Somatostatin Release in the Hippocampus in the Kindling Model of Epilepsy

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Abstract
Somatostatin biosynthesis in the hippocampus is activated during and following kindling epileptogenesis. The aim of this study was to investigate whether this phenomenon is associated with enhanced somatostatin release in vivo. Experiments have been run in awake, freely moving rats, implanted with a bipolar electrode in the right amygdala (for kindling stimulation), and with a recording electrode and a microdialysis probe in the left hippocampus. Basal somatostatin-like immunoreactivity (-LI) release was significantly greater in kindled than naive rats. In naive rats, a 2-min perfusion with 100 mM K+ did not affect behavior and EEG recordings and nonsignificantly increased somatostatin-LI release; a 10-min K+ perfusion evoked numerous wet dog shakes, electrical seizures (class 0; latency ≅8 min, duration ≅8 min), and somatostatin-LI release (≅350% of basal); and a single kindling after-discharge (4 ± 3-s duration in the hippocampus) also evoked somatostatin-LI release (≅200% of basal). In kindled rats, a 2-min 100 mM K+ perfusion evoked hippocampal discharges in three of seven animals (latency ≅2 min, mean duration ≅1.5 min) and increased somatostatin-LI release (≅250% of basal); a 10-min K+ perfusion evoked behavioral seizures (class 1 to 5, latency ≅4 min, mean duration ≅12 min) with numerous wet dog shakes and robust somatostatin-LI release (≅350% of basal); and a kindling stimulation evoked generalized seizures (class 4 or 5, 77 ± 15-s duration in the hippocampus) with remarkable somatostatin-LI release (≅300% of basal). These data demonstrate that hippocampal somatostatin release is increased in the kindling model in vivo.