The effects of alpha-neurofeedback (ANF) on electroencephalographic alpha-activity were investigated. Each session consisted of a 2.5-min eye-opened state and 17.5-min of ANF, which was divided into 16 1.25-min bins. Alpha amplitudes were gradually increased as the session was repeated. The maximum value at the start of ANF gradually decreased as time passed, but the slowdown of alpha-activity during each session was decreased as the session was repeated. The correlation between alpha-activity at the end of ANF and at the following session's eye-opened state was highly significant. These results showed that ANF enhances the ability of alpha-activity to maintain itself rather than the increase of alpha-amplitude during intrasession and that the maintained alpha-activity during former training remained until the next session.

No abstract

No abstract

Repeated psychostimulants induce electroencephalographic (EEG) changes, which reflect adaptation of the neural substrate related to dopaminergic pathways. To study the role of dopamine receptors in EEG changes, we examined the effect of apomorphine, the dopamine D1 receptor antagonist, SCH-23390, and the D2 receptor antagonist, haloperidol, on EEG in rats. For single and repeated apomorphine treatment groups, the rats received saline or apomorphine for 4 days followed by a 3-day withdrawal period and then apomorphine (2.5 mg/kg, i.p.) challenge after pretreatment with saline, SCH-23390, or haloperidol on the day of the experiment. EEGs from the frontal and parietal cortices were recorded. On the frontal cortex, apomorphine decreased the power of all the frequency bands in the single treatment group, and increased the theta (4.5∼ 8 Hz) and alpha (8∼ 13 Hz) powers in the repeated treatment group. Changes in both groups were reversed to the control values by SCH-23390. On the parietal cortex, single apomorphine treatment decreased the power of some frequency bands, which were reversed by haloperidol but not by SCH-23390. Repeated apomorphine treatment did not produce significant changes in the power profile. These results show that adaptation of dopamine pathways by repeated apomorphine treatment could be identified with EEG changes such as increases in theta and alpha power of the frontal cortex, and this adaptation may occur through changes in the D1 receptor and/or the D2 receptor.

No abstract