Hippocampal corticosterone receptors and novelty-induced behavioral activity: effect of kainic acid lesion in the hippocampus.

Rats were injected bilaterally in the dorsal and ventral hippocampus with kainic acid (KA) or with artificial CSF and their behavior and brain corticosterone (B) receptor systems were studied. The hippocampal KA injection destroyed part of the pyramidal neurons and of the dentate gyrus neurons. These neurons contain a receptor system for B. At 2 weeks after the KA lesion this B receptor system displays an increase in apparent maximal binding capacity (Bmax) of approximately 25%. The compensatory increase in B receptor concentration is reflected in an increased uptake of [3H]B in cell nuclei of hippocampal slices incubated in vitro with saturating concentrations of the steroid. Administration of a tracer dose of [3H]B shows that labelled steroid can enter in vivo the cell nuclear compartment of the KA-lesioned lobe. The role of B was investigated on novelty-induced behavioral activities of KA-lesioned and sham-lesioned animals in a large open and a small closed field at 10 days after bilateral adrenalectomy (ADX) or sham-ADX which is 14 days after the (sham) lesion. B (300 micrograms/kg rat) was administered s.c. 1 h prior to the test. KA lesion resulted in an increase in exploratory activity and a reduction in grooming and immobility. After ADX the effect of KA on exploration was reduced in the 5 min open field and abolished in the 30 min closed field. ADX animals displayed more grooming behavior (closed-field). B replacement of ADX rats reinstated the exploratory hyperactivity of KA-lesioned rats. On some components of the behavior such as ambulation in open-field and locomotion in closed field, there was even a larger responsiveness to B in the KA-lesioned rats than in the control animals. It is concluded that (1) after KA lesion of receptor containing neurons, the remaining tissue displays a compensatory increase in number of B receptor sites; (2) B is required for full expression of exploratory activity of rats with or without KA lesions; (3) the KA-lesioned rats display a larger responsiveness to B; and (4) the increased number of B receptor sites may underlie the larger responsiveness to B.