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Biomedical subjects

L Turski

Publications and source records attributed to L Turski.

At least 145 records · Page 8Linked to original sources
PubMed1982

Effect of glutamic acid diethylester on (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and kainic acid-induced changes of body temperature in rats.

A low dose (1 microgram) of intracerebroventricularly injected (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) produced a hyperthermic response in rats, while a high dose of AMPA (2.5 micrograms), similarly to kainic acid (0.1 microgram) produced a biphasic effect: short-lasting hypothermia followed by hyperthermia. These effects on body temperature were not affected by pretreatment with 200 mg/kg ip of glutamic acid diethylester (GDEE), which by itself, produced a significant hypothermia. The results indicate that the effects of kainic acid and AMPA on body temperature are not mediated by GDEE-sensitive glutamate receptors.

Animals↗
PubMed1982

Bilateral injection of kainic acid into the rat striatum potentiates morphine, arecoline and pilocarpine but not haloperidol catalepsy.

Bilateral injections of 3 nmol of kainic acid into the rat caudate nucleus potentiated morphine, arecoline and pilocarpine catalepsy but attenuated the cataleptic response to haloperidol. These results confirm the primary importance of caudate nucleus in the appearance of neuroleptic catalepsy and suggest that this nucleus plays an important role in the inhibitory control of cataleptic responses to narcotics and cholinomimetics.

Animals↗
PubMed1982

Convulsant action of pentetrazol in rats with selective lesions of the hippocampal pyramidal cells with intracerebroventricular kainic acid.

Rats were injected uni- or bilaterally with intracerebroventricular kainic acid (0.1 micrograms per one ventricle in a volume of 5 microliters) and the animals were subsequently challenged with penetetrazol (PTZ) on the 21st day after the administration of the neurotoxin. PTZ was given either subcutaneously in a single dose of 70 mg/kg or intraperitoneally, one injection every 48 hours for a total of 15 trials, in doses of 20 mg/kg to induce kindled seizures. It was found that kainic acid-lesioned animals (especially those injected bilaterally) were more sensitive to the convulsant action of PTZ both in acute and kindled convulsions. The disruption of the hippocampal pyramidal projection to the septum may be responsible for these effects.

Animals↗
PubMed1981

Evidence against the involvement of serotonergic mechanisms in wet dog shake behavior induced by carbachol chloride in rats.

The intracerebroventricular administration of carbachol chloride induced a characteristic wet dog shake response in rats. Neither 5,6-dihydroxytryptamine, a serotonergic depletor, nor DL-p-chlorophenylalanine, an inhibitor of 5-HT synthesis, affected wet dog shakes induced by carbachol. Putative antiserotonergic drugs such as cyproheptadine, danitracen and pizotifen antagonized carbachol-induced wet dog shakes, but the 5-HT-receptor antagonist methergoline did not significantly affect the response. These results indicated that carbachol-induced wet dog shakes in rats are probably not related to increased activity of central serotonergic mechanisms. Additionally, the present experiments showed that the anticholinergic properties of the potent serotonergic blockers cyproheptadine, danitracen and pizotifen must be taken into account, and these drugs should be used with care as relatively selective pharmacological tools.

5,6-Dihydroxytryptamine↗
PubMed1981

Studies of carbachol-induced wet-dog shake behavior in rats.

Intraventricular administration of carbachol chloride evoked wet-dog shakes (WDS) in rats in a dose-related manner. WDS induced by carbachol at the dose of 20 microgram were antagonized by scopolamine, atropine, cyproheptadine, morphine, clonidine, phentolamine, haloperidol, and L-5-hydroxytryptophan (5-HTP). Methergoline, propranolol, bicuculline, and aminooxyacetic acid had no effect on carbachol-induced shaking behavior. The present experiments show the existence of different types of shaking behavior, not exclusively related to the stimulation of central 5-HT structures.

Animals↗
PubMed1981

Effects of morphine and nalorphine on kainic acid-induced hypothermia in rats.

Intraventricular administration of kainic acid at the dose of 0.1 microgram induces a significant depression of rectal temperature followed rapidly by its slight elevation. Morphine (40.0 mg.kg-1 IP), which by itself elicited biphasic effect on the body temperature of rats--initially hypothermia followed by hyperthermia--slightly increased the kainic acid-induced hypothermia. Kainic acid did not cause any changes in the hyperthermic effect of low doses of morphine (10.0 mg.kg-1). Pretreatment of rats with nalorphine enhanced the kainic acid-induced hypothermia. On the contrary, nalorphine reversed the hypothermic effect produced by morphine at the dose of 40.0 mg.kg-1. The results suggest that morphine and kainic acid-induced hypothermia are not mediated by the influence on the same type of receptors.

Animals↗
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

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↗