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Biomedical subjects

Z Kleinrok

Publications and source records attributed to Z Kleinrok.

At least 217 records · Page 12Linked to original sources
PubMed1981

(RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid: wet dog shakes, catalepsy and body temperature changes in rats.

(RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) was microinjected into the lateral brain ventricle of conscious rats in order to evaluate its pharmacological effects. Microinjection (5 microliter) were made unilaterally and the effects of AMPA were assessed for 6 hr. AMPA produced generalized myoclonic seizures, short lasting hypoactivity followed by hyperactivity and hyperthermia when low doses were injected (0.25-1.0 microgram). When AMPA was injected at higher doses (1.5-5.0 microgram) it produced generalized myoclonic seizures, a hypoactive phase and hypothermia rapidly followed by hyperthermia. As the seizure activity and hypoactive phase receded, AMPA at doses of less than 2.5 microgram produced hyperactivity and wet dog shakes in a dose-related manner. After receiving AMPA at doses of 2.5 and 5.0 microgram, rats developed transient catalepsy. High quantities (5.0 microgram) evoked a spectrum of generalized convulsive seizures lasting for 2-3 hr (1 seizure every 15 min). Biochemical assays showed that AMPA had complex effects on brain aminergic systems. AMPA decreased brain NA while brain DA concentration was slightly increased in a dose dependent manner. Moreover, AMPA increased brain 5-HT and 5-HIAA concentration in a dose- and time-related manner.

Animals↗
PubMed1981

Effects of some antiepileptic drugs in pentetrazol-induced convulsions in mice lesioned with kainic acid.

Mice were injected with intracerebroventricular (i.c.v.) kainic acid (KA; 0.1 micrograms per animal) and the pentetrazol test was carried out on the fifth day after the administration of the amino acid. The following antiepileptic drugs were tested for anticonvulsant activity in mice lesioned with KA: diazepam (0.4 mg/kg), phenobarbital (12.5 and 25 mg/kg), trimethadione (200 and 400 mg/kg), depakine (200 and 400 mg/kg), carbamazepine (10 and 20 mg/kg), lefadol (bromophenylsuccinimide; 20 mg/kg), and acetazolamide (320 mg/kg). All drugs were given intraperitoneally, except for carbamazepine, which was also given orally in doses of 100 and 200 mg/kg. Pentetrazol was administered subcutaneously in a dose of 110 mg/kg, and the animals were subsequently observed for the occurrence of clonic and tonic convulsions within 30 min. The protective effects of diazepam and phenobarbital were significantly reduced in the KA-lesioned animals, while the actions of the remaining anticonvulsants were unaltered. Moreover, a substantial loss of pyramidal cells in the CA 3 field of the hippocampus was noted after i.c.v. injection of KA. It may therefore be concluded that the mechanism of the action of diazepam and phenobarbital are partially dependent on the intact functions of the hippocampal formation.

Acetazolamide↗
PubMed1981

Biochemical consequences of kainic acid injection into the lateral brain ventricle in rat.

Effects of a single intraventricular injection of kainic acid (KA) in a dose of 0.1 microgram per rat on the activity of different brain neurotransmitter systems were investigated. A decreased level of norepinephrine at 3 and 24 h and acceleration of its utilization at 3 h after application of KA were observed. These changes were also accompanied by a decreased level of dopamine at 24 h, increased utilization of dopamine at 3 h, increased levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid at 3 and 24 h, as well as by shortened time of the turnover of 5-hydroxytryptamine. No disturbances in the function of the aminergic systems were noted at 120 h after injection of KA. Lowered activity of glutamic acid decarboxylase in the striatum, hippocampus, hypothalamus and cerebellum was observed at 24 h after administration of KA. At 480 h following application of KA, this lowering persisted in the hippocampus only. The most prominent changes in the level of gamma-aminobutyric were observed at 120 h in the striatum, hippocampus and cerebellum. A decreased level of gamma-aminobutyric acid was found in the striatum and cerebellum at 480 h following injection of KA. The observed changes in the dynamic equilibrium between various neurotransmitter systems may be a consequence of the direct or indirect influence of KA.

Animals↗
PubMed1981

Preliminary investigation on the central action of prostacyclin (PGI2) in rats.

Prostacyclin (PGI2) injected ivc in doses of 25 and 100 micrograms/rat increased body temperature, decreased spontaneous locomotor activity and amphetamine-induced locomotor hyperactivity in Wistar rats, in a dose of 100 micrograms inhibited apomorphine-induced stereotypy and potentiated haloperidol-induced catalepsy. PGI2 in both doses decreased noradrenaline level, in a dose of 100 micrograms it increased the cerebral level of dopamine but did not influence the utilization of these amines in the rat brain. PGI2 in a dose of 100 micrograms also increased the concentration of serotonin, but did not change the cerebral 5-hydroxyindoloacetic acid concentration.

Animals↗
PubMed1981

Effects of morphine, nalorphine and morphine withdrawal on lethal toxicity of intracerebroventricular kainic acid in mice.

The effects of morphine, nalorphine and morphine withdrawal on intracerebroventricular kainic acid (0.1 and 0.2 micrometers) lethal toxicity were examined. Morphine (40 mg/kg) potentiated the lethal effect of a low (0.1 micrometer) but not that of a higher dose (0.2 micrometer) of kainic acid. Nalorphine (20 mg/kg) did not affect the toxic action of kainic acid. The mice during morphine withdrawal were very sensitive to the lethal effects of both doses of the amino acid. Kainic acid toxicity seems to be closely related to the functional state of the opiate system. Moreover, it seems that in tolerant animals a supersensitivity of glutamatergic receptors is likely to occur.

Animals↗
PubMed1980

Effects of kainic acid on body temperature of rats: role of catecholaminergic and serotonergic systems.

Intraventricular (IV) administration of doses of 0.1 microgram kainic acid caused diphasic effects on the body temperature of rats--initially hypothermia, rapidly followed by hyperthermia. Pretreatment of rats with 6-OHDA effectively blocked the hypothermic and significantly increased the hyperthermic effects of kainic acid. The hyperthermic effect of kainic acid was reversed in the 5,6-DHT- and dorsal raphe-lesioned rats. However, the electrolytic lesion of the medial raphe nucleus did not cause any changes in the thermic activity of kainic acid. The thermic effects of kainic acid injected IV appear to be dependent on the balance between serotonergic and catecholaminergic influences on central thermoregulation.

5,6-Dihydroxytryptamine↗
PubMed1980

Effect of dopaminergic and GABA-ergic drugs given alone or in combination on the anticonvulsant action of phenobarbital and diphenylhydantoin in the electroshock test in mice.

In the electroshock test--taking hind-limb tonic extension as the end point--apomorphine (10 mg/kg) exerted no effect on the anticonvulsant action of phenobarbital (PB; 20 mg/kg) or diphenylhydantoin (DPH; 8 mg/kg); amantadine (25 and 100 mg/kg) decreased that of DPH, while L-DOPA (500 mg/kg) and d,l-amphetamine (10 mg/kg) potentiated the action of both anticonvulsants. Fluphenazine (4 mg/kg) had no influence on the effects of the two anticonvulsants, but haloperidol lessened that of DPH. All GABA-ergic stimulants used, i.e., gamma-hydroxybutyric acid (GHBA/250 mg/kg), baclofen (2.5 and 10 mg/kg) and aminooxoacetic acid (AOAA; 15 and 20 mg/kg) potentiated the action of PB; the action of DHP was unaffected by these drugs except for AOAA (20 mg/kg). The combined treatment with dopaminergic and GABA-ergic stimulants, being ineffective in terms of anticonvulsant activity, resulted in a marked potentiation of the action of the anticonvulsants tested in this study. The most distinct potentiation was noted in the case of PB, baclofen (1 mg/kg), and amantadine (25 mg/kg).

Amantadine↗
PubMed1980

Central action of intraventricularly-injected midodrine in rats.

The aim of the present paper was to investigate the effect of intracerebroventricular (i.v.c.) injections of midodrine on the central nervous system of the rat. It was shown that midodrine increased locomotor activity, decreased body temperature, increased sedation in reserpinized rats and the cataleptic effect of haloperidol. Midodrine enhanced amphetamine-stimulated locomotor activity and reduced the amphetamine and apomorphine sterotypy. Phenoxybenzamine, yohimbine and clonidine inhibited the midodrine-induced hyperactivity. Midodrine depressed the whole brain noradrenaline (NA) and dopamine (DA) concentrations and reduced NA turnover. The results suggest a stimulating action of midodrine on the catecholaminergic neurons.

Animals↗