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Biomedical subjects

W Turski

Publications and source records attributed to W Turski.

At least 19 recordsLinked to original sources
PubMed1992

Age dependency of the susceptibility of rats to aminooxyacetic acid seizures.

Immature rats are more susceptible to clonic seizures induced by aminooxyacetic acid (AOAA) than mature and senile rats. Highest susceptibility to AOAA seizures was observed in 7-14-day-old rat pups. The lowest susceptibility was recorded in 10-20 month-old rats. AOAA seizures in 14-day-old rats were blocked by clonazepam and valproate, but not by phenobarbital, carbamazepine, diphenylhydantoin, trimethadione or ethosuximide. Morphological analysis of brains from 14-day- and 3-month-old rats which experienced AOAA seizures did not reveal epilepsy-related damage. These observations suggest that immature rat brain is highly prone to convulsions induced by AOAA and that such convulsions are difficult to control by available antiepileptic treatment.

Aging↗
PubMed1990

[24-hour fluctuations of the values of certain components of the saliva and dental plaque in school children].

24-hours changes were studied in the saliva and dental plaque of the concentrations of total fluorine, inorganic phosphate and protein, and of pH value. The study was carried out in two groups of school children: I--control, II--subjected to contact fluoridation. The obtained results showed that circadian changes occurred in controls and in children subjected to fluoridation.

Child↗
PubMed1987

Substantia nigra and motor control in the rat: effect of intranigral alpha-kainate and gamma-D-glutamylaminomethylsulphonate on motility.

Bilateral microinjections of an excitatory amino acid, alpha-kainate (KA), 5-50 ng, into the substantia nigra pars reticulata (SNR) result in an increase in the muscle tone and catalepsy in rats. The preferential KA/quisqualate antagonist, gamma-D-glutamylaminomethylsulphonate (gamma-D-GAMS), 10 micrograms, blocks the actions of KA, 25 ng, when coadministered into the SNR. The chemical lesion of the caudate-putamen with 6-hydroxydopamine (6-OHDA) does not affect either increases in the muscle tone or catalepsy produced by KA, 25 ng, from the SNR. The lesion of the caudate-putamen with ibotenate moderately enhances the effect of KA, 25 ng, on the muscle tone. Microinjections of KA, 25 ng, into the substantia nigra pars compacta (SNC) do not increase the muscle tone and lead to significantly less pronounced catalepsy relative to that observed following the injections of KA into the SNR. Unilateral microinjections of KA, 10-50 ng, into the SNR elicit ipsilateral turning in rats in a dose- and time-dependent manner. Unilateral application of gamma-D-GAMS, 1-10 micrograms, into the SNR produces contralateral turning. The turning evoked by KA, 25 ng, or gamma-D-GAMS, 10 micrograms, is affected neither by 6-OHDA nor by ibotenate lesion of the caudate-putamen. These results demonstrate that excitatory neurotransmission in the substantia nigra participates in the regulation of the muscle tone and posture in rats.

Animals↗
PubMed1982

Dyphenylhydantoin enhancement of diazepam effects on locomotor activity in mice.

The interaction of diazepam and diphenylhydantoin on locomotor activity and rearing behavior was studied in mice. Pretreatment of mice with diphenylhydantoin (4.0 and 8.0 mg/kg) significantly reversed the stimulatory effects of low doses of diazepam and considerably increased the depressant effects of the benzodiazepine on locomotor activity and rearing. Neither diazepam (up to 4.0 mg/kg), diphenylhydantoin (8.0 mg/kg) alone, nor combined treatment with both drugs affected brain GABA level and glutamic acid decarboxylase (GAD) activity at any dosage used. The present behavioral and biochemical data suggests that some of the pharmacological effects of diazepam need not be related to GABAergic mechanisms.

Animals↗
PubMed1982

Induction of wet dog shakes by intracerebroventricular bethanechol in rats. Antagonism by neurotransmitter receptor blockers.

Bethanechol chloride, administered intracerebroventricularly, induces a characteristic wet dog shake (WDS) response in rats in a dose-related manner. WDS induced by bethanechol at the dose of 100 micrograms was antagonized by atropine, scopolamine and spiperone (muscarinic cholinergic and dopaminergic antagonists, respectively), whilst metergoline, methysergide, phentolamine, propranolol and bicuculline (serotonergic, alpha-adrenergic, beta-adrenergic and GABA-ergic antagonists) fail to inhibit this effect. The present experiments show that the shaking response may be produced by bethanechol, a potent muscarinic agent administered by the intracerebral route, and suggest that bethanechol-induced shaking behavior in rats may be a useful animal model for delineating agents with antimuscarinic activity.

Animals↗
PubMed1982

The involvement of catecholaminergic mechanisms in the appearance of wet dog shakes produced by carbachol chloride in rats.

Noradrenaline (NA), methoxamine, dopamine (DA), given intracerebroventricularly (ICV), and L-DOPA, administered systemically, significantly blocked wet dog shakes (WDS) produced by carbachol chloride (10 microgram/10 microliter, ICV) in rats. Reserpine, alpha-methyl-p-tyrosine and FLA 63 did not affect WDS, while diethyldithiocarbamic acid depressed it. Aceperone and yohimbine weakened shaking response to carbachol but phentolamine given ICV showed no effect on WDS. Propranolol and isoproterenol administered ICV did not significantly influence WDS. Apomorphine failed to affect WDS induced by carbachol. Pimozide and spiperone were also ineffective against WDS, but amphetamine and metoclopramide efficiently blocked it. Selective depletion of brain NA concentration considerably enhanced WDS, while selective depletion of brain DA concentration failed to affect it. These results suggest that carbachol-induced WDS behavior is under the inhibitory control of noradrenergic neurons.

Animals↗
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↗