Distribution of Calbindin-D28K (CaBP) in the cerebral cortex and hippocampus of the epileptic (E1) mouse
β Scribed by I. Mody; K.G. Baimbridge; J.J. Miller
- Publisher
- Elsevier Science
- Year
- 1987
- Tongue
- English
- Weight
- 627 KB
- Volume
- 1
- Category
- Article
- ISSN
- 0920-1211
No coin nor oath required. For personal study only.
β¦ Synopsis
The distribution of Calbindin-D28K (CaBP), a calcium-binding protein that binds Ca2+ with high affinity, was measured by radioimmunoassay in various cortical regions of the epileptic strain of mice El. The El strain, in which seizures are induced by repeated vestibular stimulation, had significantly lower levels of CaBP in the hippocampus and dorsal occipital cortical areas than the control CF-1 strain. Following induction of seizures in the El strain, a further decrease in CaBP levels was observed in the hippocampal formation and ventral temporal cortical regions, areas where paroxysmal activity is generated in this strain. Considering the role of CaBP as an intraneuronal calcium buffer, the present findings indicate that neuronal calcium regulation is genetically altered in the El strain and is further disturbed during the events that lead to induction of seizures.
π SIMILAR VOLUMES
## Abstract Interictal brain energy metabolism and glutamateβglutamine cycling are impaired in epilepsy and may contribute to seizure generation. We used the zeroβflow microdialysis method to measure the extracellular levels of glutamate, glutamine, and the major energy substrates glucose and lacta
Inbred mutant El mice are highly susceptible to convulsive seizures upon 'throwing' stimulation, and the inhibition of 5-hydroxytryptamine (5-HT) and taurine activities appears to be involved in the El mouse seizures. Uptake and release of [3H]5-HT and [3H]taurine into and from cerebral neurocortica
The contribution of the cytosolic calcium binding protein calbindin D 28K (CaBP) to glutamatergic neurotransmission and synaptic plasticity was investigated in hippocampal CA1 area of wild-type and antisense transgenic CaBP-deficient mice, with the use of extracellular recordings in the ex vivo slic