal mitochondria in form of strong condensation and, finally, formation of intrasynaptosomal vacuoles with dense core inclusions. The mitochondrial reaction was characterized by two antagonistic configurations: condensation of the matrix with secondary enlargement of the intracistal spaces and of the outer compartment and, finally, the decay of the matrix condensate in several crumbs. On the other hand, swelling of the matrix with strong enlargement of the whole mitochondrium, later defects in the outer membrane and the degeneration into empty mitochondrial ghosts, appearing in the upper fractions. Some characteristic marker enzymes were tested in the fractions. The results hint at an elevated vulnerability of synaptosomes obtained from animals exposed to postnatal hypoxia, as indicated by the lowered quotient of LDH activities after and before addition of Triton X-100. Furthermore, there are clues to a decrease in the number of synaptic connections within the cortex of hypoxia exposed animals, as is concluded from the diminished AChE activity in the subcellular fractions of these animals. However, no different effect of early or late postnatal hypoxia exposition was evident in the biochemical parameters.
D000110:Acetylcholinesterase / Q000378:metabolism; D000367:Age Factors; D000818:Animals; D002540:Cerebral Cortex / Q000473:pathology*; D003712:Dendrites / Q000648:ultrastructure; D002534:Hypoxia, Brain / Q000473:pathology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008854:Microscopy, Electron; D008928:Mitochondria / Q000648:ultrastructure; D009186:Myelin Sheath / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D013347:Subcellular Fractions / Q000648:ultrastructure; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013570:Synaptic Membranes / Q000648:ultrastructure; D013574:Synaptosomes / Q000648:ultrastructure*
D007770:L-Lactate Dehydrogenase; D013385:Succinate Dehydrogenase; D000110:Acetylcholinesterase