SHORT AND LONG‐TERM EFFECTS OF RESERPINE ON THE CONCENTRATION OF 1‐(4‐HYDROXY‐3‐METHOXYPHENYL)‐ETHANE‐1,2‐DIOL (MOPEG‐S04) IN THE BRAIN OF THE RAT

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Abstract
1 Reserpine (1.25 mg/kg i.p.) induced an increase (172% of controls) in the concentration of 1-(4-hydroxy-3-methoxyphenyl)-etnane-1,2-diol sulphate (MOPEG-S04) in rat brain and a decrease in the noradrenaline (NA) concentration to 50% of controls 2 h after injection. At this time the MOPEG-S04/NA ratio was 0.28. Thereafter the MOPEG-SO4 concentration declined and the NA concentration decreased further to 28% of control. 2 Higher doses of reserpine (2.5 and 5 mg/kg i.p.) did not induce a larger increase in the concentration of MOPEG-SO4. 3 While a second dose of reserpine (1.25 mg/kg i.p.) given 24 h after the first did not increase the MOPEG-SO4 concentration, amphetamine (5.0 mg/kg i.p.) administration or electrical stimulation significantly increased the concentration of MOPEG-SO4. 4 NA and MOPEG-SO4 concentrations were examined during 5 days after a single dose of reserpine (1.25 mg/kg i.p.). While the concentration of NA started to return towards normal after 24 h, that of MOPEG-SO4 remained at approximately 70% of controls during the entire period. 5 The probenecid-induced accumulation rate of MOPEG-SO4 was significantly lower 3 and 4 days after reserpine and returned to the control value on the fifth day. At this time the concentration of NA had reached 50% of the control value. 6 These experiments indicate that MOPEG-SO4 is not the major metabolite of NA during the initial phase of reserpine-induced NA release. Reserpine acts on the storage pool while amphetamine (like electrical stimulation) acts on the functional pool. During the first phase of post-drug recovery, there is a clear decrease in NA output which appears to be regulated by the concentration of NA in the storage pool.