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T Bolwig

Publications and source records attributed to T Bolwig.

5 recordsLinked to original sources
PubMed1994

Transient decrease in calbindin immunoreactivity of the rat fascia dentata granule cells after repeated electroconvulsive shocks.

Changes in hippocampal calbindin immunoreactivity were investigated after repeated electroconvulsive shocks. Adult rats were subjected to 10, 20, or 36 electroconvulsive shocks (50 mA, 0.5 seconds), given as on shock per day, 5 days a week. The rats were sacrificed and processed for calbindin immunohistochemistry 1, 2, and 30 days after the last electroconvulsive shock. In the rats receiving 10 or 20 electroconvulsive shocks, a selective reduction of the calbindin immunoreactivity of the dentate granule cell bodies, dendrites, and mossy fibers was noted 1 and 2 days after the last electroconvulsive shock. After 36 electroconvulsive shocks there was an almost complete loss of calbindin immunoreactivity from the granule cell bodies and dendrites, and the calbindin immunoreactivity of the mossy fibers was markedly reduced. Thirty days after the last of 36 electroconvulsive shocks, the calbindin immunoreactivity was back to normal. Besides demonstrating pronounced changes associated with repeated electroconvulsive shocks, the results confirm the transient nature of these changes.

Animals↗
PubMed1990

Increased somatostatin and enkephalin-like immunoreactivity in the rat hippocampus following hippocampal kindling.

As neuropeptides may play a role in the electrical kindling model of epileptogenesis, hippocampal somatostatin, Met-enkephalin and cholecystokinin were studied by immunocytochemistry in rats 24 h following full hippocampal kindling (three stage 5 seizures). As control animals we used sham-kindled rats, unoperated rats and rats subjected to a single electroshock-induced seizure. In addition, the distribution of septohippocampal, cholinergic fibers and hippocampal mossy fibers were studied by histochemistry. The important finding was that after kindling there was, as compared to unoperated control, (1) a marked increase of somatostatin immunoreactivity in cell bodies in the dentate hilus and their presumed projections area in the outer parts of the dentate molecular layer, and (2) a marked increase of Met-enkephalin immunoreactivity in hippocampal mossy fiber terminals. We found no evidence of aberrant sprouting of mossy fiber collaterals in the fascia dentata.

Acetylcholinesterase↗
PubMed1984

Does seizure activity produce Purkinje cell loss?

Eight Wistar rats were exposed to 140 electroconvulsive seizures over 50 days. Ten rats served as controls. The density of Purkinje cells in cerebellum ranged from 15.3 to 18.5/mm in the treated rats and from 15.2 to 19.1/mm in the controls. No Purkinje cell loss was disclosed in the rats subjected to electroconvulsive seizures. Twenty-five Mongolian gerbils of the seizure-susceptible strain were selected according to seizure score with five animals in each group. Five Mongolian gerbils of a seizure-resistant strain served as controls. The density of the Purkinje cells ranged from 21.4 to 29.8/mm in the seizure-susceptible animals and from 27.6 to 31.5/mm in the controls, with a lower density in the gerbils with seizures compared with the controls (p less than 0.05). There was no relation to type or number of seizures. Eight gerbils of the seizure-susceptible strain were included as a supplementary group, to disclose any possible genetic trait as an explanation of the lower Purkinje cell density. The Purkinje cell density in these animals ranged from 24.8 to 30.9/mm and did not differ from the density in the seizure-resistant gerbils. Thus the lower density of Purkinje cells in the seizure-susceptible Mongolian gerbils is a result of seizure activity. The excessive epileptic input with stimulation of the glutamatergic innervation of the Purkinje cells resulting in a persistent elevated gamma-aminobutyric acid (GABA) tone may explain the damage to the Purkinje cells in the gerbils and the loss of Purkinje cells found in patients with severe epilepsy.

Animals↗