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Biomedical subjects

T G Bolwig

Publications and source records attributed to T G Bolwig.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

Electroconvulsive shock and lidocaine-induced seizures in the rat activate astrocytes as measured by glial fibrillary acidic protein.

The effects of repeated electroconvulsive shock (ECS) and/or lidocaine treatment in the rat were studied by means of biochemical markers: GFAP (glial fibrillary acidic protein), NCAM (neural cell adhesion molecule), NSE (neuron specific enolase) and D3-protein. In adult rats given daily either ECS alone or in combination with lidocaine (experiment 1) we found that ECS significantly increased the concentration of the glial marker GFAP in limbic areas: hippocampus, amygdala, and piriform cortex. The maximal increase in GFAP was found in the piriform cortex (77%). In both piriform cortex and amygdala ECS also induced a significant decrease in D3-protein (a marker of mature synapses), but no change in NCAM (especially enriched in newly formed synapses). In piriform cortex the ratio between NCAM and D3-protein was significantly increased (4%) by ECS. The lidocaine treatment, which induced seizures in some of the animals, was without significant effect on the biochemical markers. However, multiple lidocaine-induced seizures (experiment 2) were found to be associated with a significant increase in GFAP in amygdala and piriform cortex. The study shows that seizures, whether electrically or pharmacologically induced, activate astrocytes in certain brain regions. This activation is especially pronounced in the piriform cortex and may be caused by a particularly marked synaptic vulnerability and remodeling in this area, as demonstrated by the increased NCAM/D3-ratio. Synaptic remodeling and activation of astrocytes may well influence brain function and could play a role in the chain of neurobiological events underlying the clinical effects of electroconvulsive therapy (ECT).

Analysis of Variance↗
PubMedDate not supplied

Long-term effects of repeated electroconvulsive shock on exploratory behaviour and seizure susceptibility to lidocaine in rats.

Electroconvulsive shock (ECS) has anticonvulsant properties while a proconvulsant effect has not, so far, been documented. In the present experiments, we determine whether repeated ECSs lead to an increased seizure susceptibility to lidocaine (lignocaine) in rats. Furthermore, we investigated whether ECS will cause prolonged changes in the locomotion and exploratory activity of the animals. Two groups of rats received 18 ECSs: the first group (ECS-WEEKLY) was given ECS once a week, the second (ECS-DAILY) once a day. A third group (ECS-SHAM) received only sham ECS. Five, as well as 10 weeks after the last ECS, the ECS-WEEKLY group made significantly fewer "hole visits" in an eight hole box than did the ECS-SHAM group. The ECS-DAILY group also made fewer hole visits than the ECS-SHAM group, but the difference was only significant ten weeks after the last ECS. No significant difference in locomotor activity was found. Twelve weeks after the last ECS, all rats received an injection of a high dose of lidocaine (65 mg/kg i.p.). ECS was observed to have a significant effect on the number of animals convulsing in response to the lidocaine challenge. Sixty percent (6/10) of the animals in the ECS-WEEKLY group and 20% (2/10) of those in the ECS-DAILY group convulsed, whereas none of the animals (0/12) in the ECS-SHAM group had convulsions. Thus, the present study shows that ECS may induce prolonged changes in the exploratory behaviour of rats and in their sensitivity to the convulsant effects of lidocaine.

Animals↗
PubMedDate not supplied

Electrical amygdala kindling in alcohol-withdrawal kindled rats.

Repeated alcohol withdrawal has been shown to kindle seizure activity. The purpose of the present investigation was to study electrical amygdala kindling in rats previously exposed to alcohol-withdrawal kindling. In three independent experiments, male Wistar rats were subjected to multiple episodes each consisting of 2 days of severe alcohol intoxication and 5 days of alcohol withdrawal. In the first experiment, the alcohol-withdrawal kindled animals were divided into two groups depending on whether spontaneous alcohol-withdrawal seizures were observed in episodes 10-13. In the second and third experiments, the alcohol-withdrawal kindled animals were compared to a group in which alcohol-withdrawal kindling was prevented by diazepam treatment during the withdrawal reactions in order to discriminate between the effect of withdrawal and intoxication. Electrical kindling was initiated 28-35 days after the last alcohol dose by exposing the animals to daily electrical stimulations of the right amygdala. The results showed that amygdala kindling was facilitated in alcohol-withdrawal kindled animals which showed spontaneous withdrawal seizure activity, compared with animals exposed to multiple episodes of alcohol withdrawal which did not develop withdrawal seizures or with animals exposed to a single episode of alcohol intoxication. When compared to the control group, the alcohol-withdrawal kindled group with seizures also kindled at a faster rate, but the difference did not reach statistical significance and therefore the results must be regarded as preliminary at present.

Alcohol Withdrawal Delirium↗