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Biomedical subjects

W B Stavinoha

Publications and source records attributed to W B Stavinoha.

At least 37 records · Page 2Linked to original sources
PubMed1979

Involvement of the cholinergic system in the precocious puberty caused by estradiol in immature female rats.

Subcutaneous administration of 0.05 mug estradiol benzoate to sexually immature female rats caused precocious ovulation and a decreased acetylcholine content in the hypothalamus and the amygdala. A higher dose of estradiol benzoate, 2 mug/rat, did not stimulate ovulation but did cause a further decrease in the acetylcholine content in the hypothalamus and the amygdala. The steady state levels of acetylcholine in the hippocampus and the striatum were unchanged with either dose of estradiol. These observations suggest a relationship between the occurrence of ovulation and the decrease in the steady state level of acetylcholine in the hypothalamus and amygdala in sexually immature rats after estradiol treatment.

Acetylcholine↗
PubMed1979

Magnesium deficiency: brain acetylcholine and motor activity.

Deprivation of magnesium ion in the diet caused a significant decrease in whole brain acetylcholine content. At the reginal level, the most pronounced effect was seen in the corpus striatum, diencephalon and cerebellum. The rate of depletion and recovery varied from region to region, and what appeared to be a return to normal acetylcholine in whole brain was the total of regions either higher or lower than control. The data presented here suggest that a positive relationship exists between the lowered cholinergic activity in the corpus striatum and increased nocturnal spontaneous motor activity.

Acetylcholine↗
PubMed1978

Role of neuroleptic agents on mouse pulmonary cyclic nucleotide systems.

The norepinephrine (NE)-induced accumulation of cyclic AMP in incubated tissue slices of mouse lung was inhibited by chlorpromazine (CPZ) and to a lesser extent by haloperidol. In particulate lung fractions both agents blocked dopamine-sensitive adenylate cyclase to a greater degree than the NE-responsive enzyme. Again CPZ was more potent than haloperidol. Acute injections (1/2--8h) of the neuroleptics usually resulted in lower steady state levels of pulmonary cyclic AMP and cyclic GMP following rapid (0.5 sec) tissue inactivation by microwave irradiation. On a subchronic injection schedule, the in vivo levels of pulmonary cyclic AMP tended to increase.

Adenylyl Cyclases↗
PubMed1977

Identification of acetylcholine and propionylcholine in bull spermatozoa by integrated pyrolysis, gas chromatography and mass spectrometry.

Acetylcholine was identified in fertile bull spermatozoa using combined pyrolysis gas-chromatography and mass spectrometry. Bull spermatozoa contain other minor choline esters in smaller quantities than acetylcholine. One of the minor choline esters is possibly propionylcholine. The spermatozoa from infertile bulls exhibited low motility and very low levels of acetylcholine.

Acetylcholine↗
PubMed1977

Regional acetylcholine content in mouse brain after morphine tablet implantation.

Implantation of a 75 mg morphine tablet in mice caused a significant decrease in the body weight and hypothermia. After 3 days, the concentration of acetylcholine decreased in all brain regions with the exception of the cerebellum. A significant decrease in acetylcholine content was observed in the midbrain, corpus striatum and the cerebral cortex 3 days after implantation. It is postulated that the decrease in Ach content is due to an increased release of acetylcholine as a result of development of tolerance to morphine.

Acetylcholine↗
PubMed1976

Use of 300-msec microwave irradiation for enzyme inactivation: a study of effects of sodium pentobarbital on acetylcholine concentration in mouse brain regions.

Microwave irradiation of 6 kw at 2450 MHz for 300 msec was sufficient to completely inactivate mouse brain cholinesterase and choline acetyltransferase. After this method of sacrifice, the acetylcholine contents of mouse brain regions, given in nanomoles per gram, were found to be: striatum, 81; medulla-pons, 44; diencephalon-midbrain, 34; hippocampus, 31; cerebral cortex, 26; and cerebellum, 17. Sodium pentobarbital caused a dose-dependent increase in whole brain acetylcholine. A maximal increase of 81% in whole brain was seen at 15 minutes with 80 mg/kg of sodium pentobarbital. The increase in acetylcholine after sodium pentobarbital treatment was not caused by anoxia from respiratory depression or by hypothermia. All brain regions except the cerebellum exhibited an increase in acetylcholine after pentobarbital treatment. Fifteen minutes after treatment, cerebellar acetylcholine was significantly decreased. However, at the time when half of the animals had regained the righting reflex, the unconscious mice showed an increase in cerebellar acetylcholine which was statistically significant as compared to control. The relative accumulation rate of acetylcholine calculated for cerebral cortex and hippocampus was higher than that for striatum although the absolute rate of accumulation of ACh was higher in the striatum. Thus, after sodium pentobarbital treatment, the cerebral cortex and hippocampus exhibit a greater cholinergic response than the striatum.

Acetylcholine↗