Biomedical subjects

A D Levy

Publications and source records attributed to A D Levy.

43 records · Page 3Linked to original sources

PubMed1991

Microinjection of sulpiride into the nucleus accumbens increases ethanol drinking in alcohol-preferring (P) rats.

The effects of dopamine antagonists microinjected into the nucleus accumbens (Acb) on alcohol-drinking behavior were studied in the selectively bred alcohol-preferring (P) line of rats. P female rats (N = 8) were given access to food and water ad lib, while availability of a 10% (v/v) ethanol solution was limited to 1 hr/day. After implantation of guide cannulas bilaterally into the Acb and recovery from surgery, the rats were microinjected with either the D1 antagonist SCH 23390 (0.1 to 2.0 micrograms/side), the D2 antagonist sulpiride (0.1 to 2.0 micrograms/side) or vehicle, and ethanol intake was monitored. The D1 antagonist SCH 23390 had little effect on alcohol intake although the 0.5 ug/side dose produced a small increase which was not statistically significant. The D2 antagonist sulpiride increased, in a dose dependent manner, the intake of ethanol to as high as 215% of control values (F(4,28) = 39.9; p < 0.001). Additional experiments indicated that the 2.0 micrograms/side dose of sulpiride did not alter the consumption of a 14% glucose nor a 0.25% saccharin solution. These data suggest that D2 receptors in the Acb are important in the regulation of alcohol drinking by the P line of rats.

Alcohol Drinking↗

PubMed1988

Chronic amphetamine alters D-2 but not D-1 agonist-induced behavioral responses in rats.

In two experiments, using different drug doses and periods of drug administration, rats were given amphetamine (AMPH) either continuously (via slow-release pellets), or intermittently (via injections). In both experiments, only the rats pretreated with intermittent AMPH subsequently showed heightened responsivity to the selective D-2 dopamine agonist LY171555 but not to SKF38393 (a D-1 agonist). This altered response to LY171555 was still present 30 days after the AMPH withdrawal, implying that D-2 dopamine receptors at least partially mediate AMPH inverse tolerance effects. The behavioral response to the D-2 agonist was clearly different in animals receiving high versus low doses of AMPH, suggesting that different drug-state learning may have occurred during pretreatment. In a third experiment, in which rats were given repeated daily injections of either the D-1 or the D-2 agonist, only rats pretreated with the D-2 agonist and subsequently injected with the D-2 agonist clearly showed heightened responsivity. These data imply an important role of D-2 receptors in the AMPH inverse tolerance effect.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1987

Neuroleptic-induced oral movements in rats: methodological issues.

In three separate experiments groups of rats were chronically administered neuroleptics in a variety of ways (chronic injections, subcutaneous implants, and decanoate injections) and examined for oral movements (OMs) in two different tests: in an open cage using a human observer, or in a plexiglas tube enclosure, where OMs were monitored both by a human observer and computerized video analysis system. These two testing methods showed different effects of neuroleptic administration. In the open cage, OMs tended to be enhanced during chronic neuroleptic exposure and to rapidly subside upon drug withdrawal. The enhanced OMs were especially present just after drug injections, when activity levels were low. In the observation tube environment, however, OMs tended to be low soon after drug treatments, and elevated upon withdrawal. Thus, the type of behavioral test used determines how neuroleptic-induced increases in oral activity should be interpreted.

Animals↗

PubMed1987

Interaction between chronic amphetamine and neuroleptic treatments on oral behavior in rats.

The interaction of concurrently administered amphetamine (AMPH) and haloperidol (HAL) on behavior was examined. Rats were divided into four groups: drug naive controls; HAL-treated for 6 months; AMPH-treated for 1 month; and rats administered both continuous HAL for 6 months and concurrent AMPH treatment during the 2nd month of HAL administration. AMPH alone increased locomotor activity, and this effect was blocked by concurrent haloperidol administration; however, the AMPH-induced reduction of body weight was unaltered by concurrent haloperidol treatment. Oral behavior, monitored both by a human observer and a computerized system, was not significantly altered by HAL alone, or by AMPH alone, but increases in tremorous oral behavior appeared in the concurrent administration group 4 months after AMPH treatment was discontinued. These results could have implications for tardive dyskinesia.

Amphetamine↗

PubMed1985

Amphetamine-induced enhancement of ethanol consumption: role of central catecholamines.

Rats administered continuous low levels of amphetamine increase their free choice consumption of a 10% ethanol solution. The present experiment sought to determine the roles of central catecholamines in producing this effect by comparing the changes of ethanol consumption in rats implanted with control pellets or amphetamine pellets following intracerebral injections of 2 X 250 micrograms of 6-hydroxydopamine (6-OHDA), 6-OHDA preceded by 25 mg/kg of desipramine (to protect noradrenergic neurons from damage), or vehicle. The increase of ethanol consumption associated with continuous amphetamine administration was prevented by intracerebral 6-OHDA administration, but not by intracerebral 6-OHDA preceded by desipramine. There were no significant changes of ethanol consumption in animals receiving either 6-OHDA regimen followed by control pellet implantation. These data indicate that the increased consumption of ethanol obtained with continuous amphetamine administration is mediated by central noradrenergic systems.

Alcohol Drinking↗

PubMedDate not supplied

Repeated cocaine exposure inhibits the adrenocorticotropic hormone response to the serotonin releaser d-fenfluramine and the 5-HT1A agonist, 8-OH-DPAT.

The influence of cocaine exposure on serotonergic neurons and postsynaptic 5-HT1A receptor-mediated responses was evaluated by measuring neuroendocrine responses to a serotonin (5-HT) releaser or a 5-HT1A agonist. Male rats received cocaine (15 mg/kg, i.p.) or saline twice daily for 7 days. Forty-two hr after the final cocaine injection, the 5-HT releaser d-fenfluramine (0, 0.2, 0.6, 2, or 5 mg/kg, i.p.) or the 5-HT1A agonist, 8-OH-DPAT (0, 10, 50, 200 or 500 micrograms/kg, s.c.) were administered. Blood samples were then collected for analysis of plasma ACTH, prolactin, and renin concentrations. The ACTH responses to d-fenfluramine and 8-OH-DPAT were inhibited in cocaine pretreated rats. However, the prolactin responses to d-fenfluramine and 8-OH-DPAT were not significantly modified by cocaine exposure. Additionally, the renin response to d-fenfluramine was unaltered by repeated cocaine administration, while 8-OH-DPAT did not alter renin secretion in either pretreatment group. In contrast to published reports which show that cocaine exposure produces supersensitive 5-HT2A and/or 5-HT2C receptor-mediated responses, the present data suggest that repeated cocaine exposure produces subsensitivity to at least some postsynaptic 5-HT1A receptors. Cocaine-induced deficits in the ACTH response to 5-HT releasers may reflect 5-HT1A receptor subsensitivity, but presynaptic deficits cannot be excluded. Examination of the ACTH response to 5-HT1A agonists may represent a valuable approach to determine deficits in 5-HT function in human cocaine abusers.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMedDate not supplied

Gallbladder carcinoma: radiologic-pathologic correlation.

Primary carcinoma of the gallbladder is an uncommon, aggressive malignancy that affects women more frequently than men. Older age groups are most often affected, and coexisting gallstones are present in the vast majority of cases. The symptoms at presentation are vague and are most often related to adjacent organ invasion. Therefore, despite advances in cross-sectional imaging, early-stage tumors are not often encountered. Imaging studies may reveal a mass replacing the normal gallbladder, diffuse or focal thickening of the gallbladder wall, or a polypoid mass within the gallbladder lumen. Adjacent organ invasion, most commonly involving the liver, is typically present at diagnosis, as is biliary obstruction. Periportal and peripancreatic lymphadenopathy, hematogenous metastases, and peritoneal metastases may also be seen. The vast majority of gallbladder carcinomas are adenocarcinomas. Because most patients present with advanced disease, the prognosis is poor, with a reported 5-year survival rate of less than 5% in most large series. The radiologic differential diagnosis includes the more frequently encountered inflammatory conditions of the gallbladder, xanthogranulomatous cholecystitis, adenomyomatosis, other hepatobiliary malignancies, and metastatic disease.

Diagnosis, Differential↗