CBA mouse convulsion and brain monoamine

Convulsions were induced in 80% of CBA mice by throwing stimulation six from eight weeks after birth, and continued for more than one year. The procedure for causing a CBA mouse convulsion was as follows: the mouse was rolled over suddenly by throwing stimulation and set in tonic flexion. After a few seconds of clonic convulsion, tonic extension followed, and opisthotonus was observed in this stage. After a convulsion, the mouse rose, seemed stunned for a few seconds, then recovered to a normal state. This convulsive process took about 10-15 seconds for the whole procedure. Urinary incontinence was observed. Bilateral sporadic spikes of about 100-150μV were induced in the resting stage of stimulated CBA mice, but the EEG was not abnormal in normal untreated mice. Dopamine (DA) in the cortex and brainstem of the CBA mouse at the pre-convulsive stage was significantly decreased compared with the resting stage, and these changes recovered during the convulsion stage. DA in the cerebellum was also significantly decreased one hour after convulsion. Norepinephrine (NE) of CBA cortex was significantly decreased before, during, and one hour after, a convulsion, compared with the resting stage. 5-Hydroxytryptamine (5-HT) in the CBA brainstem was significantly decreased compared with the resting stage, and this change recovered to the normal level one hour after a convulsion. DA and 5 HT of the cortex of CBA mice, which convulsions had induced for more than one year, were significantly decreased compared with untreated CBA mice of the same age. There was no difference in the monoamines of CBA mouse brain between females and males