Differential Effects of Antiepileptic Drugs on Focal Seizures in the Intrahippocampal Kainate Mouse Model of Mesial Temporal Lobe Epilepsy.

Aims: Mesial temporal lobe epilepsy (MTLE) is the most common form of drug-refractory epilepsy. Most of the morphological and electrophysiological features of human MTLE can be reproduced in a mouse by a unilateral intrahippocampal injection of kainate (MTLE mouse model). The effects of antiepileptic drugs (AEDs) on the occurrence of recurrent focal hippocampal seizures in this model remain to be specified.

Chronic administration of atypical antipsychotics improves behavioral and synaptic defects of STOP null mice.

Introduction: Recent studies have suggested that schizophrenia is associated with alterations in the synaptic connectivity involving cytoskeletal proteins. The microtubule-associated protein stable tubule only polypeptide (STOP) plays a key role in neuronal architecture and synaptic plasticity, and it has been demonstrated that STOP gene deletion in mice leads to a phenotype mimicking aspects of positive and negative symptoms and cognitive deficits classically observed in schizophrenic patients. In STOP null mice, behavioral defects are associated with synaptic plasticity abnormalities including defects in long-term potentiation.

Superior colliculus firing changes after lesion or electrical stimulation of the subthalamic nucleus in the rat.

Recent data have suggested a critical role for the basal ganglia in the remote control of epileptic seizures. In particular, it has been shown that inhibition of either substantia nigra pars reticulata or subthalamic nucleus as well as activation of the superior colliculus suppresses generalized seizures in several animal models. It was previously shown that high frequency stimulation of the subthalamic nucleus, thought to act as functional inhibition, stopped ongoing non-convulsive generalized seizures in rats.