Modulation of acetylcholine release was studied in slices of the rabbit hippocampus preincubated with 3H-choline and then continuously superfused with a medium containing 10 mumol/l hemicholinium-3. Electrical field stimulation of the superfused slices elicited an increase in tritium outflow, which was tetrodotoxin-sensitive and largely calcium-dependent. Stimulus-evoked acetylcholine release in the rabbit hippocampal slices was modulated by presynaptic muscarinic autoreceptors, as has been shown previously for the rat hippocampus. Drugs with affinity for alpha- and or beta-adrenoceptors did not affect the evoked overflow of tritium from rabbit hippocampal slices. In contrast, the dopamine receptor agonist apomorphine (0.1 or 1 mumol/l) and exogenous dopamine (1 or 10 mumol/l) significantly reduced the evoked outflow by about 10 or 20%, respectively. This effect was antagonized by haloperidol (0.01 mumol/l) but not by phentolamine (1 mumol/l). Attempts to enhance (using nomifensine 10 mumol/l) or reduce (using haloperidol, up to 1 mumol/l; or bretylium, 1 mmol/l for 5 min) endogenous dopaminergic transmission in the hippocampal slices did not affect stimulation evoked acetylcholine release. In conclusion, presynaptic dopamine receptors modulating acetylcholine release are present in the rabbit hippocampus, but they seem not to be of physiological significance.