Kainic Acid‐Induced Dorsal and Ventral Hippocampal Seizures in Rats

Abstract

PLATFORM AND POSTER SESSIONSintracellular recordings. A Ca2+ spike was elicited by applying a depolarizing pulse (InA, 120ms) in the cell through the recording electrode under a blockadc of Na' and K+ channels using 1 p M tetrodotoxin and I 0mM tctraethylammonium added to the artificial CSF, respectivcly. Nicardipine (I-IOOnM), a Ca2+ channel blocker, was applicd to the bath.Results: Thirty-seven slices from I9 NER and 6 slices from 4 normal Wishr rats were used. There were no obvious changes in the resting membrane potentials of CA3 neurons between NER and Wistar rats tested. When a single stimulus was delivered to the mossy fibers, a long-lasting depolarization shift accompanied by repetitive firings followed by after-hyperpolarization werc also obtained in hippocampal CA3 neurons of young NER (4-5 weeks of age) before occurrence of any seizurcs, although the depolarization shift in younger NER was shorter than that in NER aged more than 6 weeks. These abnormal firings werc evokcd in 58% and 30% of all CA3 neurons tested in the younger and mature NER (6-1 5 weeks of age), respectively. Furthermore, abnormal firing was not elicited in NER aged after I6 weeks. Agc-matched Wistar rats showed only single action potentials without any depolarization shift with single mossy fiber stimulation. Bath application of nicardipine (IOnM) inhibited this long-lasting depolarization shift and the accompanying repetitive firing followed by afterhypcrpolarization without affecting the first spike induced by mossy fiber stimulations. Furthermore, nicai-dipine ( IOnM) inhibited the Ca2' spikes elicited by applying a depolarizing pulse in the neurons of NER with seizures, although a higher dose (100nM) did not affect those in Wistar rats.Conclusions: These findings indicate that abnormal excitability of the NER CA3 pyramidal neurons is probably due to abnormality in the Ca2+ channcls. The abnorinal excitability was observed in NER at an age when tonic-clonic convulsions were not detected, suggesting that thc hippocampus may probably scrve as an epileptogenic focus in younger NER and the seizure impulses originating in this area are transinittcd to the new other seizurc foci in mature NER. Purpose: Though many previous studies dealing with experimental epilepsy have focused on the amygdala and hippocampus, regional differenccs of dorsal and ventral hippocampus are undefined, We investigated thc electrical and behavioral characteristics of seizures after the iiijection of the kainic acid (KA) into left dorsal hippocampus (LdH) or ventral hippocampus (LvH).Methods: Twenty male Wistar rats (250 to 300 g) undcrwent stereotactic operation under pcntobarbital anesthesia. A stainless steel screw was placed in contact with the dura over the left sensorimotor cortex (LCx) with an additional screw placed in the frontal sinus as an indiffcrent elcctrodc. In LdH group (KA microinjection into dorsal hippocampus, n = lo), a stainless steel cannula with an inner needle guide was inserted into the LdH in preparation for microinjection. Bipolar de...

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Model of frequent, recurrent, and spontaneous seizures in the intact mouse hippocampus

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