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J Neurophysiol 90: 2253-2260, 2003; doi:10.1152/jn.00241.2003
0022-3077/03 $5.00
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Low-Calcium Epileptiform Activity in the Hippocampus In Vivo

Zhouyan Feng and Dominique M. Durand

Neural Engineering Center, Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106

Submitted 13 March 2003; accepted in final form 10 June 2003

It has been clearly established that nonsynaptic interactions are sufficient for generating epileptiform activity in brain slices. However, it is not known whether this type of epilepsy model can be generated in vivo. In this paper we investigate low-calcium nonsynaptic epileptiform activity in an intact hippocampus. The calcium chelator EGTA was used to lower [Ca2+]o in the hippocampus of urethane anesthetized rats. Spontaneous and evoked field potentials in CA1 pyramidal stratum and in CA1 stratum radiatum were recorded using four-channel silicon recording probes. Three different types of epileptic activity were observed while synaptic transmission was gradually blocked by a decline in hippocampal [Ca2+]o. A short latency burst, named early-burst, occurred during the early period of EGTA application. Periodic slow-waves and a long latency high-frequency burst, named late-burst, were seen after synaptic transmission was mostly blocked. Therefore these activities appear to be associated with nonsynaptic mechanisms. Moreover, the slow-waves were similar in appearance to the depolarization potential shifts in vitro with low calcium. In addition, excitatory postsynaptic amino acid antagonists could not eliminate the development of slow-waves and late-bursts. The slow-waves and late-bursts were morphologically similar to electrographic seizure activity seen in patients with temporal lobe epilepsy. These results clearly show that epileptic activity can be generated in vivo in the absence of synaptic transmission. This type of low-calcium nonsynaptic epilepsy model in an intact hippocampus could play an important role in revealing additional mechanisms of epilepsy disorders and in developing novel anti-convulsant drugs.


Address for reprint requests and other correspondence: D. M. Durand, Dept. of Biomedical Engineering, 112 Wickenden Bldg., Case Western Reserve Univ., 10900 Euclid Ave., Cleveland, OH 44106 (E-mail: dxd6{at}po.cwru.edu).




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Z. Feng and D. M. Durand
Decrease in Synaptic Transmission Can Reverse the Propagation Direction of Epileptiform Activity in Hippocampus In Vivo
J Neurophysiol, March 1, 2005; 93(3): 1158 - 1164.
[Abstract] [Full Text] [PDF]




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