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Biomedical subjects

S Liljequist

Publications and source records attributed to S Liljequist.

At least 73 records · Page 4Linked to original sources
PubMed1982

The effect of chronic ethanol administration of high affinity 3H-nicotinic binding in rat brain.

The effect of chronic ethanol administration on high affinity 3H-nicotinic binding rat brain was investigated. Chronic ethanol administration for 5 months included a significant decrease in the number of specific nicotinic binding sites in the hippocampus, whereas a significantly increase in the number of nicotinic binding sites both in the hypothalamus and in the thalamus was found. Similar effects were observed both after administration of a lower concentration (8% W/V) ethanol and a higher concentration (16% W/V) indicating that the duration of the administration seems to be of importance for the biochemical changes observed.

Animals↗
PubMed1982

Increased salsolinol levels in rat striatum and limbic forebrain following chronic ethanol treatment.

Endogenous levels of salsolinol and its methylated metabolite were measured by combined gas chromatography and mass spectrometry in rats chronically exposed to ethanol for 150 days. The chronic ethanol administration produced a significant increase of salsolinol concentrations in dopamine-rich brain areas, e.g., the striatum and the limbic forebrain. A negative correlation was observed between plasma ethanol concentration and the level of salsolinol in the brain. A possible role for salsolinol in the regulation of ethanol drinking and/or in the development of ethanol dependence is discussed.

Alcoholism↗
PubMed1982

The effect of chronic ethanol administration on lipids and fatty acids in subcellular fractions of rat brain.

In this study we have investigated the proportion of lipids and of fatty acids in brain membranes and blood serum from rats which received ethanol over a long period. Nine Sprague-Dawley rats were given ethanol in their drinking water for five months. Nine age-matched rats given pure water served as controls. Subcellular fractions (myelin, synaptosomes and mitochondria) were prepared in a discontinuous gradient of sucrose from each of the 18 rats. Blood serum was collected at decapitation. The fractions were assayed for their concentrations of protein, cholesterol, phospholipids and for the proportions of fatty acids in individual phosphoglycerides. No significant differences in the concentration of the major lipids were obtained between the ethanol-exposed rats and the control rats. In the synaptosomal fraction from ethanol-exposed rats, the proportion of oleic acid in phosphatidylcholine was increased and that of arachidonic acid in phosphatidylethanolamine decreased. These two fatty acids were also changed in the blood serum and there was a significant correlation between the changes in the brain and blood serum. The results suggest that during ethanol exposure there is an increased disposition toward modification of synaptosomal membranes by changes in the blood plasma fatty acid pattern.

Animals↗
PubMed1981

The effect of lithium on the locomotor stimulation induced by dependence-producing drugs.

The present study was performed to investigate how lithium affects locomotor stimulation induced by dependence-producing drugs such as amphetamine, ethanol and morphine. Acute lithium alone was found to suppress exploratory hyperactivity in mice without affecting basal locomotor activity, further supporting the contention that lithium has a neurolept-like behavioural profile. Acute lithium pretreatment suppressed locomotor stimulation in mice induced by all the dependence-producing drugs in a dose-dependent manner. Locomotor stimulation seen after amphetamine and ethanol appeared to be more suppressed by lithium than that seen after morphine. Taken together with the finding that lithium had no effect on apomorphine-clonidine-induced locomotor stimulation after elimination of presynaptic activity the present data suggest that the suppressive effect of lithium is mediated via presynaptic catecholaminergic mechanisms.

Amphetamine↗
PubMed1981

The effect of catecholamine receptor antagonists on ethanol-induced locomotor stimulation.

The effect of various catecholamine receptor antagonists, which differ in their potency to block central dopamine and noradrenaline receptors, respectively, on ethanol-induced locomotor stimulation was investigated. It was shown that small doses of both specific dopamine (pimozide, haloperidol) and noradrenaline (phenoxybenzamine, yohimbine) receptor blocking agents statistically significantly suppressed the ethanol-induced locomotor stimulation. Of special interest in this study was the observation that remarkably small doses of clozapine completely antagonized the ethanol-induced locomotor stimulation. The possibility that this effect of clozapine is mediated via its interference with the activity of central noradrenaline and/or GABA neurons is discussed.

Adrenergic alpha-Antagonists↗
PubMed1980

Altered response to cessation of nerve impulse flow in dopamine neurons after chronic ethanol administration.

Rats were chronically treated with ethanol for 150 and 270 days, respectively. The influence of chronic ethanol treatment on the activation of tyrosine hydroxylation (measured as the accumulation of dopa after inhibition of amino acid decarboxylase) produced by gamma-butyrolactone (GBL) was studied. It appeared that the ability of GBL to enhance the dopa accumulation was attenuated in rats subjected to ethanol, thus indicating that subsensitivity will develop at or beyong GABA receptors following chronic ethanol treatment. Preliminary findings concerning the effects of chronic ethanol administration on dopamine autoreceptor sensitivity are also reported.

4-Butyrolactone↗
PubMed1979

Attenuation of the gamma-butyrolactone-induced increase in DOPA accumulation by chronic ethanol administration.

The effect of gamma-butyrolactone (GBL) on the accumulation of dopa after inhibition of aromatic amino acid decarboxylase was studied in rats following chronic treatment with ethanol. The GBL-induced dopa accumulation was significantly decreased in ethanol-treated rats. With the increased duration of the ethanol treatment this effect appears to be more marked in the limbic forebrain. It is suggested that chronic ethanol treatment may produce a decreased sensitivity of central GABA receptors.

4-Butyrolactone↗
PubMed1979

The effect of chronic ethanol administration on central neurotransmitter mechanisms.

Rats were maintained on ad lib food and a forced-intake regimen of ehtanol for up to 270 days. The ethanol treatment induced alterations in the metabolism of central catecholamines seen as increased endogenous concentrations of dopamine concomitantly with decreased concentrations of noradrenaline in the limbic forebrain. The synthesis of catecholamines, measured as the accumulation of dopa following inhibition of aromatic amino acid decarboxylase, was unchanged during chronic ethanol treatment. Local application of dopamine into the nucleus accumbens caused a greater increase in locomotor activity in chronic ethanol rats than in controls thus indicating that chronic ethanol treatment increased the sensitivity at or beyond central dopamine receptors. This phenomenon of functional dopamine receptor supersensitivity was first observed after 5 months of ethanol treatment and lasted for about 4 weeks after cessation of the ethanol treatment. The sensitivity of noradrenergic and cholinergic receptor mechanisms appeared to be unchanged after chronic exposure to ethanol. The effect of the GABAergic drug, gamma-butyrolactone (GBL) on the accumulation of dopa after inhibition of aromatic amino acid decarboxylase was studied in chronic ethanol rats. The enhancement of the dopa formation in dopaminergic neurons induced by GBL was markedly attenuated after chronic ethanol treatment. The gross behavioural depression by GBL was also weakened. This may indicate that chronic ethanol treatment causes subsensitivity of GABA receptors.

4-Butyrolactone↗
PubMed1978

Noradrenaline receptor sensitivity after chronic ethanol administration.

The effects of the central noradrenaline receptor stimulating agent clonidine on blood pressure, heart rate, and flexor reflex activity were studied in intact rats and in rats chronically treated with ethanol. The clonidine-induced changes were similar in ethanol-treated animals and in animals never subjected to ethanol. The results suggest that the sensitivity of central noradrenaline receptors involved in the mediation of the circulatory changes and of the flexor reflex activity after clonidine is not altered by chronic administration of ethanol.

Animals↗
PubMed1978

Changes in the sensitivity of dopamine receptors in the nucleus accumbens and in the striatum induced by chronic ethanol administration.

Rats of the Sprague-Dawley strain were maintained on ad libitum food and a forced-intake regimen of ethanol for up to 270 days. Bilateral application of dapamine (DA) into the nucleus accumbens of both chronic ethanol rats and rats undergoing withdrawal produced a pronounced increase in coordinated locomotor activity which was 8--10 times higher than that of untreated water control rats. This phenomenon was first observed after 5 months of ethanol treatment and lasted for about 4 weeks after cessation of the treatment. It is concluded that prolonged ethanol administration produces an increased sensitivity of the DA-receptors in the nucleus accumbens and further supports the contention that central catecholamine mechanisms are involved in the mediation of the withdrawal syndrome observed after chronic treatment with ethanol.

Aging↗
PubMed1977

Behavioral changes after chronic ethanol treatment.

Rats were maintained on ad lib food and a forced-intake regimen of ethanol for up to 270 days. Termination of the long-term ethanol treatment caused two types of withdrawal syncromes. The first, an acute withdrawal syndrome was observed within 12 hr after the discontinuation of the ethanol treatment and was characterized by extreme hyper-excitability. The second, a delayed withdrawal syndrome was characterized by a more coordinated behavioral stimulation and developed first after about 3 days after the discontinuation of the ethanol treatment. Bilateral application of dopamine (DA) into the nucleus accumbens of both chronic ethanol and ethanol rats undergoing withdrawal produced a pronounced increase in coordinated locomotor activity which was 8-10 times higher than that of untreated water control rats. This phenomenon was observed first after 5 months of ethanol treatment and lasted for about 4 weeks after the termination of the treatment. This effect of DA was antagonized by haloperidol indicating a specific effect on DA-receptors. It is concluded that prolonged ethanol administration produces an increased sensitivity of the DA- receptors in the nucleus accumbens and further supports the contention that central catecholamine mechanisms are involved in the mediation of the withdrawal syndrome observed after long-term treatment with ethanol.

Alcoholism↗
PubMed1977

The effect of chronic ethanol treatment on behaviour and central monoamines in the rat.

Rats weaned at 16 days of age were treated with various ethanol concentrations (8--24% w/v) for 270 days. The effect of the chronic ethanol treatment on the growth rate, the diurnal pattern of drinking, the open field activity, and the conditioned avoidance acquisition and retention of the rats were studied. Termination of the chronic ethanol administration caused two types of withdrawal syndromes. The first, an acute withdrawal syndrome was observed within 12 h after the discontinuation of the ethanol treatment and was characterized by extreme hyperexcitability. The second, a delayed withdrawal syndrome was characterized by a more coordinated behavioural stimulation and developed first after about 3 days after the discontinuation of the ethanol treatment. Biochemically, the latter withdrawal syndrome was accompanied by an increased rate of tyrosine hydroxylation (measured as the accumulation of dopa after inhibition of aromatic amino acid decarboxylase) in the striatum and dopamine-rich limbic structures. No differences in the accumulation of 5-hydroxytryptophan were observed. Furthermore, there was an increased level of dopamine concomitant with a decreased level of noradrenaline in the limbic areas during ongoing ethanol treatment. On the 4th day after withdrawal of ethanol the endogenous levels of dopamine and noradrenaline were statistically significantly reduced in the limbic structures. The data of the present study indicate that chronic ethanol administration induces various kinds of behavioural changes and that these changes at least partially are mediated via central catecholamine mechanisms.

Animals↗
PubMed1976

The effect of long-term ethanol treatment on the sensitivity of the dopamine receptors in the nucleus accumbens.

The effect of local application of dopamine into the nucleus accumbens on locomotor activity was studied in rats during and after withdrawal of long-term ethanol treatment. The bilateral application of dopamine into the nucleus accumbens of both the ethanol and withdrawal rats produced a pronounced increase in coordinated locomotor activity, which was 8-10 times higher than that of untreated water control rats. This effect of dopamine was antagonized by intraperitoneally administered haloperidol indicating a specific effect on dopamine receptors. It is concluded that prolonged ethanol administration may produce an increased sensitivity of the dopamine receptors in the nucleus accumbens and further support the contention that central catecholamine mechanisms are involved in the mediation of the withdrawal syndrome observed after long-term treatment with ethanol.

Animals↗
PubMed1975

The effect of long-term penfluridol treatment on the sensitivity of the dopamine receptors in the nucleus accumbens and in the corpus striatum.

The effect of local application of dopamine to the nucleus accumbens or corpus striatum on locomotor activity was studied in rats 4 days after withdrawal from a 6 weeks term of penfluridol medication. The bilateral application of dopamine into the nucleus accumbens of penfluridol-treated rats produced a very marked increase in coordinated locomotor activity which was 3-5 times higher than that of rats not treated with penfluridol. This effect of dopamine in both penfluridol-treated and control rats was antagonized by intraperitoneally administered haloperidol. The bilateral application of dopamine into the corpus striatum of penfluridol-treated animals produced a marked stereotyped behavioural syndrome in all rats studied, whereas no signs of stereotyped behaviour were observed in any of the rats not treated with penfluridol. The results indicate that long-term treatment of rats with the dopamine receptor blocking agent penfluridol produces an increase in the sensitivity of the dopamine receptors in the nucleus accumbens and corpus striatum and that the nucleus accumbens may play a role in locomotor activity.

Animals↗