This paper deals with the action of Clonazepam on Penicillin induced interictal discharges. In 7 rabbits Penicillin was applied epicortically in a concentration of 25,000 or 50,000 I.U. The intracortical recordings were made with an 8 fold electrode, made by thin-film technology. Clonazepam (0.5 or 1.0 mg/kg) was given intravenously 30 to 45 min after the Penicillin application. Under Clonazepam the occurrence of double-und multiple interictal discharge is abolished. Single spikes become shorter and are significantly reduced in amplitude. Current Source-Density analysis showed that the configuration of sources and sinks is not altered under the action of this drug. However the spatio-temporal distribution is reduced drastically. If the shape of interictal spikes is compared by means of averaging technique before and after the application of Clonazepam, one observes a significant decrease in the standard deviation. These results indicate that excitatory processes are reduced by an enhancement of inhibitory phenomena within the cerebral cortex.
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Luminescence
December 2024
Addiction and Neuroscience Research Unit, Health Science Campus, Taif University, Taif, Saudi Arabia.
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Department of Psychiatry, London Health Sciences Centre, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Medicine (Baltimore)
October 2024
Clinical Department of Traditional Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, China.
Sci Rep
August 2024
Department of Chemical Engineering, Federal University of Pernambuco (UFPE), 1235 Prof. Moraes Rego Av, Cidade Universitária, Recife, PE, 50670-901, Brazil.
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View Article and Find Full Text PDFCereb Cortex
May 2024
Groningen Institute for Evolutionary Life Sciences, University of Groningen, Nijenborgh 7, 9747 AG, Groningen, The Netherlands.
In vitro and ex vivo studies have shown consistent indications of hyperexcitability in the Fragile X Messenger Ribonucleoprotein 1 (Fmr1) knockout mouse model of autism spectrum disorder. We recently introduced a method to quantify network-level functional excitation-inhibition ratio from the neuronal oscillations. Here, we used this measure to study whether the implicated synaptic excitation-inhibition disturbances translate to disturbances in network physiology in the Fragile X Messenger Ribonucleoprotein 1 (Fmr1) gene knockout model.
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