Systemic injections of morphine to rats produced a moderate, biphasic increase in dopamine (DA) overflow in the n. accumbens. Pretreatment with nomifensine did not increase the morphine effect significantly. Micro-injections of DALA met-enkephalin into the ventral tegmental area (VTA) elicited behavioral activation as well as a moderate DA overflow in the n. accumbens. Electrical stimulation of the VTA produced effects similar to enkephalin injections. It appears that merely a modest elevation of DA in the n. accumbens may be required to enhance behavioral activation. Infusions of ethanol through microdialysis probes situated in the striatum and n. accumbens produced dose-dependent increases in DA overflow in either structure. The effects were calcium dependent, suggesting that the release of DA by ethanol is exocytotic in nature. The relative potency of other alcohols tested on DA release was butanol > ethanol > methanol. A serotonergic component may be involved in mediating the effects of ethanol on DA overflow since pretreatment with a 5-HT, antagonist was effective in attenuating the increases in extracellular DA by ethanol. Recovery of adenosine from the striatum with microdialysis procedures revealed levels of 41.4 nM in the dialysate following probe insertion which rapidly declined to approximately 2.5 nM. Basal levels of adenosine were not altered following perfusion with TTX, Mg++ or Ca++. TTX and Ca++, however, did antagonize K+-evoked adenosine release. It appears that while K+-induced increases in adenosine are derived from an exocytotic process, the basal levels are not.
