Somatostatin release in the hippocampus in the kindling model of epilepsy:A microdialysis study

Somatostatin biosynthesis in the hippocampus is activated during and follow ing kindling epileptogenesis. The aim of this study was to investigate whet her this phenomenon is associated with enhanced somatostatin release in viv o. Experiments have been run in awake, freely moving rats, implanted with a bipolar electrode in the right amygdala (for kindling stimulation), and wi th a recording electrode and a microdialysis probe in the left hippocampus. Basal somatostatin-like immunoreactivity (-LI) release was significantly g reater in kindled than naive rats. In naive rats, a 2-min perfusion with 10 0 mM K+ did not affect behavior and EEG recordings and nonsignificantly inc reased somatostatin-LI release; a 10-min K+ perfusion evoked numerous wet d og shakes, electrical seizures (class 0; latency congruent to 8 min, durati on congruent to 8 min), and somatostatin-ll release (congruent to 350% of b asal); and a single kindling after-discharge (4 +/- 3-s duration in the hip pocampus) also evoked somatostatin-ll release (congruent to 200% of basal), In kindled rats, a 2-min 100 mM K+ perfusion evoked hippocampal discharges in three of seven animals (latency congruent to 2 min, mean duration congr uent to 1.5 min) and increased somatostatin-LI release (congruent to 250% o f basal); a 10-min K+ perfusion evoked behavioral seizures (class 1 to 5, l atency congruent to 4 min, mean duration congruent to 12 min) with numerous wet dog shakes and robust somatostatin-LI release (congruent to 350% of ba sal); and a kindling stimulation evoked generalized seizures (class 4 or 5, 77 +/- 15-s duration in the hippocampus) with remarkable somatostatin-LI r elease (congruent to 300% of basal). These data demonstrate that hippocampa l somatostatin release is increased in the kindling model in vivo.