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PubMedDate not supplied

[Reflection of evolutionary trends in the recovery pattern of the electrical activity in the human brain after unilateral electroshock].

After unilateral electroshocks the following stages of the recovery of EEG may be defferentiated in man: residual seizure activity, flat EEG, low-amplitude polyform arrhythmia, monoform delta-rhythm, synchronized teta- and alpha-rhythms. It is assumed that changes of these stages reflect the migration of EEG pacemakers within the system of hierarchically interrelated brain structures, which provide for various forms of regulation of the electrical activity of the cortex. It was shown that in each of the hemispheres, pacemakers operate relatively independently and that electrical stimulation of the dominant (left) hemisphere affects brain activity to a greater extent than stimulation of nondominant (right) hemisphere. The ascending influences of desynchronizing systems of the brain stem are less lateral as compared to the ascending pathways of hypothalamic and thalamic structures.

Biological Evolution↗
PubMedDate not supplied

Classification of compounds for prevention of NMDLA-induced seizures/mortality, or maximal electroshock and pentylenetetrazol seizures in mice and antagonism of MK801 binding in vitro.

Intravenous injection of N-methyl-D,L-aspartic acid (NMDLA) into mice produces characteristic convulsions followed by death. The present study was designed to determine the degree of blockade of these seizures/mortality by compounds acting at various subsites on the N-methyl-D-aspartic acid (NMDA) receptor complex (competitive and noncompetitive antagonists, as well as inhibitors of the strychnine-insensitive glycine subsite, and Zn++ subsite agonists), and also calcium channel blockers, clinically used anticonvulsants, plus selected compounds with activities or structures similar to specific agents chosen. Activity among compounds was correlated to in vitro potency regarding inhibition of binding of MK801 to the ionic channel subsite associated with the NMDA receptor. Furthermore, all compounds were examined for antiseizure properties with respect to tonic hindlimb extension elicited by maximal electroshock (MES) and clonus induced by pentylenetetrazol (PTZ). Drugs were subsequently classified according to their spectra of efficacy in these tests. The following characteristics emerged: 1) agents active at all 3 NMDA mechanisms (convulsions/mortality/MK801 binding) plus MES and PTZ, were MK801 and CPP [3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid]; 2) active at all the NMDA mechanisms and MES were ketamine and dextromethorphan; 3) active against NMDLA-induced convulsions/mortality, MES and PTZ, but not MK801 binding, were doxepin, desipramine and diazepam; 4) active against NMDLA-induced convulsions/mortality and MES were des-Me-doxepin, flunarizine and remacemide; 5) active against NMDLA-induced convulsions/mortality and PTZ was nisoldipine; 6) active against only NMDLA-induced convulsions/mortality were chlorpheniramine and iproniazid; 7) active in the MES and PTZ tests were phenobarbital, pentobarbital and valproate; 8) active in the MES test alone were phenytoin and carbamazepine; 9) active against PTZ only was ethosuximide; 10) active only in the in vitro MK801 binding assay were HA966, 7-Cl-kynurenate and AP7 (2-amino-7-phosphonoheptanoic acid); and 11) no demonstrable actions had AP4 (2-amino-4-phosphonobutyric acid) and mianserin. In conclusion, inhibition of NMDLA-induced convulsions/mortality in vivo is not necessarily correlated to a noncompetitive displacement of MK801 binding to NMDA receptor sites in vitro, nor is inhibition of NMDA-elicited convulsions/mortality correlated with a specific ability of a compound to inhibit either MES or PTZ seizures.

Animals↗
PubMedDate not supplied

Influence of some convulsant agents on the protective activity of a novel antiepileptic drug, felbamate, against maximal electroshock in mice.

The aim of this study was to evaluate effects of strychnine, as well as bicuculline and picrotoxin on the anticonvulsant action of felbamate against maximal electroshock (MES)-induced seizures in mice. Strychnine (up to 0.5 mg/kg), bicuculline (up to 2 mg/kg) and picrotoxin (3 mg/kg) did not affect the seizure threshold. However, strychnine (0.25-0.5 mg/kg) and picrotoxin (3 mg/kg) impaired the protective activity of felbamate against MES. It may be concluded that GABAergic inhibition and strychnine-insensitive glycine receptor-mediated events may contribute to the anticonvulsant activity of felbamate.

Animals↗
PubMedDate not supplied

Allopurinol does not affect the anticonvulsant activity of carbamazepine and valproate in maximal electroshock-induced convulsions in mice.

Allopurinol, an inhibitor of xanthine oxidase, is indicated in the management of patients with elevated serum and urinary uric acid levels. It was also reported to be beneficial in patients with epilepsy when added to traditional antiepileptic drug. Here, we investigated the effect of allopurinol upon the electrical seizure threshold and its effect on the protective efficacy of common antiepileptic drugs, carbamazepine (CBZ) and valproate (VPA) against maximal electroshock (MES)-induced convulsions in mice. We found that allopurinol administered at doses of 5, 15 or 45 mg/kg, did not affect electrical seizure threshold. When administered acutely or for a prolonged period of time (5 times every 24 h), it did not affect anticonvulsant activity of CBZ and VPAin MES. Free plasma concentration of both anticonvulsants was not affected by allopurinol given at a dose of 45 mg/kg for 5 days. Thus, our results did not support suggestions that allopurinol can be beneficial as add-on drug in the management of epilepsy at least in patients treated with CBZ or VPA.

Allopurinol↗
PubMedDate not supplied

Effects of some convulsant agents on the protective activity of topiramate against maximal electroshock-induced seizures in mice.

The anticonvulsant activity of topiramate combined with some convulsant agents (bicuculline--BIC, N-methyl-D-aspartate--NMDA, and kainic acid--KA), given at subconvulsive doses, was evaluated in the maximal electroshock (MES)-test in mice. BIC (1.5 mg/kg), KA (10 mg/kg) and NMDA (50 mg/kg) significantly decreased the anticonvulsant activity of topiramate raising its ED(50) from 76.2 mg/kg to 135, 102, and 107 mg/kg, respectively. BIC (0.75 mg/kg) and KA (5 mg/kg) did not alter the protective activity of topiramate in the MES-test. Moreover, topiramate injected alone (up to 135 mg/kg) did not affect motor performance and long-term memory of animals tested in the chimney and passive avoidance tests, respectively. In contrast, combinations of topiramate with BIC (1.5 mg/kg), NMDA (50 mg/kg) or KA (10 mg/kg) considerably disturbed long-term memory in mice. Additionally, co-administration of topiramate with KA (10 mg/kg) or BIC (1.5 mg/kg) significantly impaired motor performance, whereas topiramate co-administered with NMDA (50 mg/kg) had no impact on motor coordination in mice. None of the studied convulsants affected the free plasma concentration of topiramate assayed with immunofluorescence method. The results of this study seem to indicate the expression of the anticonvulsant activity of topiramate is dependent on all ionotropic glutamate and GABAA receptor-mediated events.

Animals↗
PubMedDate not supplied

2-Chloro-N6-cyclopentyladenosine enhances the anticonvulsant action of carbamazepine in the mouse maximal electroshock-induced seizure model.

This study examines the anticonvulsant profile of interactions between 2-chloro-N6-cyclopentyladenosine (CCPA, a selective adenosine A1 receptor agonist) and four conventional antiepileptic drugs (AEDs: carbamazepine--CBZ, phenobarbital, phenytoin and valproate) in the mouse maximal electroshock seizure (MES) model. Acute adverse effects produced by AEDs in combination with CCPA were determined in the chimney test (motor performance) and passive avoidance task (long-term memory). Results indicate that CCPA administered alone at 0.25 and 0.5 mg/kg significantly elevated the electroconvulsive threshold in mice. Additionally, the agent at a sub-threshold dose of 0.125 mg/kg potentiated the anticonvulsant activity of CBZ by reducing its ED50 in the MES test from 11.2 to 7.7 mg/kg (p < 0.01). In contrast, 8-cyclopentyl-1,3-dimethylxanthine (DPCPX, a selective adenosine A1 receptor antagonist at 5 mg/kg) abolished the enhanced anticonvulsant effects offered by the combination of CBZ with CCPA (0.125 mg/kg). Moreover, CCPA (0.125 mg/kg) co-administered with other tested AEDs had no significant impact on their antiseizure properties in the MES test in mice. Neither CCPA (0.125 mg/kg) administered singly, nor in combinations with conventional AEDs (at their ED50s) affected motor performance in the chimney test and long-term memory in the passive avoidance task. No pharmacokinetic alterations in brain CBZ concentrations were observed after administration of CCPA at 0.125 mg/kg. It may be concluded that CCPA, acting selectively on adenosine A1 receptors, enhances pharmacodynamically the antiseizure effect of CBZ in the MES test.

Adenosine↗
PubMedDate not supplied

Fluoxetine enhances the anticonvulsant effects of conventional antiepileptic drugs in maximal electroshock seizures in mice.

The present study was designed to investigate the effects of fluoxetine (FXT), a selective serotonin reuptake inhibitor, on the effect of antiepileptic drugs (AEDs) in the maximal electroshock seizure (MES) model in mice. FXT at the doses of 25, 20 and 15 mg/kg significantly increased the electroconvulsive threshold. The antidepressant applied at the lower doses (10, 5 and 2.5 mg/kg) did not influence the threshold. Moreover, FXT (at the highest subprotective dose of 10 mg/kg) increased the anticonvulsive potential of carbamazepine (CBZ), diphenylhydantoin (DPH), valproate (VPA) and phenobarbital (PB), producing a dose-related decrease in their ED50 values against MES. Nevertheless, pharmacokinetic events may be involved in the interaction between FXT and PB or CBZ, since the antidepressant raised the total brain concentration of the two antiepileptics. FXT in combination with AEDs did not influence the motor performance in the chimney test and long-term memory. In conclusion, the data suggest that FXT modulates seizure processes in the brain and may be advantageous in the treatment of epilepsy in depressed patients, improving the seizure control in epilepsy.

Animals↗
PubMedDate not supplied

7-Nitroindazole enhances dose-dependently the anticonvulsant activities of conventional antiepileptic drugs in the mouse maximal electroshock-induced seizure model.

7-Nitroindazole (7NI, a nitric oxide synthase [NOS] inhibitor) administered intraperitoneally (ip), 30 min before the test, at doses ranging between 50-200 mg/kg, raised the threshold for electroconvulsions in mice. Linear regression analysis revealed that the doses increasing the threshold by 50% (TID50) and 100% (TID100) over the control value for 7NI were 115.2 and 173.4 mg/kg, respectively. Moreover, 7NI dose-dependently potentiated the anticonvulsant effects of four conventional antiepileptic drugs (AEDs: carbamazepine - CBZ, phenobarbital - PB, phenytoin - PHT, and valproate - VPA) in the mouse maximal electroshock-induced seizure (MES) model. 7NI at 50 mg/kg enhanced only the anticonvulsant effect of PB, whereas the drug at 75 and 100 mg/kg potentiated the antiseizure effects of PB, PHT and VPA, but not those of CBZ against MES-induced seizures. Only 7NI at 150 mg/kg enhanced considerably the antielectroshock action of all studied AEDs in the MES test. Pharmacokinetic evaluation of interactions between 7NI and the investigated AEDs revealed that 7NI (150 mg/kg; ip) did not alter total brain concentrations of conventional AEDs in mice. L-arginine (L-Arg - a natural precursor of NO; administered ip, 500 mg/kg, 60 min before electroconvulsions) did not reverse the activity of 7NI (150 mg/kg), but in contrast, it significantly potentiated the anticonvulsant action of conventional AEDs combined with 7NI (150 mg/kg). Pharmacokinetic increase in total brain AED concentrations was observed for the combinations of L-Arg (500 mg/kg) with 7NI (150 mg/kg) and PHT (by 32%; p<0.01) or VPA (by 22%; p<0.05). Neither total brain CBZ nor PB concentrations were altered following the co-administration of L-Arg (500 mg/kg) with 7NI (150 mg/kg). 7NI at doses of 100-200 mg/kg significantly impaired spontaneous ambulatory activity in mice subjected to the Y-maze task. The NOS inhibitor at doses of 50 and 75 mg/kg had no significant effect on locomotor activity of animals, although the number of arm entries within the 5 min of observational time was reduced. Finally, it can be concluded that the enhancement of anticonvulsive efficacy of CBZ, PB, PHT and VPA by 7NI alone or in combination with L-Arg in the MES test, deserves more attention and further neurochemical studies are required to elucidate the exact role of NO in the brain.

Animals↗
PubMedDate not supplied

Gabapentin synergistically interacts with topiramate in the mouse maximal electroshock seizure model: an isobolographic analysis.

The anticonvulsant effects produced by topiramate (TPM) and gabapentin (GBP)--two second-generation antiepileptic drugs, in numerous fixed-ratio combinations of 8:1, 4:1, 2:1, 1:1, 1:2, 1:4 and 1:8 were examined by isobolographic analysis in the mouse maximal electroshock seizure (MES) model. Results indicate that the combinations of TPM and GBP at the fixed-ratios of 2:1, 1:1, 1:2, 1:4 and 1:8 resulted in supra-additive (synergistic) interaction against MES-induced seizures. Moreover, the combinations of TPM and GBP (at their median effective doses) did not affect motor performance of animals challenged with the chimney test and had no impact on neuromuscular tone in the grip-strength test. Additionally, GBP had no impact on total brain TPM concentrations, and simultaneously, TPM did not alter brain GBP concentrations, indicating that the interaction between drugs was pharmacodynamic in nature. In conclusion, supra-additive interaction of TPM with GBP against MES-induced seizures, lack of motor coordination and neuromuscular tone impairments as well as lack of pharmacokinetic interactions between TPM and GBP in preclinical study, strongly support the combined application of both antiepileptic drugs in patients with refractory partial epilepsy.

Amines↗
PubMedDate not supplied

Influence of NG-nitro-L-arginine on the anticonvulsant and acute adverse effects of some newer antiepileptic drugs in the maximal electroshock-induced seizures and chimney test in mice.

Overwhelming evidence indicates that nitric oxide (NO) plays an important role in epileptogenesis and seizure activity in the brain. The results of experimental studies on animals provide, however, discrepant information reporting that NO has both anti- and pro-convulsant action in the brain. The objective of this study was to determine the effect of N(G)-nitro-L-arginine (L-NA--a non-specific NO synthase inhibitor) on the anticonvulsant and acute adverse-effect profiles of four second-generation antiepileptic drugs (felbamate [FBM], lamotrigine [LTG], oxcarbazepine [OXC] and topiramate [TPM]) in the maximal electroshock (MES)-induced seizure model and the chimney test in mice. Results indicated that L-NA(at 40 mg/kg, ip) did not affect significantly the antiseizure activity of all examined drugs. However, the antielectroshock action of FBM and LTG after co-administration of L-NA was attenuated by 36% and 28%. In contrast, the anticonvulsant effects of TPM and OXC were almost unchanged after L-NA administration. Moreover, the NO synthase inhibitor (40 mg/kg, ip) did not enhance the acute adverse-effect profiles of the studied antiepileptic drugs in the chimney test. In conclusion, the observed reduction of the anticonvulsant effects of FBM and LTG after co-administration of L-NA may suggest a pro-convulsant activity of L-NA and the cooperation of NO with the antiseizure properties of FBM and LTG in the MES test in mice.

Animals↗
PubMed1991

Effects of muscarinic receptor agonists and antagonists on response of non-extensor rats to maximal electroshock.

Rats which do not respond consistently to maximal electroshock by exhibiting the classical hindlimb extensor response, are designated as 'flexors', and can serve as a useful experimental model for investigating seizure mechanisms. 20-25% Charles Foster rats exhibit the flexor status and were used in this study. The flexor rats were converted to extensors by acetylcholine (icv), physostigmine (ip) and the selective muscarinic M1 receptor agonists, arecholine (ip) and McN-A-343 (icv). This conversion of flexors to extensors was significantly attenuated by M1 receptor antagonists scopolamine (ip) and pirenzepine (icv). The M2 receptor agonist, carbachol (icv), had no effect in lower doses but induced conversion of flexor rats to the extensor status only in very high doses which may be due to loss of receptor specificity on dose increment. The M2 receptor antagonists, gallamine (icv) and AF-DX 116 (ip), also induced significant conversion of flexors to extensors, which was dependent upon the availability of neuronal acetylcholine since the effects were attenuated following pretreatment with hemicholinium, an inhibitor of acetylcholine synthesis. The results suggest that the central cholinergic system has a facilitatory pro-convulsant effect, mediated through the muscarinic M1 receptors, an action modulated by the M2 receptors.

Acetylcholine↗
PubMed1989

Effect of beta-adrenoceptor antagonists and some related drugs on maximal electroshock seizures in mice.

(+/-) Propranolol (1-50 mg/kg), (+) propranolol (50 mg/kg) and pindolol (10-50 mg/kg) exhibited significant protective effects against MES (maximum electroshock seizures), whereas, timolol (1 mg/kg), the propranolol analog, UM-272 (1 and 10 mg/kg), and the beta-agonist, terbutaline (1 and 10 mg/kg) were ineffective. Cholinergic agents, physostigmine (0.01-1.0 mg/kg), and atropine (1 and 10 mg/kg), the serotonin antagonist, cyproheptadine (0.05 mg/kg), and the prostaglandin synthesis inhibitor, indomethacin (10 mg/kg), were also without effect on the MES extensor phase. Further, pretreatment of mice with terbutaline, atropine, cyproheptadine or indomethacin did not influence the anti-MES effect of propranolol to any significant extent. The results indicate that the observed anticonvulsant effects of beta-adrenoceptor antagonists are unrelated to noradrenergic or other central neurotransmitter systems and that a non-specific mechanism, probably a membrane stabilizing effect is involved.

Adrenergic beta-Antagonists↗
PubMed1988

Pharmacological modulation of central monoaminergic systems and influence on the anticonvulsant effectiveness of standard antiepileptics in maximal electroshock seizure.

The influence of various substances modulating the activity of central noradrenergic, serotonergic or dopaminergic neurotransmission systems on the anticonvulsant effectiveness of phenobarbital (phenytoin, carbamazepine) was investigated in mice using the maximal electroshock seizure test (MES). The results demonstrated that especially the noradrenergic system might play a predominant role in modulating the efficiency of the standard antiepileptics tested. In general, pharmacological stimulation with different sympathomimetic drugs (e.g. methamphetamine, maprotiline, tranylcypromine, yohimbine) increased the anticonvulsant activity significantly. Conversely, pharmacological suppression of the noradrenergic system (e.g. 6-OHDA, phenoxybenzamine) reduced the activity of the antiepileptics. In contrast, some beta-receptor blockers with local anesthetic properties (e.g. propranolol, alprenolol, pindolol) were also able to enhance the protective effect of phenobarbital in higher concentrations. The influence of manipulations of serotonergic mechanisms was not so pronounced. However, substances such as 5-HTP, clomipramine, citalopram, zimelidine, showed also additive anticonvulsive effects. On the other hand, the dopaminergic system seemed to exert no significant influence in this respect. These findings give further support to the view that the noradrenergic system may play a remarkable role via the inhibitory function of noradrenaline in the CNS in suppression of epileptic activity and reveal also interesting aspects for a possible comedication in convulsive disorders.

Animals↗
PubMed1985

Infusion of opiates into substantia nigra protects against maximal electroshock seizures in rats.

Microinfusion of morphine sulfate (50 nmol), [d-Ala2]-Met-enkephalin (35 nmol) or dynorphin A 1-13 (1 nmol) bilaterally into the substantia nigra significantly attenuated seizures induced by maximal electroshock in rats. This action was accompanied by stereotyped behavioral hyperactivity. These anticonvulsant and behavioral effects were antagonized by systemic naloxone administration; neither effect was observed after intranigral microinjection of dynorphin A 1-17 amide (1 nmol). These results are consistent with a mu opiate receptor-mediated inhibition of substantia nigra efferent neurons, and with the proposal that bilateral inhibition of nigral efferents attenuates seizure propagation. However, intranigral morphine failed to alter the severity of i.v. bicuculline seizures, indicating that opiate-mediated inhibition in substantia nigra is distinct from that produced by gamma-aminobutyric acid.

Animals↗
PubMed1987

Inhibition of electroshock-induced seizures by cholecystokinin-related peptides in mice.

The effects of several doses of cholecystokinin octapeptide sulphate ester (CCK-8-SE) and nonsulphated cholecystokinin octapeptide (CCK-8-NS), and two CCK-related peptide analogues Ac-Thr5-caerulein, and nonsulphated Ac-Thr5-caerulein were investigated on electroshock-(ES)-induced seizures after intraperitoneal administration in mice. As parameters, the duration of the tonic and clonic phase of the fit, and those of postictal coma and behavioural depression were measured. CCK-8-SE decreased the duration of the clonic phase; its highest dose, 3.2 mumol/kg, shortened the coma. CCK-8-NS antagonized only slightly the clonic phase of seizure. Ac-Thr5-caerulein did not influence ES-induced seizures in any dose, only increased the duration of behavioural depression. Similarly to CCK-8-NS, the nonsulphated form of Ac-Thr5-caerulein inhibited selectively the clonic phase of seizures. The reference drugs, diazepam and phenobarbital, antagonized dose-dependently and most effectively the tonic phase of ES-induced seizures, but in much higher doses than did the CCK-related peptides. Besides, diazepam increased and phenobarbital decreased the duration of postictal coma. The results showed that the tested CCK-related peptides inhibit prevalently the clonic phase of ES-induced seizures after peripheral administration.

Animals↗
PubMedDate not supplied

Effect of foot-electroshock stress on cholinergic activity, tissue glycogen and blood sugar in albino rats.

The immediate or 24 hr delayed effects of 1-day (1-DS) or (7-DS) foot-electroshock stress in albino rats were studied on cardiac acetylcholine (ACh), blood and cardiac cholinesterase (ChE) activities, cardiac, hepatic and muscle glycogen contents and blood sugar concentrations. The effects of physostigmine (PHY), atropine, 6-hydroxydopamine (6-HD), vagotomy and adrenalectomy on 1-DS induced changes were also studied. 1-DS produced an increase in cardiac ACh content which lasted for 24 hr but repeated stress showed phenomenon of adaptation. There seems to be activation of autonomic cholinergic system in stress. 1-DS and 7-DS produced a short-lived inhibition of blood ChE activity and 7-DS also of cardiac ChE activity. Inhibition of ChE activity was probably related to release of adrenaline from adrenal medulla. 1-DS produced hepatic and muscle glycogenolysis with slight hypoglycaemia but without any effect on cardiac glycogen. Following repeated stress there was a phenomenon of adaptation. The hepatic and muscle glycogenolysis produced by stress is due to the release of adrenaline from adrenal medulla. Normally functioning cardiac cholinergic system seems to have a protective effect on heart against stress, in the absence of which cardiac glycogenolysis is induced by stress.

Acetylcholine↗
PubMed1981

Comparative assessment of the anticonvulsant activity of some benzodiazepines, phenobarbitone and diphenylhydantoin against maximal electroshock seizures in rats: a time-distribution study.

The anticonvulsant activity of three benzodiazepines (BZDP) and two standard antiepileptic drugs were investigated comparatively against maximal electroshock seizures in rats in a time-distribution study. While phenobarbitone (PHB) and diphenylhydantoin (DPH) gave marked to moderate protection (100%-67%) against tonic seizures up to 6-7 h post-treatment, the BZDP provided significant protection (100%-60%) only up to 1.5 h, with clonazepam being the strongest and diazepam the weakest. Clonic seizures occurred in all treatment groups, whether tonic seizures preceded them or not, but their duration was longer in the DPH and PHB groups than in the BZDP groups. Total seizure durations were often significantly reduced in the BZDP groups, notably with clonazepam, whereas it was invariably longer in the DPH and PHB groups when compared with the vehicle treated controls. The BZDP treated rats generally required longer time to recover from postictal coma, the effect being dose-related. the DPH and PHB treated rats needed longer recovery time when the treatment-test interval was 18-20 h.

Animals↗