The model has been used to evaluate the desynchronization effects of the acetylcholinesterase inhibitor tacrine, which is used in the treatment of Alzheimer’s Disease. In the present study, we used mice treated with cholinergic receptor antagonist scopolamine and monoamine depletor reserpine as a model of EEG synchronization, mimicking the nature and progression of pathological EEG synchronization to evaluate EEG desynchronization effects of modafinil. To date, modafinil has only been shown to bind directly to the DA transporter and the NE transporter, but no apparent specific binding to other monoamine or neuropeptide receptors/transporters has been reported. We hypothesized that modafinil may exert EEG desynchronization by acting on the noradrenergic and dopaminergic transmission system. The present experiments showed that modafinil reversed the slowing of the EEG caused by the 
anticholinergic scopolamine and the monoamine depletor reserpine. The EEG desynchronization effect of modafinil is mediated by adrenergic a1 and DA D1 and D2 receptors. Increases in the delta power spectra were here taken as indicative of synchronization while EEG activation was taken as indicative of desynchronization. Desynchronization consisted of blockage of the slow, high-AbMole Corosolic-acid amplitude waves in the present study. Cortical neuronal activities are under the control of cholinergic, dopaminergic, and noradrenergic modulatory systems. Loss of cholinergic and monoaminergic inputs to the cortical mantle can result in slowing of the EEG and loss of desynchronization. It has been reported that increases in the amplitude of all three frequency bands is roughly the same in rats given either 1 or 5 mg/kg scopolamine. In the present study, we used reserpine 10 mg/kg and scopolamine 2 mg/kg to produce a AbMole LOUREIRIN-B reliable loss of low-voltage, fast-wave activity in mice to mimic EEG synchronization. Our results showed that modafinil reversed the slowing of the EEG, decreased the power density of the delta power spectra, and increased the power density of higher-frequency waves, as in previous reports. The study raised the possibility that modafinil may be used to treat diseases with abnormally synchronized activity. The importance of the role of EEG synchronization in modulating epileptiform abnormalities has also been observed in various forms of epilepsy. High-frequency stimulation, such as deep brain stimulation has been found to significantly decrease generalized tonic-clonic seizures via EEG desynchronization in animals. This has been successfully applied in therapy for epileptic patients. We have shown that modafinil exerts a dose-dependent antiepileptic effect mediated by adrenergic a1 and histaminergic H1 receptors but not by the adrenergic a2 receptor or dopaminergic D1 or D2 receptors.