Diazepam attenuates the post-traumatic hyperactivity of excitatory synapses in rat hippocampal CA1 neurons.

The effect of diazepam, a benzodiazepine derivative, on the post-traumatic hyperactivity of excitatory synaptic transmission was examined in rat hippocampal CA1 area. Optical recordings showed that the activity of hippocampal neurons was enhanced in rats treated with fluid percussion injury (FPI) as compared with that of sham-operated rats. The optical response was characterized by fast and slow components. FPI did not affect the fast component that reflects presynaptic action potentials, but enhanced the slow component that reflects excitatory synaptic responses. Intracellular recordings showed that the amplitude and duration of the excitatory postsynaptic potential (EPSP) were increased after FPI. However, FPI did not affect the resting membrane potential and action potentials of hippocampal neurons. Intraperitoneal (i.p.) administration of diazepam (30 and 90 min after FPI) attenuated the post-traumatic hyperactivity of the slow optical response. The slope of input-to-output relation of excitatory synapses was decreased by acute administration of diazepam to FPI rats, but not by delayed administration of diazepam (4 and 5 h after FPI). The fast optical responses were not affected by either FPI or i.p. administration of diazepam. These results suggest that administration of diazepam at early post-traumatic period prevents the FPI-induced delayed enhancement of excitatory synaptic transmission in rat hippocampal CA1 neurons.