What is it about?

Antiepileptic and network inhibitory actions of Q5 (2-methyl-4-oxo-3H-quinazoline-3-acetyl piperidine) have recently been described in hippocampal slices. Here we present evidence on the in vivo antiabsence effect of Q5. All doses of Q5 tested (0.3 mg/kg, 0.9 mg/kg, 2.8 mg/kg) decreased the number, but not the duration and the frequency of absence spike-wave discharges (SWDs) in freely moving WAG/Rij rats. In vivo network inhibitory action of Q5 was monitored by following c-fos expression in different brain areas of Wistar rats. Significant depletion of c-fos expression was observed after single or repeated injections of Q5 (2.8 mg/kg and 2×2.8 mg/kg) in various brain areas, including hypothalamic paraventricular nucleus, medial amygdaloid nucleus, piriform cortex, somatosensory cortex, periventricular thalamic nucleus and periaqueductal central gray.

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Why is it important?

Thus, our in vivo results demonstrate that in addition to the prevention of absence seizures, Q5 effectively suppresses neuronal activation in various stress- and pain-sensitive brain areas.

Perspectives

Q5 is an effective antiabsence compound, and it suppresses neuronal activation in specific brain areas in vivo.

Dr Zsolt Kovacs
Eötvös Loránd University

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This page is a summary of: Suppression of spike-wave discharge activity and c-fos expression by 2-methyl-4-oxo-3H-quinazoline-3-acetyl piperidine (Q5) in vivo, Neuroscience Letters, August 2007, Elsevier,
DOI: 10.1016/j.neulet.2007.06.035.
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