The intent of the present study was to determine the effects of systemic injections of the sympathomimetic agent ephedrine (EPH) on extracellular dopamine (DA) levels within the rat nucleus accumbens (NAC) and to compare these effects with those of EPH on locomotion and on feeding. In experiment 1, adult male rats were prepared with an indwelling 3 mm microdialysis probe positioned within the NAC. The rats were injected (i.p.) with vehicle, 5, 10, or 20 mg/kg (-)-EPH with dialysates collected every 20 min for 100 min after drug injection. Systemic injections of 5, 10 or 20 mg/kg (-)-EPH significantly enhanced extracellular levels of NAC DA over baseline by 79%, 130%, and 400%. Systemic injection of 20 mg/kg EPH significantly reduced NAC levels of DOPAC and HVA by 37% and 31%. The effects of EPH on brain dopamine activity were stereospecific given that an additional group of rats injected with 20 mg/kg (+)-EPH exhibited smaller changes in NAC DA (< 25%), DOPAC (< 10%), and HVA levels (< 20%) than did rats injected with 20 mg/kg (-)-EPH. In experiment 2, adult male rats were injected (i.p.) with 0, 5, 10, or 20 mg/kg (-)-EPH prior to placement in automated activity chambers. Total distance traveled was significantly increased by 10 and 20 mg/kg (-)-EPH, but not by 5 mg/kg (-)-EPH. In experiment 3, adult male rats were injected (i.p.) with 0, 2.5, 5, or 10 mg/kg (-)-EPH or with 0, 2.5, 5, or 10 mg/kg (+)-EPH prior to a 30-min feeding test. Although each EPH enantiomer decreased feeding, (-)-EPH was more potent in feeding suppression than was (+)-EPH. The present results suggest that EPH may alter locomotion and feeding via an indirect action on brain dopamine activity.

Russell-Silver Syndrome (RSS) is a rare genetic developmental disorder characterized by prenatal and postnatal growth delays and other physical abnormalities. Neuropsychological screening was completed with LP, a 20-year-old college male diagnosed at one year of age with Russell-Silver Syndrome. LP's history and test findings yielded a profile consistent with a nonverbal learning disability, with significantly higher verbal compared to nonverbal intelligence, deficient visual-spatial memory, fine motor coordination and motor planning problems, relatively greater difficulty in math compared to other achievement areas, decreased writing fluency, and social behavior impediments. LP also experienced attention and concentration problems along with a ruminative cognitive-emotional style and mild depression. His pattern of processing weaknesses indicated a need for academic accommodations to complete his college-level academic work, along with counseling to address emotional issues. Further studies of individuals with RSS should consider neuropsychological assessment to address patterns of cognitive processing and possible need for educational and psychosocial intervention.

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Adult male rats (Rattus norvegicus) were exposed to a water supply in the home cage containing 100 ppm cadmium chloride and sodium saccharin (.65% wt/vol; cadmium group) or water containing only the saccharin amendment (group control). On Day 65 of exposure, animals from each group received jugular catheter implants and were subsequently trained over the course of 15 daily 2-hr sessions to self-administer a .25 mg/kg/infusion of cocaine HC1 under a fixed-ratio 1 schedule. Immediately following acquisition training, the full dose-effect function was determined for all animals by using cocaine doses of .03, .06, .125, .25, .50, and 1.0 mg/kg. Cadmium-exposed animals executed more active (cocaine) lever responses during acquisition training but were not different from controls in depressing a pharmacologically inactive lever. For dose-effect testing, cadmiumexposed animals exhibited greater self-administration than controls at the higher doses of cocaine, and there was evidence that the cocaine dose that produced maximum responding was higher in cadmium-exposed than control animals.The pathologic consequences of recurrent exposure to metallic pollutants have been a research priority in toxicology for many years (see Klaassen, 1990, for a review). Within this investigatory framework, attempts to document human health risks attendant to repeated contact with cadmium have accelerated. The increasing interest in cadmium stems partly from the expanding literature on the links between the toxicant and the use of tobacco. Cadmium selectively accrues in tobacco leaves and is present in all commercial tobacco products (Landsberger & Larson, 1995;Piascik, Champney, Kasarskis, & Forrester, 1985;Yue 1992). Consequently, it is not surprising that cigarette smokers suffer greater body burdens of cadmium than nonsmokers (e.g., Klaassen, 1990;Piascik et al., 1985;Wolfsperger, Hauser, Gossler, & Schlagenhaufen, 1994), to an extent that individuals smoking 10-20 cigarettes or more per day have more than double the levels of blood cadmium as compared with the nonsmoking population (Maranelli, Apostoli, & Ferrari, 1990). Even filtering the tobacco smoke confers no protection, as it has been shown that unlike other heavy metals, cadmium is not prominently retained in the filter (Kalcher, Kern, & Pietsch, 1993).Included in the list of health concerns associated with cadmium toxicity are the effects of the contaminant on drugs that possess abuse liability. Using an animal model, it has been shown that chronic low-level exposure to cadmium results in