In male Wistar rats, shuttle-box avoidance test (5 daily sessions of 50 min) significantly decreased (P less than 0.001) by 30% ascorbic acid (AsAc) level in hypothalamus (HYP), while it left it unmodified in striatum (ST) and in the remaining brain (RB), as opposed to untested rats; AsAc level in HYP showed a significant (P less than 0.001) trend to recovery 24 hours after the end of the test. No correlation was found between the rate of conditioned avoidance responses (CAR) and AsAc levels in the above brain regions. d-Amphetamine (d-A), given s.c. at the dose of 1.0 mg/kg/day for 5 consecutive days, significantly increased AsAc levels by 26% in HYP (P less than 0.005), by 14% in ST (P less than 0.05), and by 33% in RB (P less than 0.001), as opposed to untreated rats; return of AsAc toward baseline levels was negligible 24 hours after d-A withdrawal. The above d-A treatment schedule significantly increased (P 0.05) the rate of CAR in the shuttle-box test. AsAc levels resulted also significantly higher (P less than 0.001) in HYP (+81%) and in RB (+46%) at the end of the test; the AsAc level increase was negligible in ST. Twenty-four hours later, AsAc levels were still significantly higher in RB, but returned toward baseline level in HYP. Again, no correlation was found between CAR rate and regional brain AsAc levels. These results demonstrate that d-A is able to increase regional brain AsAc levels both in control and in tested rats. Since it is well known that systemic administration of AsAc antagonizes some d-A behavioral effects, it is suggested, as a working hypothesis, that the d-A CNS stimulating effect may cause a recruitment of endogenous AsAc, whose task could be a negative neuromodulatory action on the overall effect of d-A on neuronal activity.