Linda R. Nelson

Ethanol intake increases during continuous administration of amphetamine and nicotine, but not several other drugs

Groups of rats, acclimated to drinking both water and 10% v/v ethanol were implanted with a variety of slow-release devices containing d-amphetamine (d-amp), nicotine, caffeine, phencyclidine (PCP), secobarbital, LSD, mescaline or haloperidol. Ethanol intake was elevated only during treatment with d-amp or nicotine; none of the other drugs affected ethanol consumption even though the amounts of all drugs released were pharmacologically sufficient to affect behavior. Nicotine treated rats were not simply seeking calories provided by the EtOH solution, since nicotine treatment did not enhance intake of a distinctively flavored solution isocaloric to 10% ethanol. These results support a self-medication model of ethanol intake.

Is there atypical handedness in schizophrenia

Ninety-three schizophrenic patients and 105 normal controls were tested in a single session on an 8-item repeat-administration handedness test. The schizophrenic group, in contrast to the normal controls, showed a shift in the distribution away from right-handedness, which was due to an increase in the proportion of mixed-handers. Additional analyses revealed that the increase in mixed-handedness was largely due to an increase of within-item variability in the schizophrenic group, which we refer to as ambiguous handedness. Nearly 20% of the schizophrenic patients were inconsistent on 3 or more items compared with 3.8% of the normal controls. This increased incidence of atypical handedness is discussed within the context of disorders of attention and neurodevelopment.

Enhanced stereotypies after repeated injections but not continuous amphetamines

Abstract Immediately following repeated daily injections of d-amphetamine, rats showed enhanced motor stereotypies when injected with amphetamine or apomorphine. Other rats administered the same amount of amphetamine but in a continuous regime using silicone pellets were conversely hyperactive when initially tested with amphetamine and subsensitive to apomorphine. It is the continuous regime which most clearly produces amphetamine psychosis in humans.

Prenatal ethanol and ontogeny of pituitary-adrenal responses to ethanol and morphine

The development of pituitary-adrenal activity was examined in the offspring of rat dams fed a 5.0% w/v ethanol-containing liquid diet or pair-fed an isocaloric diet, as a nutritional control, from day 8 of gestation to parturition. Serum corticosterone responses of the pups to challenges with ethanol (1.5 g/kg) or morphine (3.0 mg/kg) were determined at 5, 7, 10, 12 and 18 days of age. The pituitary-adrenal axis of normal neonates was activated by the drugs at each age, with a characteristic biphasic developmental pattern in which a trough occurred at day 7. The overall pattern was unaffected by prenatal ethanol exposure or pair-feeding. However, both prenatal treatments intensified the trough. Already on day 5 and also on day 7, corticosterone responses of both the ethanol-exposed and pair-fed offspring to ethanol were significantly lower than responses of normal pups. Additionally, on day 7, ethanol-exposed offspring had significantly lower responses to ethanol than pair-fed offspring and significantly lower responses to morphine than normal pups. Thus, both the prenatal ethanol and pair-feeding treatments suppressed pituitary-adrenal responsiveness of 5 and 7 day-old neonates to the drug challenges. This is in marked contrast to our previous findings for adult prenatally ethanol-exposed offspring whose pituitary-adrenal responses to the same drugs, as well as to other stressors, are consistently enhanced in comparison to pair-fed derived rats, whose responses in adulthood no longer differ from normals.

Opioid but not nonopioid stress-induced analgesia is enhanced following prenatal exposure to ethanol

Two neurochemically distinct forms of stress-induced analgesia were examined in adult rats following prenatal ethanol exposure. Rats were exposed to ethanol during the last 2 weeks of gestation through a liquid diet presented to the dams. Analgesia testing was conducted when the offspring were 150–210 days of age. Two forms of footshock stress were administered; one that resulted in a naloxone-sensitive (opioid-mediated) analgesia and one that resulted in a naloxone-insensitive (nonopioid) form of analgesia. Rats prenatally exposed to ethanol demonstrated significantly enhanced opioid-mediated analgesia, but unaltered nonpoioid analgesia compared to controls. These results confirm previous findings that prenatal exposure to ethanol leads to long-term alterations in responding to some, but not all forms of stress. The possibility that prenatal exposure to ethanol leads to perturbations in the endogenous opioid systems is discussed.

Morphine Analgesia is potentiated in adult rats prenatally exposed to ethanol

Exposure to inescapable, intermittent footshock elicits an opioid-mediated stress-induced analgesia in rats. We have previously shown that this response is markedly potentiated in adult rats, prenatally exposed to ethanol. To further investigate our hypothesis that endogenous opioid pain-inhibitory systems are modified by prenatal ethanol exposure, we have measured the analgesic response to morphine, in vitro brain opiate receptor binding characteristics, and occupation of brain opiate receptors following systemic administration of morphine. Compared to controls, rats prenatally exposed to ethanol had significantly enhanced morphine analgesia. This enhancement, however, does not appear attributable to changes in number or affinity of mu or delta opiate receptors, or to altered occupation of receptors by morphine.

Ambiguous-handedness: incidence in a non-clinical sample.

Using a handedness demonstration preference test under simple and complex task conditions, incidence rates for right, left, and mixed hand preferences were identified in a non-clinical sample. A relatively low incidence rate of ambiguous-handedness was also demonstrated, supporting earlier hypotheses that this subtype is rare among normals.

Increased consumption of diazepam during continuous amphetamine administration.

Previous investigations in our laboratory have demonstrated that after implantation of slow-release d-amphetamine pellets, rats with free access to water and a 10% ethanol solution selectively increase their consumption of the ethanol solution. We now report that this d-amphetamine treatment produces a similar increase in drinking of a benzodiazepine (diazepam) solution. Female albino rats were given free access to water and a 0.060 mg/ml diazepam solution and fluid intake was recorded every two days. The baseline consumption of diazepam averaged 25% of the total daily fluid intake. After d-amphetamine pellet implantation, rats increased their diazepam consumption to an average of 48% of total fluid intake, whereas rats implanted with control pellets containing vehicle only showed no change in diazepam drinking.