Methylprednisolone modulates intracranial pressure in the brain cellular edema induced by water intoxication.

Continuous monitoring of the intracranial pressure (ICP) detects impending intracranial hypertension resulting from the impaired intracranial volume homeostasis, when expanding volume generates pressure increase. In this study, cellular brain edema (CE) was induced in rats by water intoxication (WI). Methylprednisolone (MP) was administered intraperitoneally (i.p.) before the start of CE induction, during the induction and after the induction. ICP was monitored for 60 min within 20 h after the completion of the CE induction by fibreoptic pressure transmitter. In rats with induced CE, ICP was increased (Mean+/-SEM: 14.25+/-2.12) as well as in rats with MP administration before the start of CE induction (10.55+/-1.27). In control rats without CE induction (4.62+/-0.24) as well as in rats with MP applied during CE induction (5.52+/-1.32) and in rats with MP applied after the end of CE induction (6.23+/-0.73) ICP was normal. In the last two groups of rats, though the CE was induced, intracranial volume homeostasis was not impaired, intracranial volume as well as ICP were not increased. It is possible to conclude that methylprednisolone significantly influenced intracranial homeostasis and thus also the ICP values in the model of cellular brain edema.

Effect of selenium pre-treatment on evoked cortical afterdischarges in young rats.

Prenatal or perinatal hypoxia is among the most frequent pathogenic factors of encephalopaties. It can induce wide-range of morphological, biochemical, energetic and functional alterations. Accordingly we tested changes of excitability of the sensorimotor cortex in 12, 25 and 35-day-old rats exposed and not exposed to short-term (1 hour) hypobaric and normobaric hypoxia. We studied whether sodium selenate (0,26 mg/kg b.w.) can influence character and/or intensity of evoked cortical afterdischarges or if a pre-treatment by selenium changes effects of hypoxia on such seizures. According to the results we can conclude that in our experiment arrangement sodium selenate only partially alters duration of evoked cortical afterdischarges.

[The effect of ethosuximide on epileptic after-discharges induced by thalamic stimulation in young laboratory rats]. / Ucinek ethosuximidu na epileptické následné výboje vyvolané drázdením talamu u mládat laboratorního potkana.

An influence of ethosuximide on thalamically induced epileptic afterdischarges was studied in 47 rats aged 12 and 18 days. An afterdischarge formed by spike-and-wave rhythm was induced only in 18-day-old rats. It exhibited a tendency to progressive prolongation with repeated stimulations (with 15 min intervals). Ethosuximide in a dose of 125 mg/kg i.p. immediately after the first afterdischarge did not change the duration of subsequent afterdischarges. The second type of epileptic afterdischarge formed by spikes and/or serrated waves could be induced in both age groups studied. Ethosuximide even worsened the tendency to progression of epileptic afterdischarges in 12- as well as 18-day-old animals. Ethosuximide did not exhibit an anticonvulsant action against the spike-and-wave afterdischarge in 18-day-old rats. On the contrary, it aggravated the course of progressive changes with repeated stimulations in both age groups.

Excitability cycles of epileptic after-discharges in rats.

An epileptic seizure is regularly followed by a postictal depression and then by a phase of increased excitability. The time course of these two phases was described for two types of epileptic after-discharges induced by stimulation of the hippocampus and/or the thalamus in acute experiments in rats. Using hippocampal stimulation, an interval of 10 min was necessary for induction of the second self-sustained after-discharge (SSAD) of the same duration as the first one. Significant prolongation of the second SSAD appeared with a 30-min interstimulation interval. The spike-and-wave rhythm induced by stimulation of thalamic nuclei exhibited a shorter refractory phase - up to 5 min - and also the facilitation took place sooner: with 15-min intervals a significant increase in duration of SSAD was recovered. The results are discussed in connection with the kindling model of epilepsy.

Effect of anticonvulsant drugs on thalamo-cortical and hippocampo-cortical self-sustained after-discharges in the rat.

The action of four antiepileptic drugs was studied in acute experiments in 98 rats. Two types of cortical self-sustained afterdischarges ( SSADs ) induced by rhythmic electrical stimulation of subcortical structures were used as models. SSAD formed by the spike-and-wave rhythm (most frequently induced by stimulation of thalamic somatosensory relay nucleus) was almost completely blocked by dipropylacetate (valproate, 400 mg/kg i.p.) and significantly shortened by ethosuximide (125 mg/kg i.p.). Diphenylhydantoin (60 mg/kg i.p.) tended to prolong this type of SSAD whereas carbamazepine did not influence it. SSAD formed by serrated waves (induced usually by stimulation of the dorsal hippocampus) was augmented by ethosuximide, uninfluenced by dipropylacetate and diphenylhydantoin, and significantly shortened by carbamazepine. The pharmacological profile of the two types of SSADs is in agreement with our hypothesis that the spike-and-wave type of SSAD represents a model of primary generalized seizures of the absence type whereas hippocampo -cortical SSAD could be used as a model of partial seizures with complex symptomatology.

Ontogenetic development of rhythmic thalamo-cortical phenomena in the rat.

Three rhythmic cortical phenomena (rhythmic after-discharges, incremental responses and self-sustained after-discharges formed by spike-and-wave rhythm) were elicited by electrical stimulation of thalamic nuclei during ontogenesis in rats. All three phenomena could be recorded for the first time at the age of 12 days and they matured until the 18th postnatal day. Possible explanation for the delayed development of these rhythmic thalamo-cortical phenomena in comparison with single thalamo-cortical responses are discussed.