1 The effects of (+)-amphetamine on electrically evoked dopamine overflow were examined in the rat brain slice containing either anterior caudate putamen (aCPu) 6 t,12, the rate of removal of [dopamine],x following electrical stimulation was not significantly different in the aCPu and NAc for any of the stimulation conditions. After a 40 min superfusion with (+)-amphetamine (1 AM), t1/2 for ip, 4p/10 Hz and 20p/20 Hz was significantly increased in both the aCPu and NAc, the increase in t1/2 being significantly greater in the aCPu than in the NAc. 7 In conclusion, this study indicates that the dopamine displacement and uptake inhibitory actions of (+ )-amphetamine result in complex and differential effects on electrically evoked dopamine overflow in the aCPu and NAc.
We examined the effects of pressure ejected 3, 4-methylenedioxymethamphetamine (MDMA) from a micropipette on direct chemically stimulated release, and on electrically stimulated serotonin (5-HT) or dopamine (DA) release in the caudate putamen (CPu), nucleus accumbens (NAc), substantia nigra pars reticulata (SNr), and the dorsal raphé nucleus (DRN) brain slices of rat, using fast cyclic voltammetry (FCV). MDMA is electroactive, oxidising at +1100 mV. When the anodic input waveform was reduced from +1.4 to +1.0 volt, MDMA was not electroactive. Using this waveform, pressure ejection of MDMA did not release 5-HT or DA in brain slices prepared from any of the nuclei studied. MDMA significantly potentiated electrically stimulated 5-HT release in the SNr and DA release in CPu. In the DRN or in the NAc, MDMA was without effect on peak electrically stimulated 5-HT or DA release. The rates of neurotransmitter uptake, expressed as t(1/2), were in all cases significantly decreased after MDMA. The results indicate that MDMA, unlike (+)amphetamine, is not as a releaser of DA or 5-HT, it is a potent inhibitor of both DA and 5-HT uptake.
Chronic exposure to mild unpredictable stress caused a decrease in rats' consumption of a palatable weak sucrose solution, which was reversed by chronic (5 weeks) administration of imipramine (5 mg/kg/day). Dopamine (DA) release in the nucleus accumbens (NAc) and caudate putamen (CPu) was measured in vivo using fast cyclic voltammetry, following electrical stimulation of the medial forebrain bundle. Experiments were performed under chloral hydrate anaesthesia 48 h after the termination of stress and the final imipramine injection. DA release was increased in the NAc of both stressed and imipramine-treated animals; imipramine did not normalize the increased DA release in stressed animals. In a further experiment, brain slices from stressed animals tended to be subsensitive to the inhibition of DA release in the NAc by quinpirole. No changes were observed in the CPu in any experiment. We discuss the relationship of these effects to stress-induced anhedonia.
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