Electroencephalographic and evoked response correlates of trimethyltin induced neuronal damage in the rat hippocampus
✍ Scribed by D. E. Ray
- Publisher
- John Wiley and Sons
- Year
- 1981
- Tongue
- English
- Weight
- 408 KB
- Volume
- 1
- Category
- Article
- ISSN
- 0260-437X
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Trimethyltin produces localized neuronal damage in the rat hippocampus, amygdala and pyriform cortex when given systemically. In the present study the behavioural, electroencephalographic and auditory evoked responses of conscious rats were followed over an 11 day period after oral administration of trimethyltin. An early increase in hippocampal and, to a lesser extent, neocortical evoked response was seen, this preceding the behavioural symptoms. Development of symptoms (hyperactivity, tremor and fear) was accompanied by an increase in the incidence of theta rhythm in the electroencephalogram (EEG). Finally a fall in hippocampal evoked response and theta incidence was seen. It is suggested that a phase of neuronal excitability precedes neuronal damage, and that this is more pronounced in the hippocampus than in areas not developing subsequent neuronal loss.
📜 SIMILAR VOLUMES
The effects of nitric oxide synthase (NOS) inhibitors, N(omega)-nitro-L-arginine and 7-nitroindazole, and the NOS substrate L-arginine on kainic acid (KA)-induced microglial reactivity and stress response were studied in the hippocampus 7 and 1 days after KA, respectively. Density of peripheral-type
## Abstract Synaptopodin (SP), an actin binding protein associated with the spine apparatus, has been proposed to affect the ability of neurons to undergo synaptic plasticity. In the present study, we compared the density of SP puncta in stratum radiatum of the dorsal hippocampus (DH) with that of
Interleukin-1 beta (IL-1) has been proposed as a mediator of several forms of brain damage, including that induced by excitotoxins. In vitro studies suggest that glial cells are the effector cells of IL-1-mediated neurodegeneration. We have investigated the expression of IL-1 protein by glial cel
While it is well documented that the overactivation of ionotropic glutamate receptors leads to seizures and excitotoxic injury, little is known about the role of metabotropic glutamate receptors (mGluRs) in epileptogenesis and neuronal injury. Intracerebroventricular (i.c.v.) infusion of the group I