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Biomedical subjects

Z S Herman

Publications and source records attributed to Z S Herman.

At least 181 records · Page 10Linked to original sources

Behavior of rats during one-year administration of fluphenazine and subsequent withdrawal period.

During one-year administration of fluphenazine [FLU], 1 or 5 mg/kg/d ip. two phases in the behavior of rats were observed. During the first four months of treatment the locomotor and exploratory activities were depressed, while during the following months the reversal of this phenomenon was observed, and the activity of FLU-treated rats increased, particularly in the open-field test. The irritability of rats showed a triphasic change during one year treatment with 5 mg/kg/d FLU. Catalepsy declined with the increase in length of treatment and dose of FLU during the first three months of experiment. During the first 2 weeks of FLU withdrawal the locomotor and exploratory activities and irritability of rats increased. The behavioral differences between controls and FLU-pretreated rats were observed between the 6th and 8th day of withdrawal period. The results demonstrated the occurrence of multiphasic changes in the behavior of rats during one year administration of FLU and after its withdrawal. They warrant further studies on the central nervous system reactivity during a prolonged neuroleptic therapy and after its cessation in man.

Animals↗

Behavioral effects of two dipeptides: L-phenylalanyl-L-arginine (Phe-L-Arg) and L-phenylalanyl-D-arginine (Phe-D-Arg) injected into the striatum or substantia nigra of rats.

Behavioral effects of two dipeptides: L-phenylalanyl-L-arginine (Phe-L-Arg) and L-phenylalanyl-D-arginine (Phe-D-Arg) on rat behavior after intrastriatal or intranigral injections were investigated. The L-L diastereoisomer of dipeptide (10-100 nmol) did not change the behavior while the L-D diastereoisomer induced clonic convulsions. Pretreatment by naloxone in a dose of 2 or 5 mg/kg prevented this effect. It is suggested that Phe-D-Arg might act via opioid receptors in nigrostriatal system.

Animals↗

Antinociceptive and behavioral effects of leu-enkephalin (LENK) or D-Ala2-met-enkephalinamide (DAMEA) in rats after central chemical sympathectomy or serotoninectomy.

In rats with central chemical sympathectomy induced by two injections into the lateral brain ventricle (icv) of 250 micrograms of 6-hydroxydopamine or with central chemical serotoninectomy induced by 75 micrograms of 5,6-dihydroxytryptamine icv the antinociceptive and behavioral effects of LENK (200 micrograms icv) or DAMEA (10 or 20 micrograms icv) were examined. The chemical lesion of central noradrenaline or dopamine neurons or specific lesion of serotonin neurons abolished antinociceptive effects of LENK and DAMEA. Both peptides inhibited exploratory activity of rats. Central chemical serotoninectomy but not sympathectomy reversed some behavioral effects induced by LENK and DAMEA. These results suggest modulatory influence of the central noradrenaline and serotonin neurons in the antinociceptive mechanism of action of enkephalins and the participation of the central serotonin neurons on the behavior of rats induced by enkephalins.

5,6-Dihydroxytryptamine↗

Antinociceptive effects of puromycin and bacitracin.

The aim of this paper was to examine if puromycin (PUR) and bacitracin (BAC) which delay the degradation of enkephalins (ENK) in vitro by the inhibition of aminopeptidases activity, may induce antinociceptive effects. Male Wistar rats were used. PUR in a dose of 100, 200 or 400 micrograms or BAC in a dose of 10, 25, 50 micrograms were administered intracerebroventricularly in conscious animals. As an antagonist of ENK, naloxone (NAL) was used in doses of 1, 5, 10 or 20 mg/kg ip. Antinociceptive effect was measured by the method of hot-plate. The level of ENK in the striatum was examined by biological method using mice vas deferens. PUR induced the dose-related analgesic effect abolished by NAL and increased the level of ENK in the striatum. BAC also elicited the dose-related antinociceptive effect and the increase of striatal concentration of ENK. But antinociceptive effect of BAC was not antagonized but potentiated by NAL. Moreover BAC evoked abnormal behavior of rats, namely the episodes of catalepsy and of barrel rotation. It is concluded that: PUR, but not BAC, is a useful pharmacological tool for the aminopeptidase inhibition and for activation of enkephalinergic neurons; aminopeptidases are concerned with activities of opioid peptides.

Analgesics↗

Rapid test for screening of narcotic analgesics in mice.

50 microliter of a solution of 0.35 N NH4OH containing 2.325% EDTA and 0.837% NaCl injected intradermally in mice elicited reproducible short term behavior typical for nociceptive stimulus. This behavior was inhibited specifically by narcotic analgesics. This procedure may be used as a specific test for screening and for dose--effect studies of narcotic analgetic drugs in mice.

Analgesics, Opioid↗

Behavioral effects of apomorphine during development of rats.

The behavioral effects of apomorphine in a dose of 1.5 mg/kg i.p. were studied in male Wistar rats at the age of 3,4,6 weeks and 3,5,6 months. Behavioral features typical for apomorphine were observed in rats from the 6th week of life. It is concluded that maturation of central dopaminergic receptors in rats occurs at about 6th week of life.

Age Factors↗

The effect of certain neurotransmitters on the analgesic action of enkephalinamide.

The effect of noradrenaline, dopamine, acetylcholine and 5-hydroxytryptamine on the analgesic action of enkephalinamide was studied and it was demonstrated that catecholamines and acetylcholine potentiated the analgesic action of enkephalinamide, while the effect of serotonin varied depending on the dose used. These results suggest that catecholamines, acetylcholine and 5-hydroxytryptamine can modulate the analgesic action of enkephalins.

Acetylcholine↗

Effect of stimulation or inhibition of muscarinic or nicotinic receptors on the content of biogenic amines in various parts of rat brain.

For studying the interactions of the cholinergic and noradrenergic systems in the central nervous system rats were given muscarine or nicotine and the peripheral receptors were blocked with atropine or pempidine. After killing the animals the level of biogenic amines was determined in various parts of the brain. Evident changes were found in the levels of biogenic amines after stimulation or blockade of muscarinic or nicotinic receptors.

Animals↗