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Biomedical subjects

I Geller

Publications and source records attributed to I Geller.

At least 37 records · Page 2Linked to original sources
PubMed1979

Effects of polybrominated biphenyl on a discrimination task in rats.

Learning or performance of an operant discrimination task by laboratory rats in Skinner boxes was studied as a function of subchronic treatment with polybrominated biphenyl (PBB) (1.0 mg/kg, 3.0 mg/kg or 6.0 mg/kg for 20 days). Acquisition of the discrimination task was similar for experimental and control rats at each dose level. Response times were slower for the 1.0 mg/kg rats but were like controls for the 3.0 and 6.0 mg/kg animals. Extra responses occurring in the absence of auditory discriminative stimuli increased significantly for the 1.0 mg/kg rats (hyperactivity), were no different from controls for the 3.0 mg/kg rats and decreased significantly for the 6.0 mg/kg animals (CNS depression). The weights of PBB animals did not differ significantly from controls. Analyses of brains and plasma by electron capture gas chromatography yielded detectable levels of PBB as long as 10 months following the last PBB administration. PBB in brains and plasma varied directly as a function of dose administered.

Animals↗
PubMed1979

Correlation of systemic and biochemical effects of PBB with behavioral effects.

Rats were given PBB orally at 1, 3, and 6 mg/kg (or vehicle as control) daily for 20 days. Some animals were sacrificed immediately while the food intake of remaining animals was limited to attain and maintain 80% of normal body weight. No effect of PBB upon body weight was observed for any of the dose levels employed. Immediately after dosing, liver/body weight ratios were 110% of controls for the 1 mg/kg group and 152% for the 3 and 6 mg/kg groups; after weight reduction for 2-6 months liver/body weight ratios for all 3 dose groups were 160-170% of controls. In the absence of body fat, most tissues exhibited dose-dependent retention of PBB 2-6 months after dosing with highest levels in liver followed by kidney. In 6 mg/kg rats weight-reduced for 6 months, liver AHH activity was 613% of controls; in rats sacrificed immediately after dosing, liver AHH activity was dose-related but appeared to reach maximal value at the 3 mg/kg dose. Both calcium binding to synaptic plasma membranes and calcium uptake by intact synaptosomes was significantly reduced in the brains of 1 mg/kg PBB rats, but not affected in preparations from 3 and 6 mg/kg animals.

Animals↗
PubMed1979

Use of discrimination behavior for the evaluation of toxicants.

This study involved the application of discrimination behavior for the study of effects of environmental contaminants on the behavior of laboratory animals. Polybrominated biphenyl (PBB) was evaluated for effects on the acquisition and performance of a simple auditory discrimination by rats. Methyl ethyl ketone (MEK), methyl isobutyl ketone (MIBK) and carbon monoxide (CO) were evaluated for effects on a delayed match-to-sample discrimination task in the juvenile baboon. All of the contaminants slowed response times and increased extra responses. These findings suggest that discrimination behavior may be of value for the evaluation of environmental contaminants for effects on the central nervous system.

Animals↗
PubMed1979

Effects of carbon monoxide on operant behavior of laboratory rats and baboons.

Carbon monoxide (CO) was evaluated for its effects on the operant behavior of laboratory rats and juvenile baboons. For the rat studies the procedures included a 2-min variable interval (2-min VI) or fixed interval (2-min FI) schedule of reinforcement, a 60:1 fixed ratio (FR) schedule and a multiple fixed ratio, fixed interval (FR:FI) schedule. Carbon monoxide concentrations of 50-200 ppm for 2-hr exposure periods produced minimal effects on VI rates. Response rates were increased for all animals somewhere in the concentration range of 25-200 ppm. Response rates were depressed at 500 ppm CO. Behavioral effects at 50 ppm CO were not correlated with blood CO levels. Data averaged for grops of three animals show FI rate increased slightly above controls at 50 and 100 ppm CO and decreased at 200 ppm. FR rate increased at 50 ppm and decreased at 100 and 200 ppm. For the baboon studies, a delayed match-to-sample discrimination task was used. The effects of CO (6 hr per day over a 5-day period) on the discrimination task was limited to an occasional mistake by an animal. CO did produce a slowing of the animals' response times as well as an increase of extra responses during the delay intervals. The changes in extra responses were dose related.

Animals↗
PubMed1977

Voluntary ethanol drinking by the RAT: effects of 2-aminoethylisothiouronium Salt, a modifier of NAD:NADH and norelegnine, a beta-carboline derivative.

Voluntary intake of ethanol solution (ETOH) was decreased in rats administered 2-aminoethylisothiouronium bromide hydrobromide (AET), an agent reported to alter NAD:NADH ratios in rat liver. Repeated administration of same dose of AET to ETOH-naive rats produced a significant inhibition of liver aldehyde dehydrogenase. Ethanol intake was decreased in rats given noreleagnine (NLG), a beta-carbone derivative reported to inhibit monoamine oxidase. Repeated administration of NLG exerted a significant inhibitory effect on liver alcohol dehydrogenase activity. It is concluded that the observed reduction of ethanol under AET which inhibits liver aldehyde dehydrogenase may reflect an antabuse-like reaction and the reduction of ethanol intake under NLG may be due, in part, to a build-up of alcohol in the blood and brain through inhibition of ethanol metabolism. The results are discussed in reference to the possible mechanism of action underlying voluntary intake of ethanol in rats, implicating alteration of NAD:NADH ratios in the biochemical processes underlying alcohol intake of rats.

Alcohol Drinking↗
PubMed1975

Ethanol narcosis in mice: effects of L-dopa, its metabolites and other experimental variables.

Ethanol-induced narcosis was studied in mice as a function of pretreatment with L-dopa and its metabolites administered alone or in conjunction with Ro-4-4602, an inhibitor of aromatic-L-amino acid decarboxylase. These studies suggest that L-dopa prolongation of ETOH narcosis in mice may be due to formation of one or more toxic metabolites rather than to a direct involvement of dopamine. Ethanol narcosis also was studied in mice as a function of age of animals, concentration of ETOH, ambient temperature and saline pretreatment. Since manipulation of these variables produced alterations in ETOH narcosis, the need for their rigid control is indicated.

Age Factors↗