Abstract
Previous immunocytochemical studies have shown a heterogeneous distribution of parvalbumin (PA) and calbindin (CB) in the rat hippocampal formation. The results of the present study showed a heterogeneous distribution of PA and CB in primate Ammon's horn. The density and intensity of immunoreactivity for both of these calcium-binding proteins was greatest in CA2 as compared to CA1 and CA3. CB-immunoreactivity was localized to the cell bodies, dendrites, and axon initial segments of pyramidal cells whereas PA-immunostaining was found in the axon terminals, dendrites and cell bodies of interneurons that have features similar to GABAergic inhibitory neurons. Based on previous studies that have shown a protective role of calcium-binding proteins in neurons exposed to hyperstimulation, these results suggest that the resistance of CA2 pyramidal cells in temporal lobe epilepsy is due to the high concentration of CB and PA in this region of Ammon's horn.
Highlights
In patients suffering from temporal lobe epilepsy a selective pattern of hippocampal cell loss, referred to as "hippocampal sclerosis", is a well documented observation
It was suggested that the seizure-associated brain damage in rats is caused by excessive presynaptic release of excitatory transmitters that induces intracellular postsynaptic changes leading to cell death
Other regions of the primate hippocampal formation were examined to determine the differences between the CA2 subfield and the other hippocampal areas
Summary
In patients suffering from temporal lobe epilepsy a selective pattern of hippocampal cell loss, referred to as "hippocampal sclerosis", is a well documented observation (see review in Babb et al 1984; Bruton 1988; Dam 1982; Sloviter 1983). The major loss of neurons is observed in the CA1 and CA3 subfields of the Ammon's horn and in the hilus of the dentate gyrus. The granule cells, and according to a recent statistical analysis (Kim et al 1990), more than 50% of the CA2, so called "resistant zone" pyramidal cells, are spared. A similar pattern ofhippocampal cell loss was reported for rats by Sloviter. It was suggested that the seizure-associated brain damage in rats is caused by excessive presynaptic release of excitatory transmitters that induces intracellular postsynaptic changes leading to cell death
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