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Biomedical subjects

S Liljequist

Publications and source records attributed to S Liljequist.

77 records · Page 5Linked to original sources
PubMedDate not supplied

Proteinergic profiles in cerebrospinal fluid from alcoholic subjects.

Minute amounts of cerebrospinal fluid samples from alcoholics were subjected to separation by HPLC-molecular sieving, combined with multispectral UV analysis of the acquired data. A significant difference in the protein/polypeptide pattern within the molecular weight range of 7-10 kDa has been observed between samples, taken directly after detoxification and 2 weeks later. Spectral analysis of the results suggests that the components are of peptidergic nature. On the other hand, albumin content did not differ significantly, suggesting that the blood-brain barrier was not affected. An enzyme marker, dynorphin converting enzyme, remained unchanged in both groups.

Adult↗
PubMedDate not supplied

Binding characteristics of 3H-flunitrazepam and CL-218,872 in cerebellum and cortex of C57B1 mice made tolerant to and dependent on phenobarbital or ethanol.

The influence of chronic phenobarbital (PB) or chronic ethanol administration on binding characteristics of 3H-flunitrazepam (3H-FLU) in cerebellum and cortex of C57Bl mice was examined. Chronic PB treatment for six days decreased the number of binding sites (Bmax) for 3H-FLU, whereas no change in the affinity (KD) was found. Further kinetic analysis revealed that the overall decrease in Bmax was due to a reduced number of high affinity (Type 1) benzodiazepine (BDZ) binding sites in the cerebellum, but to a decreased number of low affinity (Type 2) BDZ binding sites in the cortex. Furthermore, a marked reduction in the pentobarbital-produced enhancement of 3H-FLU binding was observed in the cerebellum of the PB-treated animals. Following chronic ethanol administration for seven days, no change in the Bmax or in the KD could be demonstrated. However, in chronically ethanol-treated mice, the pentobarbital-induced stimulation of 3H-FLU binding was reduced in the cerebellum of mice 24 hours after discontinuation of the ethanol treatment. The significance of the present findings for the development of tolerance to and dependence on barbiturates and ethanol is discussed.

Alcoholism↗
PubMedDate not supplied

NMDA receptor antagonists inhibit ethanol-produced locomotor stimulation in NMRI mice.

The effects of competitive and noncompetitive NMDA receptor antagonists on locomotor stimulation produced by low doses of ethanol were studied in NMRI mice. Both competitive (CGP 39551) and noncompetitive (MK-801) NMDA receptor antagonists inhibited ethanol-produced behavioral stimulation in doses which by themselves had no effects on the locomotor activity. In additional experiments, where the muscle relaxant actions of ethanol and the NMDA receptor antagonists were studied, it was found that the "inhibitory" effects of the NMDA receptor antagonists in the locomotor activity test situation most likely were due to a potentiation of the sedative effects of ethanol and/or the antagonists. The implications of the current observations with regard to previously reported results concerning interactions between ethanol and NMDA receptor antagonists and with regard to a possible therapeutic advantage of using competitive NMDA receptor antagonists in the management of the human alcohol abstinence syndrome are discussed.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Developmental changes in the inhibitory actions of ethanol on glutamate-induced translocation of protein kinase C in cerebellar granule neurons.

The effects of increasing concentrations of ethanol (25-200 mM) on the enhancement of [3H]phorbol-12,13-dibutyrate ([3H]PDBu) binding produced by different glutamate receptor agonists, indicative of a translocation of the intracellular enzyme protein kinase C (PKC), were studied in rat cerebellar granule cells at 2, 4, 8, and 12 days in vitro (DIV). Glutamate-produced stimulation of [3H]PDBu binding was inhibited by 50 mM ethanol at 2 DIV, whereas higher ethanol concentrations (> 100 mM) were needed to reduce the increase of [3H]PDBu binding in cells grown for 4, 8, and 12 DIV. Ethanol significantly inhibited NMDA-stimulated [3H]PDBu binding in a concentration-dependent fashion in cells maintained in culture for 4 and 8 days, respectively, with a slightly less pronounced inhibition by ethanol (50 mM) seen in cells kept for 2 and 12 DIV. Application of higher ethanol concentrations (> 100 mM), inhibited the NMDA-induced stimulation in all cell preparations. Following kainic acid-induced enhancement of [3H]PDBu binding, ethanol (100 mM) reduced the binding only in cells maintained for 2 DIV. Even higher ethanol concentrations (200 mM) inhibited the effects of kainic acid only in cells maintained for 2 and 4 DIV, respectively. Our data suggest that various subclasses of glutamate receptors display a developmentally determined differential sensitivity to ethanol at least in cerebellar granule cells in vitro.

Animals↗