PubMed Health⌕ Search

Biomedical subjects

L F Englert

Publications and source records attributed to L F Englert.

At least 19 recordsLinked to original sources
PubMed1985

Passive avoidance deficits in mice following ethylcholine aziridinium chloride treatment.

High-affinity choline uptake (HACU) appears to be the rate-limiting step in the synthesis of the neurotransmitter acetylcholine. The present experiment was designed to examine the effects of irreversible inhibition of HACU by ethylcholine aziridinium chloride (ECA) on passive avoidance retention in mice. Animals were injected intracerebroventricularly, and one-trial passive avoidance retention evaluated 21 days later. A significant retention deficit was observed in ECA-treated animals upon retest 24 hours after training. ECA-induced changes in retention were accompanied by significant reductions in choline acetyltransferase (CAT) activity in only two of seven brain regions tested, hippocampus (48% of control) and cerebellum (76% of control). The results support the involvement of hippocampal cholinergic activity in mediation of passive avoidance learning.

Animals↗
PubMed1979

Metabolism correlates of cocaine-induced stereotypy in rats.

An increase in stereotyped behavior was observed in rats injected daily with cocaine (40 mg/kg, IP), as compared with the first day. This increase persisted 14 days after discontinuation of the drug treatment, and corresponded to increased levels of 3H-cocaine norcocaine and benzoylecgonine in brain. Pretreatment of the animals with SKF-522A, an inhibitor of cocaine demethylation, produced a decrease in stereotypy rating and concomitantly a lower level of 3H-norcocaine in the brain. The role of this metabolite in the production of cocaine-induced stereotyped behavior is discussed.

Animals↗
PubMed1979

Generalization of norcocaine to the discriminative stimulus properties of cocaine.

In rats trained to discriminate 10 mg/kg cocaine from 1 mg/kg saline, norcocaine, the N-demethylated metabolite, at doses of 2.5 mg/kg, 5 mg/kg and 10 mg/kg, produced a dose response curve similar to that of cocaine and generalized to cocaine at the two higher doses. As with cocaine, the discriminative stimulus produced by the norcocaine was partially attenuated by the dopaminergic antagonist pimozide and the amine depletor reserpine. Benzoylecgonine, benzoylnorecgonine and ecgonine methyl ester in doses of 10 mg/kg and 20 mg/kg did not generalize to cocaine.

Animals↗
PubMed1977

Inhibition of the metabolism of cocaine by SKF-525A.

In vitro and in vivo studies in rats indicate cocaine to be metabolized primarily in the liver to form benzoylecgonine and norcocaine. The formation of these metabolites was significantly hindered by SKF-525A, a microsomal enzyme inhibitor. In in vivo studies, pretreatment of rats with SKF-525A prior to receiving cocaine resulted in increased amounts of unchanged cocaine in the brain. No accompanying increase in spontaneous motor activity was observed for these animals, indicating a possible role for metabolites in the stimulant action of cocaine.

Animals↗
PubMed1976

Demethylation in rats chronically treated with cocaine.

Norcocaine was prepared from cocaine utilizing diethyl azodicarboxylate. The rate of demethylation of 14C-cocaine in rats receiving either chronic or acute dosages of the drug was investigated. No significant difference in the rate of 14CO2 exhalation from the two groups was observed.

Animals↗
PubMed1976

Hydrolysis of carbon-labeled cocaine in human serum.

Hydrolysis of 14C-cocaine in human serum, separation of the metabolites on TLC, and subsequent identification on GLC is described. AT 1 H, 20 percent of the cocaine was metabolized to benzoylecgonine, ecgonine and ecgonine methylester. At this time interval the highest percent of product was in the form of the ecogonine methyl ester, a metabolite not previously reported in humans. After 4 h, 67 percent of the cocaine was hydrolyzed; of this, 45 percent was benzoylecgonine and ecgonine in a ratio of 1.6 to 1. The half-life for cocaine hydrolyzed in human serum was approximately 2.5 h.

Cocaine↗
PubMed1973

The effects of (-)-delta9-tetrahydrocannabinol on reserpine-induced hypothermia in rats.

1. An intravenous injection into rats of 1 mg/kg (-)-Delta(9)-tetrahydrocannabinol Delta(9)-THC) had no effect on rectal temperature and produced in the subcellular fractions of the brain a shift of 5-hydroxytryptamine (5-HT) from the particulate or ;bound' 5-HT to the supernatant or ;free' fraction, whereas the noradrenaline (NA) decreased in both fractions.2. Pretreatment of rats by an intravenous injection of 1 mg/kg Delta(9)-THC three times a week for four weeks, prevented the hypothermia and the reduction in brain 5-HT produced by an intraperitoneal injection of 15 mg/kg reserpine given 24 h after the last Delta(9)-THC injection.3. Pretreatment of rats by a single intravenous injection of 1 mg/kg Delta(9)-THC prevented the hypothermia and reduction in brain 5-HT produced by an intraperitoneal injection of reserpine given 1 h before. The reduction in brain NA was not prevented except at the 18 h time interval.4. An injection of 1 mg/kg Delta(9)-THC intravenously into rats 3 h after an intraperitoneal injection of reserpine accentuated the reserpine hypothermia as well as the reduction of 5-HT but not of NA in the brain.5. The reserpine hypothermia was not prevented by a single intravenous injection of 1 mg/kg Delta(9)-THC when cinanserin, a 5-HT inhibitor, was injected 30 min before the reserpine.

Anilides↗