Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 31

Abnormalities of CNS catecholamines have been reported in several genetic models of epilepsy. In the spontaneous epileptic rat, dopamine was decreased in the caudate nucleus whereas noradrenaline was increased in the midbrain and brainstem (Hara et al., 1993). Decreased levels of dopamine have been found in epileptic foci of epilepsy patients (Mori et al., 1987). In animal models of absence epilepsy, seizures are exacerbated by dopamine antagonists while alleviated by dopamine agonists (Snead, 1995). These results suggest that decreased dopamine facilitates appearance of seizures by lowering the threshold triggering such seizures. Tottering mice have an absence-like syndrome that is characterized by episodes of behavioural arrest associated with 6 to 7 Hz cortical SW EEG discharges. Selective destruction of the ascending noradrenergic system at birth prevents the onset of the syndrome. Therefore, it has been suggested that the syndrome is caused by a noradrenergic hyperinnervation of the forebrain (Engelborghs et al., 2000). Recent data indicate that the serotonergic system regulates epileptiform activity in a genetic rat model of absence epilepsy as intraperitoneal or intracerebroventricular administration of 8- OHDPAT caused marked and dose-dependent increases in number and duration of discharges (Gerber et al., 1998).