Biomedical subjects
Publications and source records attributed to C J Eriksson.
The activity of a high-Km aldehyde dehydrogenase in the liver cytosol was increased by phenobarbital induction. No corresponding increase in the oxidation rate of acetaldehyde in vivo was found, and it is concluded that cytosolic aldehyde dehydrogenase plays only a minor role in the oxidation of acetaldehyde during ethanol metabolism.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The AT and ANT rat lines, developed by selective outbreeding for differential ethanol-induced motor impairment, were tested for their sensitivity to the hypothermic and narcotic (loss of righting reflex) effects of ethanol. In contrast to the large differences between the lines in their degree of motor impairment, as measured with both the tilting-plane and rotarod tests, only minor differences were observed in duration of loss of righting reflex or hypothermia. Therefore, we suggest that genetically determined factors influencing motor impairment are for the most part dissociated from the factors determining the hypothermic and narcotic effects of ethanol.
After 37 generations, the AA and ANA rat lines developed for high and low voluntary alcohol consumption, were revitalized by crossing with hybrid (Brown Norwegian X Lewis) rats. The line difference in alcohol consumption continued, although initially diminished, after revitalization. The greater acetaldehyde accumulation and longer loss of righting reflex after ethanol administration of the ANAs persisted after revitalization, but significant line differences in motor impairment were no longer found. The line characteristics for open-field test behavior were also different than before revitalization. Of the previously-observed line differences that have now been reexamined, the level of blood acetaldehyde during ethanol metabolism appears to be the most closely related to the genetically-determined factors influencing alcohol consumption.
The plasma or serum concentrations of testosterone, LH, FSH, PRL, cortisol, 17-hydroxyprogesterone, androstenedione, dehydroepiandrosterone, estrone and estradiol were monitored in 8 healthy male volunteers for a period of 48 hr after administration of one large dose of ethanol (1.75 g/kg BW) within the first 3 hr of the experiment. Each subject served as his own control in an identical experiment without ethanol. Blood alcohol concentration reached a maximum of 1.51 +/- 0.08 g/l (mean +/- SEM) 4 hr after the start of drinking. The maximum decrease in serum testosterone was observed at 12 hr when the serum concentrations of gonadotropins were still unchanged. The decrease in serum testosterone persisted at 24 hr despite increases in the serum levels of LH and FSH. The serum or plasma concentrations of PRL, cortisol, 17-hydroxyprogesterone, androstenedione and dehydroepiandrosterone were clearly increased 4 hr after the start of drinking. The increase in serum cortisol lasted as long as the decrease in serum testosterone. No significant changes were found in plasma concentrations of estrone and estradiol. Our results suggest that in addition to direct testicular effects of alcohol, increased adrenal secretion of cortisol may contribute to the decrease in serum testosterone in men acutely intoxicated with ethanol.
The effects of acute ethanol intake (1.5 g/kg) on plasma testosterone and luteinizing hormone (LH) concentrations were examined in male Long-Evans rats. Ethanol decreased the serum LH concentrations by 21% and 42% 30 and 60 minutes after ethanol administration respectively. The testosterone concentrations decreased later (30 min: +8%; 60 min: -30%). The LH concentrations were highly correlated with subsequent (60 min later) testosterone concentrations (LH30min: r = .688, p less than 0.001, n = 25; LH60min: r = .678, p less than 0.001), but less so with concurrent testosterone concentrations (30 min: r = .187, N.S.; 60 min: r = .552, p less than 0.004). To further test the influence of LH, naloxone (11 mg/kg) was administered, which elevated the LH levels within 30 min by 103% in controls. Naloxone also increased serum LH concentration by 34% in ethanol-treated rats at 30 min, but these animals nevertheless had lower (p less than 0.01) testosterone levels at 60 min than did control animals without naloxone and ethanol treatment. It is concluded that although ethanol-induced changes in serum LH levels may play a role in the decrease of serum testosterone concentrations in rats, there are also other mechanisms by which ethanol may produce these effects.
Individual predispositions in emotional reactivity have been suggested as factors involved in the development of alcoholism. To approach this problem, we assessed emotional reactivity in alcohol-naive animals from the alcohol-preferring (AA) and alcohol-avoiding (ANA) rat lines of Alko Ltd. AA rats are known to have higher brain levels of 5-hydroxytryptamine (5-HT) than ANA rats. Emotional reactivity was therefore assessed by an audiogenic immobility reaction (freezing), which is specifically sensitive to and shortened by depletion of 5-HT. The results showed that AA rats of both sexes displayed increased immobility reactions compared to the corresponding sex of the ANA rats. During the period of adaptation to the test cage ANA rats of both sexes showed increased locomotor activity compared to the corresponding sex of the AA rats. Levels of plasma corticosterone did not differ between the rat lines, either during resting or stressful conditions. The present results suggest that a passive, inhibited style of defensive behavior is associated with a high alcohol consumption.
Several studies report that rats exposed to stressful conditions may increase their ethanol consumption. Stress is accompanied by a rise in the secretion of adrenocortical hormones, and the possibility that these hormones exert an influence on ethanol consumption should be considered. The present investigation addressed this issue by studying the effect of adrenalectomy (ADX) and subsequent corticosterone (CORT) or aldosterone (ALDO) treatment on ethanol intake. The results showed that ADX rats decreased their ethanol intake compared to the sham-operated controls and that treatment with CORT restored the intake of ethanol to the preoperative level. In contrast, treatment with ALDO (0.25 or 0.75 mg/kg) had no effect on ethanol intake. Biochemical analyses showed increases in monoamine turnover in the brain stem and limbic forebrain after ADX. The reduction of ethanol consumption caused by ADX may thus be specifically attributed to the loss of one of the adrenal hormones, CORT. The results indicate that CORT may be a factor of importance in the modulation of alcohol consumption.
This study determined the relationship between ethanol intake and spontaneous and amphetamine-induced locomotor activity. Locomotion was studied in high-preferring (HP; > 70% of total fluid intake consumed as alcohol) and low-preferring (LP; < 20% of total fluid intake consumed as alcohol) male Wistar rats with free access to water and a 6% (v/v) ethanol solution for 3 weeks. Following an alcohol-free 3-week period, the animals were tested for spontaneous motor activity for 1 h. One week later, locomotion was recorded in the same activity boxes following a subcutaneous injection with d-amphetamine sulfate (1 mg/kg). For determination of plasma levels of corticosterone, blood samples were taken immediately after each of the two tests for locomotor activity. There was no difference between HP and LP rats with regard to spontaneous locomotor activity. Neither were there any differences in plasma levels of corticosterone between the groups. Amphetamine stimulated locomotion in both HP and LP rats, but to a significantly greater extent in HP animals. Both groups had higher blood levels of corticosterone after the amphetamine test than after the drug-free test, but the corticosterone increase was significantly larger in the HP than in the LP rats. These data indicate that the same neural substrate (e.g., the mesocorticolimbic dopamine system) may mediate important aspects of both ethanol drinking and amphetamine responsiveness. Individual differences in the properties of this substrate may account for the finding that ethanol drinking and amphetamine responsiveness covary. A possible explanation for this association may be that prior consumption of ethanol sensitizes the neural substrate responsible for amphetamine-induced hyperactivity.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study investigated the influence of early weaning and separation from mother and littermates on voluntary ethanol intake and general activity during prepuberal age, and adult age corticosterone levels. On day 16 after birth the male offspring of a litter were divided in three groups, each subjected to a different rearing condition: 1)early weaned and isolated from its littermates; 2) early weaned but growing up together with two littermates; 3) staying with mother and two littermates. On day 25 the animals were tested for general activity including assessment of fearfulness. From day 30 all animals were given a free choice between water and ethanol solution. The ethanol concentration was increased by 2% during each of the following weeks until 10% was reached during the 5th week. Ten days later, after cessation of alcohol testing, blood samples were taken from the tail for assessment of plasma levels corticosterone. The isolated, early weaning pups displayed higher activity levels than both normally reared pups and group-living, early weaning pups. The quotient peripheral locomotion/total locomotion was lower for the isolated pups compared with the other groups, suggesting less fearfulness in the early weaned, isolated pups. For 2%, 4%, and 6% ethanol solutions the normal-reared rats consumed more ethanol and displayed higher ethanol preference than either of the early weaned groups of animals. No group differences were observed either at 8% or 10% ethanol solutions. Levels of plasma corticosterone in adult age in the early weaned rats were slightly reduced, not reaching statistical significance, compared to the normally weaned animals.