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L Velísek

Publications and source records attributed to L Velísek.

At least 55 records · Page 3Linked to original sources
PubMed1993

Reduced susceptibility to seizures in carbonic anhydrase II deficient mutant mice.

The seizure susceptibility of carbonic anhydrase II (CA) deficient mice and their normal littermates was determined and compared. In flurothyl-induced seizures, CA deficient mice displayed longer latencies to the onset of both clonic and tonic-clonic seizures. In pentylenetetrazole-induced seizures mutant mice exhibited a lower incidence of clonic seizures than did their normal littermates. Acetazolamide (a CA blocker) was used for the pretreatment of normal mice to compare them to CA deficient littermates. The pretreated mice displayed a lower incidence of flurothyl-induced tonic-clonic seizures and of both types of pentylenetetrazole seizures. The attempts to elicit audiogenic seizure did not reveal any difference between normal and mutant littermates. However, when the mice were primed by a loud sound during the critical period and retested for audiogenic seizures again at age 1.5 months, the CA deficient mice displayed a significantly lower incidence of seizures. The similarity between the anticonvulsant action of CA deficiency and the anticonvulsant action of acetazolamide suggests an important role of CA in seizures. The exact mechanism of anticonvulsant action by CA inhibition, however, remains to be elucidated.

Acoustic Stimulation↗
PubMed1992

N-methyl-D-aspartate (NMDA)-induced seizures in developing rats.

Intraperitoneal administration of N-methyl-D-aspartate (NMDA) elicited epileptic motor seizures in developing rats aged from 7 to 25 days as well as in young adults. The very first sign of NMDA action is locomotor hyperactivity which is followed by clonic and tonic seizures. In rat pups during the first 3 postnatal weeks flexion seizures (emprosthotonus) appeared as the first pattern of motor seizures; later they were replaced by generalized tonic clonic seizures. Only regular tonic-clonic seizures were observed in 25-day-old and adult rats. The youngest animals are the most sensitive to NMDA. CD50 for tonic-colonic seizures is 6.7 mg/kg in 7-day-old rat pups and it increases up to 86.6 mg/kg in 25-day-old animals. Similar changes could also be demonstrated for LD50, a lethal outcome being very frequent. EEG recordings demonstrated mainly suppressed activity, thus exhibiting a lack of correlation with motor phenomena.

Aging↗
PubMed1992

Differential effects of naloxone on postictal depression.

The influence of naloxone on the duration of the postictal depression was determined in 2 seizure models in the adult rats: hippocampal afterdischarges and maximal electroshock. For testing the intensity of postictal depression 2 subsequent stimulations were used. The interstimulation intervals were 3, 5, 10 and 60 min. Using interstimulation intervals 3, 5 and 10 min there was marked depression of the afterdischarge duration. Wet dog shakes accompanying hippocampal afterdischarges were suppressed only in 3- and 5-min intervals. Naioxone (1 mg/kg i.p.) abolished the suppression of afterdischarges when 10-min interstimulation interval was used. In maximal electroshock seizures where the duration of tonic flexion and extension was determined, no postictal depression was registered nor were any effects of naloxone present. The results suggest a limited role of the mu opioid receptor system in the late phases of postictal depression following hippocampal stimulation and different effects of the mu opioid system in tonic flexion/extension and behavioral depression induced by maximal electroshock.

Animals↗
PubMed1991

Excitatory amino acid antagonists and pentylenetetrazol-induced seizures during ontogenesis. II. The effects of MK-801.

MK-801 is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist with anticonvulsant and neuroprotective properties. The action of MK-801 (0.05-10 mg/kg IP) was assessed against pentylenetetrazol-induced seizures (PTZ; 100 mg/kg SC; 30 min after MK-801) in rats aged 7, 12, 18, 25, and 90 days (N = 263). We observed pronounced ataxia and hypermobility after MK-801 pretreatment during the whole ontogenesis, and the animals exhibited head-weaving and body-rolls. After the combination of MK-801 and PTZ "wet dog shakes" were detected in 18-, 25-, and 90-day-old rats (never seen in controls receiving PTZ only). MK-801 only insignificantly modified the latencies of minimal (clonic) seizures in 18-day-old and older rats where this seizure type is regularly elicited. In 12-day-old rats an increased incidence of minimal seizures was detected. MK-801 nearly completely blocked or strongly delayed major (generalized tonic-clonic) seizures and attenuated the seizure severity during ontogenesis in a dose-dependent manner. Present results suggest the important role of NMDA receptors in the genesis of generalized tonic-clonic seizures whilst the role of NMDA receptors in minimal seizures appears to be negligible during the whole ontogenetic development.

Aging↗
PubMed1991

Bicuculline-induced neocortical epileptiform foci and the effects of 6-hydroxydopamine in developing rats.

Catecholamines (dopamine and norepinephrine) are considered to be predominantly inhibitory neurotransmitters in the brain and their depletion produced by 6-hydroxydopamine may result in proconvulsant effects. In our experiments on rats aged 5, 7, 9, 12, 15, 18, 25 and 90 days under urethane anesthesia we demonstrated the development of neocortical epileptic focus evoked by topical application of bicuculline methiodide. In experimental groups aged 7, 12, 18, 25 and 90 days a chronic depletion of catecholamines was induced using pretreatment with 6-hydroxydopamine early postnatally. An epileptogenic focus was induced in all age groups; duration of a single discharge decreased with age in both control and experimental animals. The spread of activity from the primary focus to contralateral frontal cortex via callosal connections was as rapid as in controls. However, the transfer of discharge to occipital regions was delayed and the number of discharges decreased in experimental rats. Our study demonstrated a substantial role of catecholamines for synchronization of focal discharges in neocortex and a promoting role of catecholamines in association pathways within neocortex.

Animals↗
PubMed1990

Excitatory amino acid antagonists and pentylenetetrazol-induced seizures during ontogenesis. I. The effects of 2-amino-7-phosphonoheptanoate.

The anticonvulsant action of 2-amino-7-phosphonoheptanoate (AP7) was assessed during ontogenesis of the rat. Animals of five age groups (7, 12, 18, 25, and 90 days) were pretreated with AP7 i.p. in the doses from 15 to 60 mg/kg 30 min prior to pentamethylenetetrazol (PTZ; metrazol; 100 mg/kg s.c.). The incidence and latency of minimal seizures (pure clonic without the loss of righting ability) and of generalized tonic-clonic seizures (major) were evaluated and compared with the control groups. Minimal metrazol seizures were not regularly observed in controls between ages 7 and 12 days. An increased incidence was noticed in AP7-treated groups. In animals of 18 days of age and older the AP7-pretreatment did not influence incidence of minimal seizures; the latencies were significantly lengthened only in 18-day-old animals. Major seizures were significantly suppressed with the highest dose of AP7 (60 mg/kg) in all groups except 7-day-old rats. In 90-day-old rats all doses of AP7 were effective in the suppression of major seizures. The latencies of major seizures were increased in 7 and 18 days old rats. It appears that the blockade of NMDA receptor substantially influences the major seizures induced by PTZ, whereas minimal (clonic) seizures are affected weakly. This suggests an important role of NMDA receptor-mediated transmission in the genesis of generalized tonic-clonic seizure pattern.

2-Amino-5-phosphonovalerate↗
PubMed1990

Ketamine suppresses both bicuculline- and picrotoxin-induced generalized tonic-clonic seizures during ontogenesis.

An anticonvulsant action of ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) antagonist (5-40 mg/kg IP), on the bicuculline-induced (3-8 mg/kg IP) or picrotoxin-induced seizures (3-6 mg/kg IP) was assessed in male Wistar rats aged 7, 12, 18, 25 and 90 days. Ketamine alone caused moderate ataxia which was more pronounced in younger animals. In combination with both aforementioned convulsants, ketamine exerted anticonvulsant effects against generalized tonic-clonic seizures in all developmental stages studied. This effect was more pronounced in bicuculline-treated animals. Moreover, ketamine also suppressed the lethality induced by both drugs during all the development. On the contrary, the action of ketamine on minimal (clonic) seizures was moderate or absent. Our results suggest an important role of ketamine-affected transmission in the generation of the generalized tonic-clonic seizure pattern; moreover, an action of high doses of ketamine on GABA-A receptors might be present.

Aging↗
PubMed1989

Effects of ketamine on metrazol-induced seizures during ontogenesis in rats.

An anticonvulsant action of ketamine, a noncompetitive NMDA receptor antagonist (1-40 mg/kg IP), on the metrazol-induced seizures was assessed in male Wistar rats aged 7, 12, 18, 25 and 90 days. Ketamine alone caused ataxia even in the lowest dose used. As concerens its interaction with metrazol it exerted a clearcut anticonvulsant effect against generalized tonic-clonic seizures at all developmental stages. On the contrary, the effects on clonic (i.e., minimal) seizures were only moderate or absent. Higher efficacy of ketamine was observed in young animals. Our results suggest a role of excitatory amino acids in the generation of generalized tonic-clonic metrazol seizures, but their share on the induction of clonic (minimal) seizures seems to be very small.

Aging↗
PubMed1989

Ethosuximide affects both pentylenetetrazole- and kainate-induced clonic seizures but differentiates between tonic-clonic seizures.

Young (25-day-old) and adult (90-day-old) rats pretreated with ethosuximide (62.5 or 125 mg/kg i.p.) were injected with either s.c. pentylenetetrazole (100 mg/kg) or i.p. kainate (10 or 14 mg/kg). The incidences and latencies of minor (clonic) and major (tonic-clonic) seizures were registered. Ethosuximide (125 mg/kg) completely blocked clonic seizures induced by the lower dose of kainate, and slightly suppressed or delayed those induced by the higher dose of kainate or pentylenetetrazole in both age groups. The effect of ethosuximide on major kainate-induced seizures (elicited in young rats only) was insignificant (ethosuximide only partially decreased the incidence of major seizures), whereas ethosuximide abolished major pentylenetetrazole-induced seizures in both age groups. Ethosuximide also failed to affect the latencies of kainate-induced automatisms (e.g., scratching, wet dog shakes). Similarities between kainate- and pentylenetetrazole-induced clonic seizures, as well as a similar action of ethosuximide on both, suggest a common generator for the pattern of clonic seizures.

Animals↗
PubMed1989

Hippocampal afterdischarges and localization of the stimulating electrodes.

Electrically evoked hippocampal afterdischarges are used as a model of partial epileptic seizures with a complex symptomatology and for testing anticonvulsants and toxic substances. Stimulating electrodes were implanted in the dorsal hippocampus of 16 laboratory rats and when the animals had recovered they were stimulated (15-s series, 8 Hz, pulse length 1 ms) with a voltage double the threshold value for a tissue response. The following features of the evoked afterdischarge were evaluated: the duration of the first phase of the afterdischarge, the duration of the non-active interphase, the duration of the second phase and the number of "wet dog shakes" (a constant accompaniment of hippocampal afterdischarges). Localization of the electrodes in the CA1 (n = 7) and CA3 (n = 7) region of the hippocampus made no difference to these parameters and in both cases the measured and evaluated data were the same. The afterdischarges were always accompanied by a marked orientation reaction. The study showed that when using macroelectrodes to stimulate the dorsal hippocampus, their localization in the CA1/CA3 is not of critical importance.

Animals↗
PubMed1988

Epileptic phenomena produced by kainic acid in laboratory rats during ontogenesis.

Because of its preferential neuroexcitatory effects on the hippocampal neurones kainic acid (KA) is used for inducing partial seizures with a complex symptomatology. In this study the authors investigated the effect of intraperitoneal administration of KA, in doses of 2-16 mg/kg, on the laboratory rat during ontogenesis. The experimental animals were males aged 7, 12, 18, 25 and 90 days. The first signs of an effect in adult rats were automatisms; in young animals, jerks also appeared. The most important automatisms were wet dog shakes, which preponderated in 25-day-old and older animals, whereas in the young rats they consisted chiefly of intensive scratching. Minimal seizures with a motor pattern identical to minimal metrazol seizures were observed in all the age groups and so were generalized tonic-clonic convulsions, which appeared after large doses of KA. The systemic administration of KA is a convenient model of temporal seizures and their progressive generalization and could act as a model for testing broad spectrum antiepileptics.

Age Factors↗
PubMed1987

Influence of clonazepam on electrocorticographic changes induced by metrazol in rats during ontogenesis.

The action of clonazepam (CZP) pretreatment on metrazol-induced ECoG phenomena was studied in Wistar albino rats. ECoG was recorded in acute experiments in male rats 7, 12, 18, 25 and 90 days old (N = 162). CZP (0.1 or 0.02 mg/kg) was injected i.p. 10 min prior to the start of repetitive administration of metrazol (PTZ, 20 mg/kg i.p. every 5 min). Latencies of the first signs of PTZ action, of the rhythmic metrazol activity, of the first ictal activity and of the generalized seizure were measured. CZP exhibited a dose-related effect against ECoG signs elicited by PTZ. A statistically significant increase in latencies was observed with the dose of 0.1 mg/kg in 18 day old and older animals. The 0.1 mg/kg dose of CZP also completely blocked generalized ictal activity in 7 day old rats. In adult animals, CZP pretreatment led to the appearance of partial seizures, a phenomenon never seen in controls. The development of CZP effects corresponds to the maturation of benzodiazepine binding sites.

Aging↗