“…One potential source of concern when using an FCN or any traditional differentiation procedure as a baseline against which to evaluate drug effects is that drug-induced disruptions in the run distribution will produce correlated changes in reinforcement probability and rate, generally decreasing criterional run frequency and consequently reinforcement density. Increasing doses of a wide variety of drugs, including various opioid agonists and antagonists (e.g., Bronson & Moerschbaecher, 1987;Picker, Heise, & Dykstra, 1987), the nonopi-205 1991) 561, [205][206][207][208][209][210][211][212][213][214][215] NUMBER 2 (SEPrEMBER) oid analgesics clonidine and 1-nantradol (Picker & Dykstra, 1988), the anticonvulsants clonazepam, ethosuximide (Picker, Leibold, Endsley, & Poling, 1986a) valproic acid, phenytoin, phenobarbital, diazepam (Picker, Leibold, Endsley, & Poling, 1986b), methsuximide, and mephenytoin (Schlinger, Wilkenfield, & Poling, 1988), the stimulants amphetamine (Laties, 1972), methamphetamine, caffeine, and methylphenidate (Mechner & Latranyi, 1963), and the anticholinergic scopolamine (Laties, 1972) all decrease the relative frequency of runs reinforced under FCN procedures. These decreases in reinforcement density are potentially important because they have been implicated in modifying both acute (e.g., Smith & McKearney, 1977) and chronic (cf.…”