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PubMedDate not supplied

A comparative study of aminophylline and acepifylline on reversal phenomenon of anticonvulsant drug efficacy in electroshock model of seizures in rats.

The study was designed to compare the proconvulsive activity of two theophylline-containing bronchodilating agents, aminophylline and acepifylline and their antagonistic effects to diazepam, phenytoin, MK-801 and carbamazepine in electroshock seizure model in rats. Graded intensity (30-150 mA for 0.2 s) of electroshock was applied to different groups of rats pretreated either with normal saline (0.5 ml, i.p.), graded doses (25-150 mgkg-1, i.p.) of aminophylline, graded doses (70-560 mgkg-1, i.p.) of acepifylline, graded doses of the antiseizure drugs or to rats pretreated with aminophylline (25 mgkg-1, i.p.) + antiseizure drugs or acepifylline (70 mgkg-1, i.p.) + antiseizure drugs. CI 50 +/- s.e.m. value was 88.41 +/- 2.14 mA in saline treated rats. In aminophylline pretreated rats the values were 84.14 +/- 2.03, 68.06 +/- 1.24, 54.28 +/- 1.96 and 39.58 +/- 2.31 mA at 25 mgkg-1 (0.06 mmolekg-1), 50 mgkg-1 (0.12 mmolekg-1), 100 mgkg-1 (0.24 mmolekg-1) and 150 mgkg-1 (0.36 mmolekg-1), i.p. doses respectively. The values were 85.73 +/- 1.09, 64.86 +/- 2.37, 61.58 +/- 1.37 and 60.62 +/- 2.41 mA at 70 mgkg-1 (0.125 mmolekg-1), 140 mgkg-1 (0.25 mmolekg-1), 280 mgkg-1 (0.50 mmolekg-1) and 560 mgkg-1 (1.0 mmolekg-1), i.p. doses respectively for the acepifylline pretreated groups of rats. Diazepam, MK-801, phenytoin and carbamazepine significantly antagonized electroshock-induced seizure in a dose-dependent manner. Subsensitizing dose of aminophylline (25 mgkg-1, i.p.) but not that of acepifylline (70 mgkg-1, i.p.) pretreatment significantly antagonized the efficacy of all the antiseizure drugs. The study highlighted that acepifylline might be safely used in epileptic patients well controlled on antiepileptic drugs. Aminophylline, on the other hand, should be avoided since it might produce breakthrough seizure attacks due to its greater proconvulsive and anti-antiseizure drug effects.

Aminophylline↗
PubMed1990

[Effect of electroshock on learning-dependent long-term potentiation in rat hippocampal CA3 area].

Population spikes were recorded from hippocampal CA3 of freely moving rats following stimulation of the perforant path. Six rats were trained to perform conditioned drinking behavior. (1) Animals were treated with electroshock in less than 15 minutes after daily training session for a period of 6 consecutive days. Synaptic efficacy did not increase and the conditioned response could not be established during the behavioral training in four rats, synaptic efficacy was increased, the long-term potentiation (LTP) appeared and the conditioned behavior was established in other two rats. (2) After consolidation of conditioned behavior, electroshock temporarily caused suppression of the learning-dependent LTP and the correlative conditioned response. Both LTP and the correlative conditioned response recovered in one to four hours after electroshock. In these cases, the maximal development of LTP preceded the development of conditioned behavior. The results indicated that the learning-dependent LTP might be one of the neural substrates underlying learning and memory.

Animals↗
PubMed1989

[Inhibitory effects of L-threo-DOPS on electroshock seizure in mice].

Effects of L-threo-3,4-dihydroxyphenylserine (L-DOPS), a synthetic norepinephrine (NE) precursor, on electroshock seizure were studied in mice. All substances were administered intraperitoneally. Minimal electroshock seizure threshold (EST) was not significantly altered by L-DOPS at a dose of 200 or 400 mg/kg. L-DOPS was unable to abolish tonic extensions of hind legs in maximal electroshock seizure (MES) test at doses from 100 to 400 mg/kg. However, it significantly reduced extension/flexion (E/F) ratio in a dose-dependent manner. Furthermore, L-DOPS dose-dependently blocked maximal electroconvulsions in a combined use with nialamide (30 mg/kg), desipramine (20 mg/kg) or maprotiline (40 mg/kg) at so small doses as not to show any anticonvulsant effect when they were used alone. ED50 (with 95% confidence limit) of L-DOPS in the combination treatments were 210 (145-305), 160 (100-256) and 95 (50-181) mg/kg respectively. Those results indicate that L-DOPS has an anticonvulsant property, which is potentiated by a MAO inhibitor or NE uptake blockers. It was presumed that the effect of L-DOPS was caused by the inhibition of spreading of seizure discharges. It was suggested that L-DOPS would be a useful substance for the investigation on a role of NE in experimental epilepsy and could be used clinically as an adjunct drug for generalized tonic-clonic convulsions.

Animals↗
PubMed1978

Modification of electroshock convulsive responses and thresholds in neonatal rats after brain monoamine reduction.

Modification of electroshock (60 Hz; a.c.) convulsive responses and thresholds by monoamine-reducing drugs was investigated in developing rats. Throughout postnatal development, tetrabenazine (TBZ) reduced brain monoamines and increased the severity of motor responses to electroshock. The predominant maximal response in control pups progressed from hyperkinesia (day 1) to clonic convulsions (day 3) and tonic forelimb (day 7) and hindlimb (day 19) extension. The pattern in TBZ-treated pups progressed from tonic forelimb extension (day 1) to tonic hindlimb extension (day 7). On day 7, TBZ reduced the thresholds for clonic (CT) and tonic convulsions (TT) to 41 and 24% of control, respectively. Reserpine (1.25 mg/kg, 24 hours) decreased the TT but not the CT; TBZ, 4 hours before reserpine, prevented this decrease. A higher dose of reserpine (2.5 mg/kg) decreased both the CT and TT. On day 8, TBZ (25 mg/kg, 4 hours) decreased the TT (46% control); L-dihydroxyphenylalanine, but not 5-hydroxytryptophan prevented this decrease. Intracisternal 6-hydroxydopamine reduced the TT on day 8, while intracisternal 5,7-dihydroxytryptamine had no effect despite a 46% reduction in serotonin. The results indicate that in the neonatal rat brain, monoaminergic systems are sufficiently mature to attenuate electroshock convulsive responses, perhaps by limiting propagation of seizure discharge.

5,7-Dihydroxytryptamine↗
PubMedDate not supplied

[Participation of the kidney in changes in the fibrinolytic system during electroshock].

Fibrinolytic activity was studied in the renal vein of rats after electroshock. Electroshock increased distinctly the fibrinolytic activity in all parts of the venous system. The level of plasminogen activator was increased more in the renal vein and in the vena cava inferior, than in the jugular vein. In electroshock fibrinolytic activity was decreased 2-fold in kidney cortex; in the medullar layer of kidney it was unaltered.

Animals↗
PubMedDate not supplied

[Effect of electroshock on intraspecific behavior of mice maintained in isolation].

By means of probabilistic-ethological analysis it was shown on isolated mice that the direct effect of primary electroshock is manifested in an inversion of the isolant's aggressive behaviour into a defensive one. Delayed (24 hours) and chronic effects of the electroshock (applied daily during a week) were manifested in a change of behaviour pattern of the isolants (appearance of the previously absent phase of investigating the partner and the environment before aggressive attack), in diminished probability of appearance of aggression and increased intraspecies sociability. All effects of the electroshock on intraspecies behaviour had rigid temporal limitations.

Aggression↗
PubMed1994

An immediate morphopathologic response of a subpopulation of astrocytes to electroshock: "dark" astrocytes.

Varying numbers of astrocytes lining the subarachnoid and Virchow-Robin's spaces become stainable by a special silver method in brain sections of rats subjected to a single electroshock of "suitable" parameters immediately before being sacrificed by perfusion fixation. This type of argyrophilia is considered to be induced by some electrically caused morphological damage, since the affected astrocytes are dramatically shrunken and hyperchromatic at both light- and electron-microscopic levels. Based on several points of morphopathologic similarity between the electroshock-damaged astrocytes and "dark" cells of various tissues, especially electroshock-induced "dark" neurons, it is supposed that their nature is also similar ("dark" astrocytes).

Animals↗
PubMed1996

Pre- and postpubertal LH and estradiol pattern in gilts subjected to intermittent inescapable electroshock.

The effect of intermittent electroshock on LH and estradiol secretory pattern and on reaching puberty was studied in 24 prepubertal gilts. Twelve gilts 115-168 days of age received unpredictable and inescapable electroshocks 0-5 times daily between 8 am and 4 pm and 12 gilts served as controls. At an age of 168 +/- 0.7 days all gilts were moved, regrouped and exposed to a boar for 30 min. Observations for signs of oestrus were carried out twice daily. Indwelling jugular catheters were inserted into 8 gilts on each treatment after the initial boar contact. Blood samples were collected to determine LH profiles for 4 h every 15 min on day 2 and day 4 after the initial boar contact. The remaining 4 gilts on each treatment were catheterized one day prior to the initial boar contact and blood was collected to determine LH profiles the day before initial boar contact and day 1 and day 2 after initial boar contact for 6 h every 15 min. In addition, blood samples were collected and analyzed for LH and estradiol from all gilts daily at 8 am, 12 am and 4 pm for the first 3 days following the initial boar contact and thereafter every 4 h until the end of oestrus (diurnal samples). Samples taken daily at noon the first 5 days following initial boar contact were analyzed for cortisol. The electroshock treatment significantly increased the age at puberty (p = 0.04) and tended to decrease the mean LH concentration prior to the preovulatory LH surge (p = 0.08) and the maximal concentration of LH during the preovulatory LH surge (p = 0.07). The apparent down regulation of the plasma concentration of LH was not associated with increased activity in the hypothalamus-pituitary-adrenal axis in that the basal concentration of cortisol was not affected by treatment. This indicates that other physiological mechanisms are involved in stress-induced suppression of LH.

Animals↗
PubMedDate not supplied

Parenteral magnesium sulfate fails to control electroshock and pentylenetetrazol seizures in mice.

Magnesium sulfate has been used as an anticonvulsant in the treatment of eclampsia, but efficacy of magnesium in other types of seizure disorders is poorly documented. We examined the effects of magnesium sulfate (MgSO4) on seizures produced in mice by maximal electroshock (MES) and pentylenetetrazol (PTZ), MgSO4 injection (6.7 mEq/kg i.p.) caused weakness in all animals. With suprathreshold electroshock, 10/10 controls and 11/12 treated animals had seizures with tonic hind limb extension (P = NS). Electroshock threshold was unaltered by magnesium treatment (n = 48; P = 0.47). PTZ induced clonic seizures in 12/12 controls and 5/14 treated animals (P less than 0.05). This difference was likely due to muscular weakness because frequency of EEG spikes was the same in PTZ and PTZ + MgSO4 groups. Mean serum magnesium levels were 2.3 +/- 0.3 mEq/l in animals not given MgSO4; 10.9 +/- 1.4 mEq/l and 12.8 +/- 2.2 mEq/l in treated animals with and without seizures (P = NS). We conclude that magnesium sulfate had no significant anticonvulsant activity in mouse MES and PTZ models for epilepsy. The relevance of these findings to the possible efficacy of magnesium sulfate in eclamptic seizures and other types of epilepsy remains to be determined.

Animals↗
PubMedDate not supplied

Intraocular pressure changes during anesthesia for electroshock therapy.

Intraovular pressure was measured in 20 patients undergoing anesthesia for electroshock therapy. Compared to control values, determined on the day before electroshock therapy, statistically significant elevations of intraocular pressure followed the post-electroshock therapy convulsions and were still significant 5 minutes later, but not of sufficient magnitude or duration to cause concern.

Adult↗
PubMed1975

[The role of electroshock in the era of psychopharmacology].

Since the introduction of medicamental therapies in psychiatry, the electroshock technique has been put aside. After having noticed the fact "figures in hand", the speaker: --Reminds the practical conditions of electroshock, its principal indications during depressions and schizophrenia. --Compares the various convulsive techniques and especially the unilateral electroshock as well as those based on the use of pharmacological agents. --Proposes applicable therapeutical rules divided into six points and meant for "resistant" depressions.

Amnesia, Retrograde↗
PubMed1999

Effect of fluoxetine on maximal electroshock seizures in mice: acute vs chronic administration.

There are no definite reports regarding the effects of chronic fluoxetine on animal models of epilepsy. Since chronically administered fluoxetine, in comparison to acutely administered fluoxetine has different effects on CNS, the present study was undertaken to investigate the effect of acute and chronic fluoxetine pretreatment, on a median anticonvulsant dose (ED50) of phenytoin in male ICR albino mice. Additionally, the effects of fluoxetine pretreatment on median convulsive current (CC50) in the presence and absence of phenytoin were investigated and results were compared. The maximal electroshock seizure (MES) test was used to estimate the ED50of phenytoin. The electroshock threshold test was used to estimate CC50. ED50and CC50values were calculated by probit analysis. The effects of the chronic and acute fluoxetine groups on the ED50of phenytoin were significantly different (P<0.05), and on CC50this difference was not statistically significant. Chronic fluoxetine insignificantly increased the ED50of phenytoin and decreased the CC50while acute fluoxetine decreased the ED50of phenytoin and increased the CC50. Our results indicate that chronic fluoxetine does not have an antiepileptic property and it may have dubious proconvulsant properties, contrary to acute fluoxetine.

Animals↗
PubMed1992

Comparison of the effects of losigamone and its isomers on maximal electroshock induced convulsions in mice and on three different patterns of low magnesium induced epileptiform activity in slices of the rat temporal cortex.

Losigamone (AO-33) is a recemate of a tetronic acid derivative. The effects of losigamone and its three isomers (AO-242, AO-294 and AO-23) were compared on maximal electroshock (MES) induced convulsions in mice and on different patterns of extracellularly recorded, low Mg2+ induced epileptiform activity in slices of the rat temporal cortex. Lowering Mg2+ induced recurrent short discharges in areas CA3 and CA1 while ictaform events that lasted for many seconds were induced in the entorhinal cortex. In the hippocampus the activity stayed stable over a number of hours. In contrast, the ictaform events in the entorhinal cortex changed their characteristics after one to two hours to recurrent discharges of 0.8 to 10 s. Afterdischarges and interictal events were absent. 50 microM AO-242 showed a similar efficacy to 50 microM AO-33 in reducing and blocking epileptiform discharges in areas CA1 and CA3 while 50 microM AO-294 and 50 microM AO-23 had weaker effects than 50 microM AO-33. Concentrations of 50 microM and 100 microM AO-242 showed a similar efficacy to AO-33 on ictaform events in the entorhinal cortex. Late recurrent discharges were also blocked by AO-33 and AO-242 although at higher concentrations (300 microM). The in vitro observations are with respect to order of efficacy in accordance with the in vivo data obtained in the maximal electroshock test in mice. The order of potency in the MES test was AO-242 greater than AO-33 much greater than AO-294 much greater than AO-23.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Influence of CGS 15943 A (a nonxanthine adenosine antagonist) on the protection offered by a variety of antiepileptic drugs against maximal electroshock-induced seizures in mice.

CGS 15943 A (a nonxanthine adenosine antagonist) was studied on the protective efficacy of carbamazepine (60 min prior to the convulsive test), diazepam (60 min), diphenylhydantoin (120 min), phenobarbital (120 min), and valproate (30 min) against maximal electroshock-induced convulsions in mice. Moreover, the influence of the adenosine antagonist on 2-chloroadenosine (1 mg/kg, 20 min prior to the test)- and valproate (250 mg/kg, 30 min)-induced inhibitions of locomotor activity was also studied. CGS 15943 A (1 mg/kg) was given 15 min before both tests and all the drugs were administered i.p.. The adenosine antagonist (1 mg/kg) remained without influence upon the protective activity of all studied antiepileptics, reflected by their respective ED50 values against maximal electroshock. However, both 2-chloroadenosine and valproate-induced inhibitions of locomotor activity were attenuated by CGS 15943 A, which alone did not affect this parameter. However, CGS 15943 A (5 mg/kg) diminished the protection offered by diphenylhydantoin, increasing its ED50 value from 13 to 16 mg/kg. It may be concluded that the protection provided by common antiepileptic drugs against electroconvulsions seems independent of adenosine-mediated inhibition. In the case of diphenylhydantoin, one may suggest the involvement of purinergic transmission in the final anticonvulsant effect.

Adenosine↗
PubMed1996

Influence of aminophylline and strychnine on the protective activity of excitatory amino acid antagonists against maximal electroshock-induced convulsions in mice.

Aminophylline reversed the protective action of both, D-3-(2-carboxypiperazine-4-yl)-1-propenyl-1-phosphonic acid (D-CPP-ene-a competitive NMDA antagonist) and valproate (used as a conventional antiepileptic drug for comparative purposes) against maximal electroshock-induced seizures. The respective ED50 values of aminophylline were 55.7 and 98.4 mg/kg i.p. However, aminophylline (up to 100 mg/kg i.p.) did not influence the protective efficacy of 1-(4-aminophenyl)-4-methyl-7,8-methyl- enedioxy-5H-2,3-benzodiazepine (GYKI 52466-a non-NMDA antagonist). Strychnine affected the protection provided by D-CPP-ene, GYKI 52466, and valproate against maximal electroshock-the ED50 values of strychnine for the reversal of the anticonvulsive effects of D-CPP-ene, GYKI 52466 or valproate were 0.082, 0.35 and 0.28 mg/kg s.c., respectively. An involvement of strychnine sensitive glycinergic receptor-mediated events in the mechanism of the anticonvulsive activity of excitatory amino acid antagonists and valproate may be postulated. The ineffectiveness of aminophylline to reduce the anticonvulsive effects of GYKI 52466 may distinguish a new class of antiepileptic drugs offering an advantage over conventional antiepileptics in patients with epilepsy, requiring aminophylline for pulmonary reasons.

Aminophylline↗
PubMed1991

Differential effects of selective mu-, kappa- and delta-opioid antagonists on electroshock seizure threshold in mice.

The effects of the selective opioid antagonists cyprodime (mu; 1, 3, 10, 30 mg/kg IP), norbinaltorphimine (kappa; 3, 10, 30 mg/kg IP) and naltrindole (delta; 0.3, 1, 3, 10 mg/kg IP) on electroshock seizure threshold in mice were compared with those of the universal opioid antagonist naloxone (0.3, 1, 10 mg/kg IP). Seizure threshold was increased by mu-receptor blocking doses of both cyprodime and naloxone, unaltered by norbinaltorphimine and decreased (in a dose-related manner) by all doses of naltrindole. The effects of naltrindole were similar to those of the established pro-convulsant agent bicuculline (1 mg/kg IP); however, naloxone and cyprodime produced relatively small increases in seizure threshold when compared with phenytoin (doses up to 30 mg/kg IP). The differential effects of mu-, kappa- and delta-receptor antagonists obtained in this study suggest that electroshock seizure threshold in mice may be controlled, at least in part, by a balance between endogenous opioids acting either pro-convulsantly through mu-receptors or anti-convulsantly via delta-receptors.

Animals↗
PubMed2003

L-histidine is a beneficial adjuvant for antiepileptic drugs against maximal electroshock-induced seizures in mice.

Endogenous histamine has been reported to be involved in regulation of seizure susceptibility. Enhancement of histamine neurotransmission engendered by L-histidine treatment produces anticonvulsant effects in experimental animals. The present study investigated the influence of L-histidine on the protective effects of carbamazepine and phenytoin against maximal electroshock-induced seizures in mice.L-Histidine, administered at the doses that did not influence the threshold for electroconvulsions (250-500 mg/kg), enhanced by nearly 30% the protective effects of carbamazepine against maximal electroshock-induced seizures. D-Histidine (1000 mg/kg), an inactive isomer of histidine, was without any effect in this regard. L-Histidine (500 mg/kg) also augmented the protective effects of phenytoin. Importantly, the enhancement of the anticonvulsant effects of these antiepileptic drugs produced by L-histidine co-administration was not associated with augmentation of their unwanted effects on memory and motor performance. A pharmacokinetic interaction was also excluded since the free plasma levels of these antiepileptics remained unchanged in the presence of L-histidine. It may be suggested that L-histidine could serve as a beneficial adjuvant for selected antiepileptic drugs.

Animals↗
PubMed2005

Cyclosporin A aggravates electroshock-induced convulsions in mice with a transient middle cerebral artery occlusion.

1. To test whether an ischemic insult increases the susceptibility to cyclosporine A (CsA)-induced neurotoxicity, we examined the effect of CsA on the minimal electroshock-induced convulsions in mice treated with a transient middle cerebral artery occlusion (MCAO) for a short period (2 h). 2. This MCAO produced small to mid-sized infarcted regions in the cerebral hemisphere with increasing post-operative days. In MCAO mice, CsA (30 mg/kg, i.p.) elevated the incidence of minimal electroshock-induced convulsions to 90-100% over that in sham mice (20-30%) at 1-7 days but not 14 days post-surgery. 3. In light of these findings, the possibility that CsA increases the risk of convulsions in patients with cerebral infarction and/or at an early stage following focal cerebral ischemia would have to be considered.

Animals↗