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R C Schnell

Publications and source records attributed to R C Schnell.

72 records · Page 4Linked to original sources
PubMed1977

Effect of acute and chronic morphine treatment on serotonin uptake into rat hypothalamic synaptosomes.

The effect of morphine on uptake of serotonin into hypothalamic synaptosomes was determined following acute and chronic morphine treatment in the rat. The uptake of serotonin was noncompetitively inhibited by in vitro morphine (IC50 = 7 X 10(-4) M) but not by an acute morphine treatment (30 mg/kg s.c.) which produces hypothermia. Uptake of serotonin into hypothalamic synaptosomes derived from rats rendered tolerant to the hypothermic effect of morphine or rats withdrawn from morphine was not altered either in the absence or presence of in vitro morphine as compared to control rats. These data indicate that alterations in thermoregulatory responses of the rat to either acute or chronic morphine treatment do not result from morphine-induced modification of serotonin uptake into hypothalamic neurons.

Animals↗
PubMed1976

Barbital alteration of central nervous system sensitivity to hexobarbital in the rat.

Alteration in central nervous system (CNS) sensitivity to the hypnotic effect of the hexobarbital was assessed by analytical, electroencephalographic, and pharmacokinetic techniques in barbital-treated rats. Each of these conceptually diverse experimental methodologies yielded similar conclusions concerning the alteration of CNS sensitivity by barbital treatment.

Animals↗
PubMed1976

Studies relating morphine hypothermia with serotonin reuptake in the rat hypothalamus.

Experiments were conducted to determine if the acute hypothermia elicited by morphine in the rat resulted from morphine-induced inhibition of serotonin reuptake into hypothalamic nerve-endings. The acute hypothermia elicited by morphine (30 mg/kg, s.c.) was reversed by pretreatment with naloxone (10 mg/kg, s.c.), a narcotic antagonist, which alone did not alter body temperature. In vitro uptake of serotonin into synaptosomes prepared from rat hypothalamus was inhibited 53% by the addition of morphine (7 X 10(-4) M) and 53.9% by naloxone (1 X 10(-3) M). Simultaneous addition of both drugs in these same concentrations further inhibited synaptosomal serotonin uptake 77.8%. Uptake of serotonin uptake into synaptosomes isolated from rats injected with morphine (30 mg/kg, s.c.) was not altered as compared to controls. These data suggest that the acute hypothermic acition in morphine in the rat is not related to an inhibition of the serotonin reuptake mechanism in hypothalamic nerve-endings.

Animals↗
PubMed1976

Tolerance development to cadmium-induced alteration of drug action.

Cadmium administration potentiates the duration of hexobarbital-induced hypnosis and inhibits the rate of hepatic microsomal metabolism of this drug in the male rat. The threshold dose of cadmium required to produce these alterations in drug action is 0.84 mg Ck/kg. If subthreshold doses of cadmium (0.21 or 0.42 mg Cd/kg) are administered prior to the 0.84 mg Cd/kg dose, the cadmium-induced alterations in drug action are no longer observed.

Animals↗
PubMed1975

Similarity in cns sensitivity to hexobarbital in the rat and mouse as determined by an analytical, a pharmacokinetic, and an electroencephalographic measure.

Sensitivity of the central nervous system (CNS) to the hypnotic effect of hexobarbital was assessed by analytical, pharmacokinetic, and electroencephalographic techniques in male and female rats and in mice of both sexes by the first two techniques. These experimentally and conceptually diverse measures yielded strikingly similar estimates of CNS sensitivity to hexobarbital which was independent of both species and sex, while well known species ans sex (rat) differences in duration of response to hexobarbital were demonstrated.

Animals↗
PubMedDate not supplied

Sex-related differences in cadmium-induced alteration of drug action in the rat.

3 days after pretreatment of rats of both sexes with cadmium (2 mg/kg, 1.p.) the duration of hypnosis induced by hexobarbital (75 mg/kg, 1.p.) was potentiated in males but not females. Likewise similar treatment with cadmium leads to significant inhibition of the metabolism of hexobarbital by hepatic microsomal enzymes obtained from male but not female animals. These data suggest that there is a sex-related difference in the ability of cadmium to alter drug action in rats.

Animals↗
PubMedDate not supplied

Circadian variations in glutathione-S-transferase and glutathione peroxidase activities in the mouse.

Circadian variations in hepatic glutathione-S-transferase and glutathione peroxidase activities were found in male Swiss-Webster mice maintained under a 12/12 lighting schedule (L: 06.00-18.00 h) for 3 weeks prior to use. Hepatic glutathione-S-transferase activity was significantly elevated during the dark phase as compared to the light phase. The glutathione peroxidase activity, using two different substrates, was biphasic in nature. Using cumene hydroperoxide, the enzyme activity was significantly elevated at 18.00 and 06.00 h; nadirs occurred at 10.00, 14.00 and 22.00 h. Using hydrogen peroxide as the substrate, enzyme activity was greatest at 14.00 and 06.00 h; nadirs occurred at 10.00 and 22.00 h. Glutathione concentration also varied in a circadian manner with peak levels occurring between 06.00 and 10.00 h and the nadir occurring at 18.00 h. These studies have shown that glutathione levels and two enzymes utilizing glutathione as a cosubstrate vary in a similar circadian manner, with the highest values primarily occurring during the dark phase. Thus, these results may have considerable toxicological importance.

Animals↗
PubMedDate not supplied

Tolerance development to cadmium-induced decrease in hepatic oxidative xenobiotic metabolism and cytochrome P-450 content in the male rat.

Cadmium, in dose of 0.84 mg/kg (ip), produces a marked inhibition in hepatic oxidative xenobiotic metabolism which results from a decreased cytochrome P-450 content in the male rat. The inhibitions in microsomal metabolism of aniline, ethylmorphine, or p-nitroanisole were not elicited by the 0.84 mg/kg cadmium dose in rats which had been pretreated (72 hours prior) with a lower dose of cadmium (0.21 mg Cd/kg, ip). Likewise, the decreases in both microsomal cytochrome P-450 content and in microsomal spectral binding of hexobarbital or aniline produced by the 0.84 mg/kg cadmium dose were not elicited in the rats pretreated with the low cadmium dose. The 0.21 mg/kg cadmium dose produced an increase (370%) in the cadmium-binding capacity as well as an increase (395%) in total hepatic metallothionein. These data are consistent with the hypothesis that the pretreatment of animals with relatively low cadmium doses produces an increase in the cellular levels of metallothionein which can then bind and ameliorate the toxicological effects of a subsequently administered toxic dose of cadmium.

Animals↗