Fig. 4.

Hippocampal electrophysiological activation and up-regulation of CRH mRNA expression are abolished by barbiturate pre-administration. (A) Representative EEG recordings obtained via bipolar depth electrodes from the hippocampi of immature rats. Top left: the baseline theta-frequency, low-amplitude hippocampal EEG activity. The arrow shows a movement artifact. Top right: hyperthermia induced repetitive high-amplitude semi-rhythmic discharges (arrowheads), typical of electrographic seizures involving the hippocampus. The animal was motionless during these events. Pentobarbital (Pentobarb; 30 mg/kg, i.p.), given immediately prior to the onset of hyperthermia, altered the baseline activity by eliminating the theta rhythm and decreasing the EEG amplitude (left, bottom tracing). Importantly, when pentobarbital-treated animals were subjected to hyperthermia, electrographic seizures were not observed on the hippocampal EEG (right, bottom tracing), and no behavioral seizures occurred. Vertical scale: 50 μV; horizontal: 1 s. (B) Semi-quantitative analysis showing the effects of hyperthermia and barbiturates (pentobarbital, Pb) on CRH mRNA levels in the hippocampus. Bars represent CRH mRNA hybridization signal over the hippocampal formation (combined CA1, CA3 and DG) 8.5 h after hyperthermia alone or with pentobarbital pretreatment. Hyperthermia resulted in a significant increase relative to both the control and the pentobarbital-treated rats. *P < 0.05 (Student’s t-test), comparing hyperthermics to the laboratory controls and the hyperthermic (pentobarbital-treated) controls. Hippocampal CRH mRNA levels of animals injected with pentobarbital alone did not differ significantly from those who received an i.p. injection of vehicle (88 ± 5.5%; P = 0.52, Student’s t-test). Samples are the mean ± S.E.M. of a total of 30 matched sections from at least three animals per group.