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C K Erickson

Publications and source records attributed to C K Erickson.

At least 55 records · Page 3Linked to original sources
PubMed1988

A device for the sustained release of nicotine in the mouse.

A subcutaneously-implantable reservoir for the sustained release of nicotine in mice is described. The device, dubbed INRm to differentiate it from an earlier Implantable Nicotine Reservoir for Rats (INRr), is a small glass cup sealed with Silastic polymer. Three sizes are described, which release 0.75-2.05 mg of nicotine per 24 hours. When implanted into mature CD-1 female mice, the largest device produces blood nicotine levels of 445 ng/ml, which remain relatively stable for at least 19 days. These blood nicotine levels produce no weight loss and minimal body temperature reduction over the time period of testing. INRms, like the INRr, are nontoxic, reproducible, inexpensive, and adaptable for behavioral, pharmacological, and toxicological studies of nicotine in mice.

Animals↗
PubMed1987

Effects of exercise and ethanol on liver mitochondrial function.

Rates of ADP stimulated respiration for various substrates were determined in mitochondria isolated from the livers of female Sprague-Dawley rats following 8 weeks of treatment with daily swimming, ethanol consumption, or both. All rats were fed an American Institute of Nutrition (AIN) type liquid diet with the ethanol treated rats receiving 35% of the calories as ethanol. Chronic exposure to ethanol depressed both state 3 respiration with glutamate as a substrate and cytochrome oxidase activity. Respiratory control ratios and P:O ratios, however, were unaffected by the ethanol exposure. Exercise alone had no effect on hepatic mitochondrial function. There were also no significant alterations in oxidative function of hepatic mitochondria from rats which were endurance-trained by swimming while receiving the ethanol diet. This lack of alteration in mitochondrial function was in spite of the fact that these rats consumed an identical amount of ethanol as those which incurred mitochondrial dysfunction. These results indicate that regular exercise has the potential to attenuate the ethanol induced decline in hepatic mitochondria.

Animals↗
PubMed1986

Cytotoxicity of ethanol in primary cultures of rat midbrain neurons.

Primary cultures of midbrain neurons were obtained from 15-day-old rat fetuses. Neuron cultures were exposed to ethanol (27 mM, 43 mM and 120 mM) for 24 h and evaluated by light microscopy, a viability measure, and protein content. Ethanol concentrations of 43 and 120 mM appeared to affect the cultures both in terms of cell viability and protein. This effect was independent of any osmotic effect, when sucrose was run as a control. We conclude that primary cultures of midbrain neurons are sensitive to relatively low concentrations of ethanol, compared to cell culture preparations used by other investigators.

Animals↗
PubMed1986

Central cholinergic correlates of low dose ethanol-induced locomotor stimulation.

Brain area levels of acetycholine and choline plus the turnover rate of acetylcholine were measured in three strains of rats given low, locomotor-stimulating doses of ethanol. Maudsley reactive (MR/N), Sprague-Dawley, and randomly bred MR/N (MRrb) rats were killed by microwave irradiation and cholinergic function was measured by gas chromatography/mass spectroscopy methods. The results show that the MR/N strain (2 and 5 months old), which elicits enhanced locomotor stimulation after low doses of ethanol, also demonstrates significant increases in cholinergic function at the time of behavioral stimulation. However, after locomotor stimulation, cholinergic parameters returned to normal in these animals. Strains which do not show enhanced locomotor activity after ethanol did not demonstrate significant central cholinergic changes. We conclude that central cholinergic function is related to behavioral stimulation elicited by low doses of ethanol in the MR/N rat strain but not other strains.

Acetylcholine↗
PubMed1983

Effects of acute and chronic administration of antidepressant drugs on the central cholinergic nervous system. Comparison with anticholinergic drugs.

The purpose of this investigation was to study the effects of antidepressant drugs on the central cholinergic system of the rat after acute and chronic administration. Drugs (antidepressants and non-antidepressants) were first divided into highly potent, moderately potent or weak anticholinergic categories based upon the ability of each compound to displace [3H]-QNB [( 3H]quinuclidinyl benzilate from synaptosomal membranes. One antidepressant drug and one non-antidepressant drug, with similar anticholinergic properties, were chosen as representative agents of each category of anticholinergic potency. Acute administration of amitriptyline or atropine (highly potent anticholinergics) increased the level of high affinity uptake of choline in the hippocampus and striatum. Imipramine and thioridazine (moderately potent anticholinergics) increased the uptake of choline only in the striatum. After acute administration, the effects of nomifensine and d-amphetamine (weak anticholinergics) differed on striatal uptake of choline. Following 30 days pretreatment with any drug, an acute challenge dose of that drug no longer altered the uptake of choline in either region. After chronic administration, amitriptyline increased the density of muscarinic receptors in the cortex whereas atropine increased the density of receptors in the cortex, hippocampus and striatum. The other agents did not alter receptor parameters in the regions examined. Since the central cholinergic actions of the antidepressants were similar to the central actions of the non-antidepressants, it is concluded that the effects of the antidepressants on the central cholinergic nervous system are more closely related to the side effects of these agents than to their therapeutic mechanism of action.

Animals↗
PubMed1982

The interaction of endurance running and ethanol on skeletal muscle mitochondria.

This study was designed to measure the interaction of 8 weeks of endurance running and chronic ethanol consumption upon skeletal muscle mitochondria. Male Sprague-Dawley rats were assigned to 1 of 4 groups; ethanol diet sedentary (SED-E), ethanol diet trained (RUN-E), control diet sedentary (SED-E), and control diet trained (RUN-C). The ethanol groups, SED-E and RUN-E, consumed 35% of their calories as ethanol in a liquid diet. The trained groups, RUN-C and RUN-E, ran 5 days/wk for 8 weeks and were running 30 m/min for 90 min/day by the last week. The SED-E group had significantly lower body weights and gastrocnemius-plantaris weights than did the other 3 groups. The left ventricular heart weights showed no treatment effects. Mitochondrial respirations and cytochrome content were significantly depressed in the SED-E group and significantly elevated in the RUN-C and RUN-E groups. Two conclusions can be drawn from these data; (1) the ethanol diet caused a depression in mitochrondrial function of skeletal muscle, in weight gain, and in gastrocnemius-plantaris muscle mass amd (2) an endurance running program offset the deleterious effects of ethanol in all of these areas.

Alcoholism↗
PubMed1982

A new subcutaneously-implantable reservoir for sustained release of nicotine in the rat.

A subcutaneously-implantable reservoir for the sustained release of nicotine is described. The device, dubbed INR for Implantable Nicotine Reservoir, is a small glass cup sealed with Silastic polymer. It releases 3.4 mg of nicotine per 24 hours. When implanted into moderately-sized female Sprague-Dawley rats it produces blood nicotine levels of 400-500 ng/ml which remain relatively stable over at least 18 days. INRs are nontoxic, reproducible, inexpensive, and adaptable for pharmacological and toxicological studies in rats and other small animals.

Animals↗
PubMed1982

The interaction of ethanol and swimming upon cardiac mass and mitochondrial function.

Four groups of female Sprague-Dawley rats received a nutritionally adequate liquid diet formulated for rats. Two groups, one ethanol diet and one control diet swam 6 days/wk for 6 weeks and were designated swim ethanol (SWM-E) and swim control (SWM-C) respectively. Their swimming time increased from 15 min/day on the first day to 2 hrs/day during the final week. One sedentary group received an ethanol diet (SED-E) while another sedentary group received a control diet (SED-C). In the ethanol diet 35% of the calories as ethanol isoenergetically replaced dextrin. The group mean body weights were not different at the end of 6 weeks. The left ventricles of both swimming groups showed similar gains in weight, 13% for the ethanol and 15% for the control. Mitochondrial respiration in the ethanol groups showed a significant depression across substrates and across both pupulations of mitochondria (subsarcolemmal and intermyofibrillar). The swimming-ethanol interaction in the SWM-E group caused an atrophy of the gastrocnemius-plantaris muscle as evidenced by the 13% loss in weight of the muscle. We conclude that chronic ingestion of ethanol will suppress mitochondrial respiration in sedentary and swimming exercised rats, but will not suppress cardiac hypertrophy in the swimming exercised rats. Muscles that are not chronically overloaded by swimming, such as the gastrocnemius-plantaris muscles will undergo atrophy during the swimming protocol of 6 weeks.

Animals↗
PubMed1981

High performance liquid chromatographic analysis of catecholamines in growing and non-growing Tetrahymena pyriformis.

Tetrahymena pyriformis, strains NT-1 and W, harvested in logarithmic (growing) and stationary (non-growing) phases, were found by high-performance liquid chromatography to contain considerable quantities of dopamine. In addition, small amounts of epinephrine and norepinephrine were detected. Logarithmic-phase strain NT-1 cells contained 249 +/- 44 pg dopamine/10(6) cells compared to 477 +/- 42 pg/10(6) cells for logarithmic-phase strain W cells for logarithmic-phase strain W cells. The dopamine content of stationary-phase cells was approximately half the value of the logarithmic-phase cells. There was a significant amount of dopamine in the growth medium from stationary-phase cultures and, to a lesser extent, logarithmic-phase cells.

Animals↗
PubMed1980

Induction of physical dependence on and tolerance to ethanol in rats fed a new nutritionally complete and balanced liquid diet.

Rats offered a nutritionally balanced and complete liquid diet containing 35% of energy as ethanol, 12% as fat, 21% as protein, and the balance as carbohydrate consumed greater than 9 g/kg ethanol after 10 days. Rats displayed signs of physical dependence and tolerance while showing a net gain in weight. Physical dependence was indicated by severe intensity of the following signs during withdrawal from ethanol: Muscle rigidity; tail tremors; caudal tremors; and general tremors. Severity of these signs reached a maximum intensity by 19 h after withdrawal of ethanol. Tolerance was exhibited by chronically treated rats as measured by significantly reduced time off the belt after 7 days. Concentrations of ethanol in blood were documented on selected mornings and were observed to increase. These data suggest that physical dependence and tolerance can be induced through voluntary consumption of ethanol by rats and without nutritional compromises or weight loss.

Alcoholism↗
PubMed1980

Calcium enhancement of alcohol and drug-induced sleeping time in mice and rats.

Calcium injected intracerebroventricularly (IVT) at various times before a hypnotic dose of ethanol significantly enhanced the duration of sleeping time (loss of righting reflex, LRR) in mice and rats. This cation also enhanced the duration of LRR induced by t-butanol and chloral hydrate, but not that induced by sodium pentobarbital. Other cations injected IVT (manganese, cadmium, and zinc) also enhanced ethanol-induced LRR. The synergistic effects of the ionophores X537A and A23187 on calcium-enhanced LRR, and the antagonism of ethanol-induced LRR by EDTA and EGTA suggest the involvement of a membrane-associated calcium pool in the hypnotic effect of ethanol. These studies show the generality of cation enhancement of alcohol-induced sleeping time in mice and rats, and confirm earlier reports which suggested that calcium is involved with the central nervous system depressant effects of alcohols.

Animals↗
PubMed1980

Ethanol dependence produced in rats by nutritionally complete diets.

Nutritionally complete diets formulated according to American Institute of Nutrition guidelines were used to make rats dependent upon ethanol. When intubated with a diet-ethanol solution for four days maintained initial body weight. When forced to consume the solution as the sole source of nutrients and water for nineteen days, rats gained weight. All animals developed severe withdrawal signs as measured by the intensity of tremors and spastic rigidity. The diet ingredients did not alter the absorption of the ethanol. The results demonstrate that physical dependence on ethanol can be induced in the rat without nutritional impairment.

Alcoholism↗
PubMed1980

Subcutaneous silastic implants: maintenance of high blood ethanol levels in rats drinking a liquid diet.

A new subcutaneous form of ethanol exposure in rats is described. The Sustained Ethanol Release Tube (SERT) for rats is similar to an earlier device reported for mice, except that only one refill per day is required. This device, plus an intragastric loading dose for initially raising blood ethanol levels (BEL), is capable of maintaining high BEL for greater than 12 hours. Supplementation of SERT-released ethanol with a Sustacal chocolate-flavored diet with 37% of total energy as ethanol produces high, stable BEL for indefinite periods. Maintenance of such BEL for 9 days is sufficient to cause dramatic withdrawal signs when ethanol exposure is stopped. The method is useful as a model for conveniently and quickly producing physical dependence to ethanol in rats.

Animals↗