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Z Speiser

Publications and source records attributed to Z Speiser.

13 recordsLinked to original sources
PubMed1991

Behavioral and biochemical studies in rats following prenatal treatment with beta-adrenoceptor antagonists.

Increased motor activity and poor performance in the active avoidance test were observed in the offspring of rats treated with dl-propranolol or sotalol during pregnancy, but not with atenolol and d-propranolol. All substances were administered in drinking water from days 8-22 of gestation. A significant increase in the density of muscarinic acetylcholine receptors in the hippocampus was found for dl-propranolol and sotalol, at 35 and 20 days of age, respectively. Twenty-day-old pups born to dl-propranolol-treated rats exhibited a non-significant decrease in the number of beta-adrenoceptors in the frontal cortex. Assuming that all the beta-adrenoceptor antagonists tested had access to the developing fetal brain, the effect of dl-propranolol and sotalol on behavior could stem from central beta 2-adrenoceptor blockade. In view of the lack of behavioral changes after atenolol, a beta 1-selective adrenoceptor antagonist, it is suggested that the clinical use of beta 1-selective adrenoceptor antagonists during pregnancy might be safer for the fetus than beta 2-adrenoceptor antagonists.

Administration, Oral↗
PubMed1991

Different behavioral deficits are induced by anoxia/hypoxia in neonatal and senescent rats: blockade by MK-801.

Rats exposed on their first postnatal day to 100% nitrogen for 25 min developed hyperactivity and lower performance in passive avoidance task during development. Administration of MK-801 (0.5 mg/kg i.p.) 1 h before anoxia or (0.25 and 0.5 mg/kg) 1 h after completely reversed this behavioral impairment. Senescent rats (24-26 months) exposed to hypoxia (92% N2 + 8% O2) for 5 h failed in their performance in C.A.R., 30 days later. Pretreatment with MK-801 (1 mg/kg i.p.) completely reversed this impairment. These data suggest that activation of endogenous NMDA receptors produces different behavioral consequences in neonatal and senescent rats and that MK-801 administration close to exposure of animals to anoxia or hypoxia can prevent such damage, thus preventing behavioral impairments in postnatal as well as in senescent rats.

Aging↗
PubMed1990

Central catecholaminergic dysfunction and behavioural disorders following hypoxia in adult rats.

Wistar male rats, 3-4 months old, were made to breathe for 6 h a sub-lethal hypoxic atmosphere consisting of 8% oxygen and 92% nitrogen. Following this treatment, these rats were subjected to a series of behavioral and biochemical tests starting 30 days and ending at about 180 days after the hypoxic insult. an age-matched control group was subjected to the same series of tests. The following findings were made at the time interval indicated, relative to controls: (1) At 30-35 days, diurnal (3 h) and nocturnal (12 h) locomotor activities decreased by about 25%. (2) At 40-45 days, amphetamine in the dose range of 0.25-1 mg/kg proved less effective in eliciting an increase in motor activity and stereotypic behavior. (3) At about 50 days, apomorphine in the dose range 0.25-0.5 mg/kg caused an increase in stereotypic behavior. (4) At 60-65 days, alpha-methyl-p-tyrosine at the dose of 50 mg/kg caused a more pronounced hypoactive syndrome and a slower rate of recovery of motor activity. (5) At 75-90 days, performance in the active avoidance test was inferior to that of controls. (6) At 180 days, and one hour after a dose of 200 mg/kg alpha-methyl-p-tyrosine, the turnover rates of hippocampal norepinephrine and caudate-putamen dopamine were much below control. One may tentatively conclude that one of the effects of hypoxia in adult rats is a lesion producing long-term behavioral disorders which are partly ascribed to dopaminergic and, possibly noradrenergic, dysfunction.

Age Factors↗
PubMed1989

Tacrine or arecoline mediates reversal of anoxia- or AF64A-induced behavioural disorders in the developing rat.

A 25 min anoxia, or an intracerebroventricular bilateral 2 nmol dose of ethylcholine aziridinium (AF-64A), administered postnatally to male rat pups, elicited on further development of these behavioural disorders, which are partly related to central cholinergic hypofunction. These included a hyperkinetic syndrome and inferior performance in the passive avoidance test. The anoxia-lesioned group but not the AF-64-A-lesioned one, showed an inferior performance in the active avoidance test. Administration of tacrine, an inhibitor of cholinesterase, or arecoline, a cholinergic agonist, in the drinking water to the nursing mothers, at an estimated daily dose of 15 and 10 mg/kg, then directly to the juvenile rats after weaning and until the age of 40 days, partly reversed the effects of anoxia or AF-64A, normalizing the level of locomotor activity and improving performance in passive avoidance, but not in active avoidance. These beneficial effects persisted long after discontinuation of administration of either drug, suggesting that stimulation of spared cholinoceptors in brain at development had prompted the recovery of cholinergic function.

Animals↗
PubMed1989

A benzodiazepine receptor antagonist improves emergence of mice from halothane anaesthesia.

The benzodiazepine receptor antagonist, flumazenil, at a dose of 10 mg/kg given intraperitoneally to mice, had no effect on the minimum air concentration (MAC-50) of halothane causing anesthesia in 50% of the animals and which was 1.0% by volume of the inhaled air. Diazepam, 10 mg/kg, potentiated the effect of halothane. When the mice had been pretreated with diazepam and flumazenil, 10 mg/kg or 20 mg/kg, partial but not complete reversal of the potentiating effect of diazepam was observed, minimum air concentration values being 0.6% after diazepam alone and 0.8% after diazepam and flumazenil. However, mice pretreated intraperitoneally with flumazenil, in the concentration range 1-10 mg/kg, delivered as a solution in polyethylene glycol-Intralipid vehicle or as a suspension in saline, recovered control levels of spontaneous motor activity much faster than in the absence of flumazenil, on emergence from halothane-induced anaesthesia. In this range, the effect was not dose-dependent. These findings suggest that some of the effects of halothane are mediated at the level of the benzodiazepine receptor.

Anesthesia↗
PubMed1988

Behavioral differences in the developing rat following postnatal anoxia or postnatally injected AF-64A, a cholinergic neurotoxin.

Rat pups were submitted postnatally to one of two procedures: a 25-min exposure to 100% nitrogen or an i.c.v. bilateral injection of AF-64A, 2 nmol contained in 1-microliter saline. Throughout further development of either group, their performance in passive and active avoidance tests and in amphetamine-induced stereotype behavior was followed and compared. Both groups exhibited hyperactivity which persisted until 42 days of age in the anoxia group and beyond 120 days in the AF-64A group. Both groups were equally inferior to controls in the passive avoidance test, but only the anoxia group was inferior to controls in the active avoidance test. Amphetamine-induced stereotype behavior was much less pronounced in the anoxia group relative to AF-64A-treated rats or to controls. The results suggest that the lesion induced by the neurotoxin is more specific and less widespread than the one caused by anoxia.

Animals↗
PubMed1978

Changes in brain catecholamine turnover and receptor sensitivity induced by social deprivation in rats.

Catecholamine turnover was compared in two brain areas of rats housed under different social conditions. Rats reared in isolation for 6-8 weeks had a significantly lower noradrenaline turnover in the brainstem and lower noradrenaline and dopamine turnover in a brain segment comprising all other areas except the cerebellum, pineal gland, thalamus, and subthalamus. In the open-field test, isolated rats were much more active than group-housed animals. Noradrenaline turnover increased in both brain areas of isolated rats but not in grouped animals after exposure to the open field. Hyperactivity was selectively reduced in isolated rats by chronic oral treatment with d-amphetamine, 5 mg/kg/24 h. It was also reduced 15 min after pretreatment with alpha-methyl-p-tyrosine 200 mg/kg. It is suggested that a prolonged period of reduced noradrenaline release may sensitise post synaptic receptors in isolated rats. Hyperactivity appears to be associated with an increase in transmitter release onto sensitised receptors.

Animals↗
PubMed1976

Reduction by propranolol of raised urinary output of MHPG in hyperactive rats.

Prolonged isolation of rats resulted in hyperactivity in the open field and a significant increase in 24 hr urinary excretion of MHPG (3-methoxy-4-hydroxyphenylglycol). Exploratory activity of group-housed rats in open field was not associated with raised MHPG excretion, compared with that of rats remaining in home cages. Exposure of group-housed rats to 4 degrees C for 2 hr also increased urinary excretion of MHPG. Pretreatment of isolated rats with dl-, d-propranolol or practolol abolished hyperactivity of isolated rats and reduced MHPG output in these rats and in rats exposed to cold. dl-Propranolol did not reduce activity of group-housed rats in open field or their urinary excretion of MHPG. It is suggested that propranolol may have a selective inhibitory effect on stress-induced increases in noradrenaline turnover.

Animals↗
PubMed1974

Supersensitivity to isoprenaline induced in rats by prolonged isolation.

1 The effect of isoprenaline on diastolic blood pressure and heart rate was determined in anaesthetized male rats which had been housed individually for 6-8 weeks after weaning, and compared with its effect in group-housed litter-mate controls.2 Isoprenaline caused a significantly greater fall in diastolic pressure in isolated rats and a greater increase in heart rate.3 Low doses of noradrenaline (5-10 ng) caused vasodepressor responses in isolated, but not in group-housed rats.4 The pressor response to noradrenaline, which was smaller in isolated rats, was increased to the level of group-housed controls by (+/-)-propranolol.5 Prolonged isolation of rats may bring about an increase in sensitivity of beta-adrenoceptors to isoprenaline and noradrenaline.

Animals↗