48 Neuroscience Letters, 112 (1990) 48-53 Elsevier Scientific Publishers Ireland Ltd. NSL 06805 Epileptic activity following 10 minute cerebral ischemia in Mongolian gerbils: an electrophysiological study M. Grazia Marciani, Giancarlo Santone, Giuseppe Sancesario, Roberto Massa, Paolo Stanzione and Giorgio Bernardi Clinica Neurologica, Dipartimento di Sanitgt Pubblica, H Universit?l di Roma, Rome (Italy) (Received 29 August 1989; Revised version received 2 January 1990; Accepted 3 January 1990) Key words: Gerbil; Cerebral ischemia; Epileptic activity; CA 1 hippocampal neuron The effects of bilateral carotid occlusion (BCO) on electroencephalographic (EEG) activity and hippo- campal structural integrity was studied in 25 Mongolian gerbils. During BCO EEG became fiat in frontal cortex and hippocampus but bilateral spikes and motor signs were recorded during this period. Following release of clamping EEG gradually recovered within 36 h but interictal activity persisted disappearing on the 6th 7th day. At the end of 7 days a selective necrosis of CA1 hippocampal neurons was observed. The results indicate that 10 min cerebral ischemia induces a transient epileptic activity followed by the CAI neuronal loss. Mechanisms underlying ischemic damage are complex and probably they involve an altered synaptic transmission. The Mongolian gerbil (M.g.) is a very useful model for studying cerebrovascular disease because the Circle of Willis is incomplete [13] and therefore brain damage can easily be induced by clamping both carotid arteries. The hippocampus, in human as well as in experimental studies, is a structure which responds in a unique manner to cerebrovascular insult [12]. Of all pyramidal neurons, CA1 cells are most vulnerable to ischemia as already demonstrated by several bio- chemical and morphological studies [1, 4, 11, 20, 21]. Previous reports in M.g. evidenced that convulsive activity following acute bilat- eral carotid occlusion is of extracerebral origin [3]. More recently it has been demon- strated that 5 min cerebral ischemia induced abnormal hippocampal neuronal hyper- activity leading to a functional and morphological cellular death [20, 21]. In order to clarify the effects of cerebral ischemia on neuronal activity a longitudi- nal study of electroencephalographic (EEG) changes in hippocampal and cortical re- gions following 10 min bilateral carotid occlusion (BCO) was performed. Correspondence." M.G. Marciani, Clinica Neurologica, Dipartimento di Sanit~i Pubblica, II Universith di Roma, Via O. Raimondo, 00173 Rome, Italy. 0304-3940/90/$ 03.50 © 1990 Elsevier Scientific Publishers Ireland Ltd.