If an obstacle impedes the forward swing of a cat's foot, the animal responds by rapidly lifting the foot over the obstacle. In freely moving cats, the electrical activity of hindlimb flexors and extensors was recorded during such reactions elicited both mechanically and electrically. The sequencing of muscle activity was more complex and longer in duration in the mechanically elicited reactions. Anaesthesia of the foot dorsum abolished responses in ankle extensors and knee flexors, and converted the responses of ankle flexors to simple stretch reflexes. Although our findings closely resemble those reported for chronic spinal kittens, there are interesting points of difference, which should be taken into account if the notion of a purely spinal mediation of the placing reaction during stepping is to be accepted.
Reduction of blood flow to the rat retina was achieved by either clamping both carotid arteries briefly (24 min) or combining clamping of the carotid arteries with permanent occlusion of the vertebral arteries. Analysis of retinas 6 days after operations showed that GFAP immunoreactivity is expressed throughout the retinal Miiller cells, although this was variable in retinas from animals where only the carotid arteries were clamped. GFAP immunoreactivity was not associated with retinal Miiller cells from control animals and no obvious neuronal damage was observed in retinas from operated animals. These data suggest that Miiller-cell GFAP expression may be used as an index to follow possible processes leading to an ischemic insult.
The re-expression of the developmentally regulated serine protease inhibitor glia-derived nexin (GDN) was investigated 1 year after transient global ischaemia induced by the four-vessel occlusion technique in rats. The CA1 sector of the hippocampus was severely shrunken due to the absence of pyramidal cells, but still clearly discernible due to the continued presence of the parvalbumin-containing GABAergic neurons. In this partially neuron-depleted hippocampus, GDN immunoreactivity was found in reactive astrocytes containing glial fibrillary acidic protein. GDN-positive astrocytes were also found in other lesioned areas, the reticular thalamic nucleus and the cerebellar cortex. Thus, the re-expression of GDN in the adult excitotoxically lesioned brain described previously in the gerbil model of ischaemia persists. The continued presence of the protease inhibitor might disturb the proteolytic balance and lead to the deposition of pathological breakdown products of proteins, e.g. beta-amyloid.
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