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Biomedical subjects

A Bilkei-Gorzó

Publications and source records attributed to A Bilkei-Gorzó.

6 recordsLinked to original sources

mCPP-induced anxiety in the light-dark box in rats--a new method for screening anxiolytic activity.

The activity of anxiolytic and other drugs in a light-dark test situation was studied in rats treated with the anxiogenic compound m-chlorophenyl-piperazine (mCPP). mCPP 0.5 mg/kg significantly diminished the exploratory activity of the animals in the light compartment of the apparatus. Drugs to be tested against mCPP-induced anxiety when studied alone (not in combination with mCPP) did not significantly alter the activity of rats in the light-dark apparatus, except yohimbine, which reduced the movement time values in the lit area. 1,4-Benzodiazepines [diazepam (0.1-4mg/kg) and chlordiazepoxide (2-8mg/kg)], 5-HT2A/2C antagonists [ritanserin (0.25-8 mg/kg) and deramciclane (0.5-8 g/kg)], the 5-HT3 antagonist MDL-72222 (3 mg/kg) and ethanol (2-4 mg/kg) significantly reduced the effect of mCPP. A dose-dependent increase in the exploratory activity of mCPP-treated animals was found in the 2,3-benzodiazepine girisopam (2.5-5 mg/kg)-treated groups. Tofisopam, another 2,3-benzodiazepine molecule, also showed activity against mCPP, although its effect was not statistically significant. The 5-HT1A partial agonist buspirone was also active in the dose range of 0.25-0.5 mg/kg, while the 5-HT1A full agonist 8-OH-DPAT was the only drug with presumed anxiolytic activity that clearly lacked any effect in this model. Imipramine, amitriptyline, morphine, naloxone, haloperidol, clozapine, amphetamine, yohimbine, carbamazepine and diphenylhydantoin were not effective. We conclude that mCPP-induced anxiety in the light-dark box is a potent and useful method for screening and detecting anxiolytic activity of a wide range of compounds with various modes of action.

Animals↗

Some doubts about the basic concept of hole-board test.

Hole board test is a generally used method for screening the potential anxiolytic character of drugs. The test is based on the assumption, that head-dipping activity of the animals is inversely proportional to their anxiety state. We tested this assumption by measuring the head-dipping activity of animals in environments with different levels of aversive character (illumination). The anxiolytic chlordiazepoxide significantly elevated head-dipping activity in moderately aversive environment, it was not active in non-aversive environment, and it exhibited inhibitory activity in highly aversive environment. When the latency of the first head-dip was measured, we found that the proportion of animals with short latency was significantly increased in moderately and highly aversive environments. It is concluded, that the inverse relation between anxiety state and head-dipping activity is true only in a certain range of anxiety level. In more aversive situations, when the anxiety level of the animals is high, the holes nay represent a possible way to escape from the aversive environment instead of an explorable object. In this case the relation between anxiety state and head-dipping activity is directly and not inversely proportional.

Animals↗

Neurotoxic effect of enteral aluminium.

Long Evans rats were treated for 90 days with water-soluble, insoluble or chelated aluminium compounds. The daily treatments given were as follows: controls, NaCl (100 mg/kg body weight) plus citric acid (30 mg/kg); AlCl3 (30 or 100 mg/kg); Al(OH)3 (100 mg/kg) plus citric acid (30 mg/kg); Al(OH)3 (300 mg/kg). Their learning ability was determined in the labyrinth test at day 90, and the choline-acetyltransferase, acetylcholinesterase activity and aluminium content of the brains were measured. Soluble and chelated aluminium compounds seriously worsened the learning ability, and the aluminium content of the brain was elevated. Acetylcholinesterase activity increased and choline-acetyltransferase activity decreased, resulting in a diminished cholinergic activity, which is a characteristic of Alzheimer's disease.

Acetylcholinesterase↗