The effects of adenosine and magnesium ion (Mg2+) on striatal dopamine release were studied in awake rats by in vivo microdialysis. The mean striatal basal levels of dopamine release at Mg2+ free perfusate were 56.95 +/- 5.30 fmol/sample (for 20 min). By varying the Mg2+ levels in perfusate from 0 mmol/L to 1, 10 or 40 mmol/L, the dopamine release was inhibited by Mg2+ in a level-dependent manner. Perfusion with modified Ringer's solution containing zero Mg2+ and from 5 to 50 mumol/L adenosine, non-selective adenosine agonist, as well as 0.1 mumol/L 2-chloro-N6-cyclopentyladenosine (CCPA), selective adenosine A1 agonist, showed no effect on dopamine release. However, from 5 to 50 mumol/L adenosine and from 0.1 to 1 mumol/L CCPA plus Mg2+ (1 and 40 mumol/L) perfusion decreased the dopamine release. This inhibitory effect of adenosine and CCPA on striatal dopamine release was enhanced by an increase in extracellular Mg2+ levels. Levels of 50 mumol/L of 8-cyclopentyl-1,3-dimethylxanthine (CPT), a selective adenosine A1 receptor antagonist, in perfusate increased the dopamine release under conditions both with and without Mg2+. This stimulatory effect of CPT on striatal dopamine release was reduced by an increase in extracellular Mg2+ levels. As a result, CPT antagonized the inhibitory effects of adenosine and CCPA on dopamine release under conditions of the presence and absence of Mg2+. These results suggest that the inhibition of striatal dopamine release by adenosine was mediated by adenosine A1 receptor. This inhibition was intensified by Mg2+. This study also revealed that the concentrations of Mg2+, which ranged from physiological to supraphysiological, reduced the striatal dopamine release; furthermore it was found that the physiological concentration of Mg2+ potentiated the effects of adenosine agonists, but inhibited adenosine antagonist. Thus, the present study, using in vivo microdialysis preparations, suggests Mg2+ inhibits the calcium ion channels and enhances the adenosinergic function in the central nervous system.

Two hundred and one school refusers (≤18 years old), excluding schizophrenia, were treated at the Department of Neuropsychiatry, Hirosaki University Hospital between April 1975 and March 1995. Of 56 cases of school refusal, 31 did not improve for more than 2 years (group P), and 25 cases had improved in the degree of school refusal and social impairment (group B). The remaining cases were excluded from the analysis for several reasons. There was no significant difference between groups B and P in age at the first psychiatric evaluation as well as the age of onset of school refusal. The duration from school absence to the first evaluation of group P was significantly longer than that of group B. The duration of school refusal significantly and positively correlated with the duration from school absence to the first evaluation. Introversion and nervousness prolonged the duration of school refusal. The non‐presence of volition for school attendance, and a low frequency of school attendance during the 1 month prior to the first evaluation influenced the prolongation of school refusal. The ‘duration from school absence to the first evaluation’, the ‘patient’s character’, the ‘non‐presence of volition for school attendance’ and the ‘frequency of school attendance’ influenced the prolongation of school refusal. The introduction of treatment within 10 months of the onset of school refusal is an important factor in preventing the prolongation of the school refusal.