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At least 1,477 records · Page 82Linked to original sources
PubMed1984

Effects of the cholinotoxin, AF64A, on neuronal trace-metal distribution in the rat hippocampus and neocortex.

Ethylcholine mustard aziridinium ion (AF64A) is a neurotoxin which is specific for cholinergic nerve terminals. Besides its effects on elements of the acetylcholine system, we observed that, after 2 and 8 days, a single 20-nmol intracerebroventricular dose altered the Timm's staining of certain regions of the central nervous system and reduced the tissue levels of trace metals. In the hippocampal formation, there was a considerable decrease in the staining of the neuropil of the stratum radiatum and stratum oriens, which contain cholinergic nerve terminals. A reduction in staining was also demonstrated in the perikarya of cortical pyramidal cells. The diminished trace-metal level in both regions was confirmed by quantitative measurements of zinc and copper levels. A similar reduction was not observed at a lower dose (8 nmol) of the cholinotoxin. The results led to the conclusion that AF64A may cause the decrease of the trace-metal content of the postsynaptic neurons through an indirect mechanism.

Animals↗
PubMed1977

Occurrence of dark neurons in living mechanically injured rat neocortex.

In order to ascertain the immediate histopathological changes of rat brain following experimental surgical injury, fragments of left parietal cortex were obtained through craniotomy and fixed by immersion. Next, the animals were killed by perfusion with the same fixative used for the respective biopsy. Five groups of rats were tested, each for one different fixative. Dark neurons were by far the most prominent feature in surgically traumatized tissue, following both immersion and perfusion with all five fluids. They were morphologically identical at both sites, and fixatives with widely different chemical composition, e.g. Bouin's fluid and buffered glutaraldehyde, had no influence on their aspect. It is suggested that shrunken neurons are not to be interpreted systematically as artefacts, but also represent a form of short-latency cellular reaction to injury.

Animals↗
PubMed1987

Ultrastructural abnormalities in the cerebral neocortex and hippocampus associated with Alzheimer's disease and aging.

Lesions of the frontal and temporal neocortices and hippocampus typically found in Alzheimer's disease were looked for with the electron microscope in 119 autopsy cases whose ages ranged from 24-93 years. By light microscopy 11 of the cases over the age of 60 had large numbers of plaques and neurofibrillary tangles, whereas the remaining cases had few or none. From the age frequency distribution of the electron microscopic lesions in these two categories of cases amyloid fibrils and abnormal neurites, both components of plaques, were first seen at approximately the same time. This suggests that amyloid is unlikely to precede the neurites in their formation. The abnormal neurites were thought, due to the small numbers of synapses in their walls, to be largely derived from degenerating neuronal processes and not synaptic boutons.

Adult↗
PubMed1983

Neuropathological alterations in the neocortex of rats subjected to focal aminopyridine seizures.

Acute focal seizures were produced in anaesthetized albino rats by topical application of 3- and 4-aminopyridine on the exposed fronto-parietal neocortical areas. After 15 min of seizure activity neuronal and glial changes were studied by light (toluidine blue and Golgi staining) and electron microscopy. Shrinkage and increased electron density of some pyramidal cells, astrocytic swelling and depletion of 40-60 nm synaptic vesicles from the nerve terminals in layers I, II and III were found. The possible significance of the alterations in the seizure is discussed.

Aminopyridines↗
PubMed1979

Postnatal vascular growth in the neocortex of normal and protein-deprived rats. Morphometric studies.

The postnatal vascular growth in the neocortical area 18 of normal and pre- and postnatally protein-deprived rats was examined. For control rats the specific length, the specific surface and the volume fraction of vessels increased rapidly between 7 and 20 days of age. Thereafter, only a minor increase was seen. In protein-deprived rats there was no increase in the specific length of vessels between 7 and 10 days of age and this variable was still reduced at 30 days of age compared to controls. This reduction was due to a decrease in the specific length of thin vessels (luminal diameter less than 8.25 mu) whereas the specific length of wider vessels was not affected by the protein deprivation. There were no significant differences in the specific surface or volume fraction of vessels between control and protein-deprived rats. These findings indicate an adaptive increase in luminal diameter of vessels in the protein deprived rats during postnatal development. At 90 days of age no significant differences between vascular variables of control and protein-deprived rats were seen.

Age Factors↗
PubMed1992

Glutamate decarboxylase in developing rat neocortex: does it correlate with the differentiation of GABAergic neurons and synapses?

Postnatal development of glutamate decarboxylase was studied in the rat cerebral cortex. Two methods were used: estimation of the enzymatic activity of glutamate decarboxylase in homogenates of developing cortical tissue and visualization of structures containing glutamate decarboxylase-like immunoreactivity. Glutamate decarboxylase-like immunoreactivity appeared first in perikarya and dendrites and only later in axons and axon varicosities. The most rapid increase in the glutamate decarboxylase activity took place during the second postnatal week and this coincided with a rapid increase in the density of axon varicosities containing glutamate decarboxylase-like immunoreactivity but preceded the most rapid phase in the formation of GABAergic synapses by several days. However, there was a change in the characteristics of glutamate decarboxylase which correlated with GABA synaptogenesis: two fractions of glutamate decarboxylase with different sensitivities to the activating effects of Triton X-100 could be distinguished as from about the time when most of the GABAergic synapses are formed.

Animals↗
PubMed1994

Transmitter amino acid release from rat neocortex: complete versus incomplete ischemia models.

Release of the excitotoxic amino acids, glutamate and aspartate, from the ischemic rat cerebral cortex was compared in two models; the seven vessel occlusion model (7VO) of complete cerebral ischemia and the four vessel occlusion model (4VO) of incomplete cerebral ischemia. Amino acid efflux into cortical superfusates was measured using cortical cups placed on both hemispheres. Whereas a 20 min period of ischemia causes a pronounced release of glutamate and aspartate from the 4VO model, efflux was significantly reduced in the 7VO model. Release of the inhibitory transmitter GABA, was similar in the two models. This result suggests that excitotoxic amino acid efflux into the extracellular spaces of the cerebral cortex may be enhanced by the residual blood flow in an incomplete ischemia.

Animals↗