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Biomedical subjects

A Chodera

Publications and source records attributed to A Chodera.

At least 55 records · Page 3Linked to original sources
PubMedDate not supplied

Influence of olanzapine on cognitive functions and catalepsy in rats after single and chronic administration.

The aim of our investigations was to supplement the scarce information about behavioral effects of olanzapine and especially to find out if the effects change during prolonged treatment. It was established that at a dose of 0.5 mg/kg, which did not evoke sedation, olanzapine had distinct anxiolytic effects, both after acute and chronic treatment. Olanzapine improved memory in the maze test (food finding time), but only in chronic experiments after a lag of 14 days. Olanzapine at the dose of 0.5 mg/kg did not cause catalepsy but a higher dose of 1 mg/kg elicited strong sedating effects, which would interfere with the catalepsy test. The results of Porsolt's test (immobility time in swimming rats) were interesting because a shortening of immobility time occurred only after single drug injection. Our results are in agreement with the statement of other authors that olanzapine has greater potency in antagonizing responses mediated rather by 5-HT than D2 receptors.

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Behavioral and memory improving effects of mirtazapine in rats.

These experiments examined the effects of the antidepressant mirtazapine in several behavioral and memory tests. The tests were carried out on male Wistar rats weighing about 200 g. The drugs were injected 30 min before the tests. The aim of the locomotor activity test was to select a dose which had no influence on the motility of the animals and, at the same time, was active at least in one behavioral test. The chosen dose was 2.5 mg/kg. In the two-compartment exploratory test, 2.5 mg/kg of mirtazapine had a distinct anxiolytic effect after the first treatment, after 7 days the effect was weaker but still significant and it disappeared after 14 days. In the forced swimming test, the immobility time was shortened only after 14 days of administering the drug. In the maze test, mirtazapine shortened the food finding time (it improved memory) and counteracted memory loss induced by scopolamine. In the conditioned avoidance responses test (CARs), mirtazapine improved memory only after its earlier impairment by scopolamine. The authors cohclude, contrary to some published data, that after proper dose (adequate for other tests but not for the locomotor activity test), mirtazapine has a distinct memory improving activity or a memory restoring effect after scopolamine treatment.

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PubMedDate not supplied

Reversal of stress-induced memory changes by moclobemide: the role of neurotransmitters.

Studies on animals have shown that chronic stress is able to evoke behavioral changes such as locomotor activity deficit, decreased sleep, reduced food and water consumption and impaired memory. Chronic stress produces changes in concentrations of neurotransmitters, mainly in the hippocampus. The hippocampus is a vulnerable brain structure that is involved in learning and memory functions. In this study, we investigated the effects of chronic stress procedure and moclobemide in rats, and the influence of chronic stress on the levels of monoamines: noradrenaline (NE), dopamine (DA) and serotonin (5-HT) in the rat hippocampus [as well as their metabolites: dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA)]. It was found out that chronic 21-day stress caused worsening of memory: the well trained rats after stress procedure lost their ability to find food quickly. Because of many errors in finding the way, the time these animals needed was on average 2.4-times longer than that of the control group. Single, as well as prolonged (21 days) treatment with moclobemide (10 mg/kg/day) counteracted the deficit of memory induced by chronic stress. In stressed animals, we observed an increase in DA, decrease in DOPAC, 5-HT and 5-HIAA and decrease in NE levels. Moclobemide modulated the changes in the levels of neurotransmitters in the hippocampus, decreasing their turnover. The results demonstrate that moclobemide improves memory impaired by stress. They suggest also that moclobemide has a modulatory effect on stress-induced neurotransmitter changes which may be of importance for the protective effect of the drug with regard to memory impairment.

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Antidepressant effect of carbamazepine--the role of dopaminergic and noradrenergic agents.

Fourteen days of treatment with 20 mg/kg/day carbamazepine (CBZ) reduced the immobility time in the behavioral "despair" test in rats. Two blockers of dopaminergic receptors: haloperidol (0.5 mg/kg) and sulpiride (100 mg/kg) antagonized the reduction of immobility caused by CBZ. The anti-immobility effect of CBZ was also counteracted by clonidine (0.1 mg/kg) an agonist of presynaptic alpha 2 adrenoreceptors and propranolol (5 mg/kg) beta-adrenolytic drug.

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Effects of pethidine on central neurotransmitters: changes in the state of tolerance.

Cerebral concentrations of neurotransmitters: noradrenaline, dopamine, serotonin and GABA were assayed in male Wistar rats receiving either a single dose of pethidine, or a prolonged treatment with the drug (twice daily for 21 days, im), leading to tolerance development. In tolerant rats the GABA content in the cerebral tissue was increased, and the activity of serotonergic system (assessed from the changes in 5-hydroxyindoleacetic acid level and serotonin turnover rate) was augmented.

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Pharmacokinetic disposition of pethidine under tolerance.

Under tolerance, evoked by multiple doses of pethidine (PD), the serum and brain tissue content of PD was related to diminished analgesic activity. Even though in tolerant rats no enhancement of PD biotransformation in the liver could be recognized (as followed by the measurement of hepatic esterase and N-demethylase activity), the amounts of both PD and nor-PD excreted in urine were increased under tolerance. The authors conclude that the faster disposition of PD may contribute to the development of tolerance.

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Cerebral blood flow (CBF) autoregulation in spontaneously hypertensive rats (SHR) during chronic administration of a theophylline derivative (P-23).

Chronic hypertension causes the lower and upper limits of CBF autoregulation to reset to higher blood pressure levels. In the present study we examined whether the theophylline derivative P-23, which had lowered blood pressure in SHR, would influence CBF autoregulation. P-23 (10 mg/kg po) was administered once daily for 4 weeks and tail systolic pressure was measured weekly in this P-23 group and in a control group of SHR. At the end of the treatment period, CBF autoregulation was studied. CBF was determined using the intracarotid 133Xe injection method in halothane/nitrous oxide anesthetised animals. The lower and upper limits of autoregulation were studied in two subgroups of rats by, either raising blood pressure (MAP) stepwise with norepinephrine or lowering MAP stepwise by controlled bleeding and measuring CBF at MAP intervals of 10 mmHg. In the P-23-treated group, blood pressure fell significantly but in the control group, blood pressure increased slightly. The lower part of the autoregulation curve was shifted towards lower pressure in the treated group and the lower limit of autoregulation was significantly different from that in the control. The upper limit of autoregulation was above 180 mmHg in both groups. The beneficial effect of P-23 on CBF autoregulation should be taken into consideration during chronic administration in clinical studies in man.

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Differences in the development of tolerance to various benzodiazepines.

Anticonvulsant, sedative and anxiolytic effects of the following benzodiazepines, administered chronically by the intraperitoneal route, were assessed: nitrazepam (NTZ), diazepam (DZ), oxazepam (OXZ), chlordiazepoxide (CDX) and temazepam (TMZ). The action of NTZ in tests for sedative, anticonvulsant and anxiolytic effects rapidly changed upon a repeated daily treatment, which suggests development of tolerance, while no tolerance developed to such effects of OXZ. The stimulating effect of DZ was found not earlier than after 5 weeks of chronic treatment, but no tolerance to the anxiolytic action was observed, and the anticonvulsant action was even potentiated. The stimulating action and tolerance to the anxiolytic effects of CDX and TMZ developed rapidly, but was accompanied with an only slight decrease in the anticonvulsant effect.

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The effect of dopamine on blood flow in skeletal muscles.

To explain some mechanisms of the peripheral action of dopamine experiments were carried out on anesthetized rabbits in which the blood flow in calf muscles was measured during rest and during evoked twitches, using the method of 133Xe clearance of Lassen et al.; the arterial blood pressure and ECG were simultaneously recorded. Dopamine reduced the blood flow, particularly after a muscular effort. That effect of dopamine was not blocked by the alpha- and beta-adrenoceptor antagonists phentolamine and propranolol, the dopamine receptor antagonist haloperidol, or by the agent blocking sympathetic nerve endings compound BW392C60. Only low doses of dopamine given after propranolol pretreatment caused an increase in the blood flow. Dopamine depressed the arterial blood pressure, particularly the diastolic one. Pretreatment with phentolamine and haloperidol did not antagonize that effect, while pretreatment with propranolol or BW392C60 abolished or reversed the action of dopamine. The depression by dopamine of the blood flow in an important area of skeletal muscles indicates that part of the circulating blood may be shifted to other vascular beds, e.g. to the viscero - renal one.

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PubMedDate not supplied

Development of tolerance to pethidine in rats, pretreated or not, with beta-naphtoflavone or SKF 525 A.

Tolerance to the analgesic effect of pethidine (PD) in rats, treated with a dose of 15 mg/kg of the compound twice daily at 12 h intervals for 1-3 weeks, was assessed using both, heat and current irritating stimuli. Tolerance could be detected earlier by the current irritating method, than by the hot plate technique. Pretreatment with beta-naphtoflavone did only slightly affect the development of tolerance to the antinociceptive effect of PD. In contrast after one week of treatment with SKF 525 A PD retained its analgesic effect. The prolonged pretreatment with SKF 525 A did not prevent the development of tolerance to the analgesic effect of PD.

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PubMedDate not supplied

Pharmacokinetic interaction of psychotropic drugs. I. Divergent effect of mianserin on pharmacokinetics and pharmacodynamics of amphetamine.

Pharmacokinetics of amphetamine and stereotypy caused by this drug was studied after premedication with two doses of mianserin (2 and 10 mg/kg). High doses of mianserin depressed the amphetamine level in blood and cerebral tissue and increased the stereotypy. The results suggest that the potentiation of the action of amphetamine by mianserin is mainly due to pharmacodynamic synergism and depends on the blockade of central serotonergic receptors by mianserin.

Amphetamine↗