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PubMedDate not supplied

Correlation between effects of acute acetazolamide administration to mice on electroshock seizure threshold and maximal electroshock seizure pattern, and on carbonic anhydrase activity in subcellular fractions of brain.

The relationships between inhibition of carbonic anhydrase (CA) activity in cytoplasmic, microsomal, and myelin subcellular fractions obtained from cerebral cortex, subcortex, and cerebellum and electroshock seizure threshold (EST) and modification of the extension/flexion (E/F) ratio following maximal electroshock seizures (MES) were ascertained in Swiss-Webster mice given 40 and 200 mg/kg acetazolamide. The parameters were determined at 1, 4, and 24 h after administration of acetazolamide. The results showed that changes in the E/F ratio induced by acetazolamide correlated linearly (r = 0.90) with changes in CA activity in the cytoplasm of the subcortex. However, there was an inverse power function correlation (r = 0.92) between EST and CA activity in the myelin fraction of the cerebral cortex. The time course of acetazolamide inhibition of CA activity in these two fractions also paralleled the time course of its effects on EST and E/F ratio. Thus, acetazolamide decreases susceptibility to seizures (raises EST) by inhibiting myelin CA and prevents spread of seizure activity by inhibiting CA in the cytoplasm of glial cells. The CO2 that accumulates as a result of CA inhibition in these two fractions causes profound changes in brain function.

Acetazolamide↗
PubMedDate not supplied

Electroshock- and pentylenetetrazol-induced seizures in genetically epilepsy-prone rats (GEPRs): differences in threshold and pattern.

Using facial and forelimb (F&F) clonus (a proposed forebrain marker) and running-bouncing (R/B) clonus and tonus (proposed brain-stem markers), the responsiveness of forebrain and brain-stem to electroshock or pentylenetetrazol seizures was assessed in GEPRs. The most striking finding was the failure of GEPR-9s to display F&F clonus in response to transcorneal electroshock at any stimulus intensity. Indeed, GEPR-9s displayed only R/B clonus or tonus indicative of brain-stem seizure discharge. GEPR-3s and normal rats, on the other hand, displayed F&F clonus in response to the least effective electroshock stimulus, and R/B clonus and tonus at higher stimulus intensities. After treatment with phenytoin (50 mg/kg) to inhibit the tonic seizure, the least effective electroshock stimulus also produced F&F clonus in GEPR-9s. These findings suggest that the threshold for triggering brain-stem seizure discharge by electroshock is lower than that for triggering forebrain seizure discharge in GEPR-9s, whereas the reverse relationship is true in normal rats and GEPR-3s. The rank ordering of the electroshock thresholds was: normals greater than GEPR-3s greater than GEPR-9s. Both GEPR-3s and GEPR-9s were found to be hyper-responsive to pentylenetetrazol as evidenced by shorter latency for the tonic seizure and a greater seizure severity than normal rats. The rank ordering of seizure severity in response to pentylenetetrazol was: GEPR-9 greater than GEPR-3 greater than normal rats.

Animals↗
PubMed1990

Rapid rise in transcription factor mRNAs in rat brain after electroshock-induced seizures.

Recent studies have demonstrated that several transcription factor genes are rapidly activated by neuronal stimulation. For example, we have found that prolonged and repeated seizure activity produced by administration of chemical convulsants induces a rapid and transient increase in mRNA levels of four immediate early genes in rat brain. These genes, zif/268, c-fos, c-jun, and jun-B, encode sequence specific DNA binding proteins thought to act as transcription regulatory factors. To ascertain whether a brief electrically induced seizure discharge of the type utilized in clinical electroconvulsive treatment is sufficient to induce a similar genomic response, we have examined the response of these mRNAs in rat brain following single and repeated electroshock-induced seizures. After electroshock, mRNA levels of each of these genes increase within 15 min, and all except c-jun return to near baseline levels within 4 h. Although this response is most prominent in granule cell neurons of the hippocampus, increases are also apparent in neocortex and pyriform cortex. The rapid mRNA response persists in animals receiving a chronic electroshock protocol similar to that used in clinical electroconvulsive therapy. Intrahippocampal infusion of the sodium channel antagonist tetrodotoxin blocks hippocampal mRNA responses without blocking seizures, indicating a role for electrical excitation in the electroshock-induced mRNA response. By contrast, pretreatment with anticonvulsants or selective NMDA antagonists, which reduce seizure intensity and block hindlimb extension, fails to alter mRNA responses, suggesting that seizure induction, rather than spread, is linked to these mRNA responses. Because electroshock induces robust, highly reproducible mRNA responses, it may be useful to study the neuronal genomic response to stimulation.

Animals↗
PubMed1990

Pretreatment with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline accelerates the electroshock-induced decrease in density of beta-adrenoceptors but not functional downregulation.

Intrapritoneal injection of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) to rats significantly reduced the density of alpha 1- and alpha 2-adrenoceptors in the cerebral cortex, without affecting beta-adrenoceptors. A single dose of EEDQ markedly accelerated the development of downregulation of beta-adrenoceptors induced by a short series of electroshocks. The accumulation of cAMP, induced by isoproterenol, was unchanged in rats treated with EEDQ, while the effect of noradrenaline was reduced, to the level observed after isoproterenol alone, indicating the attenuation of alpha-adrenoceptor function. The isoproterenol-induced accumulation of cAMP was not changed by EEDQ nor electroshock, not by the combined treatment. The stimulatory action of noradrenaline was reduced after EEDQ alone or in combination with electroshock, but the effect of electroshock alone was insignificant. The results suggest that the acceleration of downregulation of beta-adrenoceptors after combined treatment with an alpha-adrenoceptor blocking agent is related to elimination of the alpha-adrenergic potentiation of accumulation of cAMP mediated by beta-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1991

The role of technical, biological and pharmacological factors in the laboratory evaluation of anticonvulsant drugs. II. Maximal electroshock seizure models.

Although seizure models using electrical stimulation for the induction of generalized tonic-clonic seizures in rodents are widely employed to identify potential anticonvulsants, the important role of various technical, biological and pharmacological factors in the interpretation of results obtained with these models is often not recognized. The aim of this study was to delineate factors other than sex, age, diet, climate and circadian rhythms, which are generally known. For this purpose, experiments with 8 clinically established antiepileptic drugs were undertaken in the following electroshock seizure models: (1) the maximal (tonic extensor) electroshock seizure threshold (MEST) in mice; (2) the traditional maximal electroshock seizure (MES) test with supra-threshold stimulation in mice; and (3) the MES test with suprathreshold stimulation in rats. When drugs were dissolved in vehicles which did not themselves exert effects on seizure susceptibility, the most important factors which influenced drug potencies were (1) marked differences between drugs and species in terms of peak drug effect, duration of action and the formation of active metabolites; (2) differences in drug potencies calculated on the basis of administered doses compared to potency calculations based on active drug concentrations; (3) the equipment used for seizure induction; (4) marked effects of current strength on results obtained in electroshock seizure models; (5) site of application of the electrical stimulus (transcorneal vs. transauricular). In order to reduce the variability among estimates of anticonvulsant activity, the various factors delineated in this study should be rigidly controlled in experimental situations involving assay of anticonvulsant agents.

Age Factors↗
PubMed1992

7-Chlorokynurenic acid antagonizes the anticonvulsant activity of D-cycloserine in maximal electroshock seizures.

This study evaluated the anticonvulsant activity of D-cycloserine against maximal electroshock seizures in rats. Systematically administered D-cycloserine (i.p.) inhibited maximal electroshock-induced tonic hindlimb extension in a dose-dependent manner with an ED50 of 153 mg/kg. No neurological deficit was detected at any dose of D-cycloserine. In contrast, L-cycloserine had no effect on the maximal electroshock seizures. Administration of the strychnine-insensitive glycine receptor antagonist 7-chlorokynurenic acid (100 nmol, i.c.v.) significantly antagonized the anticonvulsant activity induced by D-cycloserine. Centrally administered D-cycloserine (i.c.v.) induced significant anticonvulsant activity 1-2 h after administration with an approximate ED50 of 5 mumol. 7-Chlorokynurenic acid (100 nmol, i.c.v.) significantly antagonized the anticonvulsant activity of centrally administered D-cycloserine. L-Cycloserine (i.c.v., 2 h) induced no significant anticonvulsant activity. These results provide evidence that the anticonvulsant activity of D-cycloserine in maximal electroshock seizures may be mediated by strychnine-insensitive glycine receptors.

Animals↗
PubMed1985

Upregulation of gamma-aminobutyric acid (GABA) B binding sites in rat frontal cortex: a common action of repeated administration of different classes of antidepressants and electroshock.

The action of different classes of clinically effective antidepressants and electroshock on gamma-aminobutyric acid (GABA) B recognition sites in the frontal cortex was compared to that of other psychotropic agents. After either prolonged (6-18 days) s.c. infusion via osmotic minipumps or repeated i.p. injections of different antidepressants, or a series of electroshocks, treatment was halted and 72 hr later the animals were sacrificed, the brain was dissected and frozen. All major antidepressants (desipramine, amitryptyline or maprotiline), several newer compounds with reported antidepressant activity (viloxazine, zimelidine, fluoxetine, citalopram, progabide, fengabine, sodium valproate, mianserin, trazodone or nomifensine) as well as pargyline and repeated electroshocks, up-regulated GABA B binding in the rat frontal cortex but not hippocampus. This appeared to be a maximum binding effect, but in some instance the kinetics were more complex. Reserpine, diphenylhydantoin and phenobarbital down-regulated GABA B binding in the frontal cortex, whereas this was unaltered by haloperidol, chlorpromazine or diazepam administration. Desipramine up-regulated GABA B binding in a dose- and time-dependent manner (minimum effective dose, 1.25 mg/kg/day s.c. for 18 days; onset of action, 6 days at 5 mg/kg/day s.c.). Together with the rather sparse data in the literature on GABA in depression and antidepressant drug action, these findings support a common GABAergic mechanism of action of antidepressant drugs and electroshock, mediated via GABA B synapses.

Animals↗
PubMed1977

Blood-brain barrier during electroshock seizures in the rat.

The effect of electrically induced seizures on the permeability of the rat blood-brain barrier was investigated. The small radioactive tracers sodium (24Na+), chloride (36Cl-) carbon labelled thiourea (14C-thiourea) and glucose (14C-D-glucose) were studied in indicator dilution experiments with indium labelled diethylenetriaminepenta-acetic acid (113mIn-DTPA) as reference substance. This method allows a quantitative estimate of the transcapillary loss of solutes, the extraction (E), during a single passage through the brain. Passage of macromolecules was studied using as marker substance Evans Blue which binds to plasma albumin. In the resting state ENa, ECl, Ethiourea and Eglucose were 2.9, 4.8, 9.3 and 12.5%, respectively. During seizures and during shortlasting hypercapnia E glucose decreased while E for the other tracers was unchanged. As cerebral blood flow increased, there must be an increased transfer of test substances into the brain. This finding is in agreement with recent human studies [15]. When Evans Blue was injected intravenously prior to electroshock, there was no staining of brain tissue after one electroshock but following repeated electroshocks some staining was observed. In an attempt quantify this transcapillary loss of albumin by means of indicator dilution, 51Cr-labelled erythrocytes were used as intravascular reference substance against 113mIn-DTPA (a plasma tracer). However, the albumin loss (by pinocytosis or otherwise) occurring after ten electroshocks could not be detected during a single passage through the brain.

Animals↗
PubMed1990

[Use of electroshock for vital indications].

Electroshock therapy still remains a very controversial problem in the treatment of mental disorders. It is very effective in a narrow range of indications and has not many absolute contraindications. Epilepsy is one of the relative contraindications of electroshock therapy. The authors submit the case-history of an epileptic patient in a severe catatonic state with incipient metabolic breakdown, where electroshock therapy was followed by a rapid effect without any neurological complications. The contraindications of electroshock are rather relative than absolute and it is up to the doctor to consider whether the assumed therapeutic effect will outweigh possible complications.

Adult↗
PubMed1989

Relationship between concentration and anticonvulsant effect of phenytoin against electroshock-induced seizures in rats: comparison of sampling sites for concentration determinations.

The purpose of this investigation was to determine the optimum sampling site for phenytoin concentration measurements in the context of pharmacodynamic studies of the anticonvulsant effect of phenytoin. Determination of drug concentrations in the serum, serum water, brain, and cerebrospinal fluid (CSF) of rats as a function of time after iv injection of a 6-mg/kg dose revealed a significant disequilibrium between brain and serum water for 15 min and between CSF and serum water for 5 min after injection. The concentrations of phenytoin in serum water 1 min after injection of 3 mg/kg (0.371 +/- 0.054 microgram/mL) and 45 min after injection of 8 mg/kg (0.399 +/- 0.049 microgram/mL) were not significantly different, but drug concentrations in the CSF and brain were appreciably higher after the latter dose. There was no protection against electroshock-induced seizures 1 min after the 3-mg/kg dose, but there was complete protection 45 min after the 8-mg/kg dose. At 15 min after drug injection, phenytoin concentrations in CSF and serum water were essentially identical over a wide concentration range. Fifty female Lewis rats weighing approximately 225 g, that consistently exhibited maximal electroshock-induced seizures in three preliminary trials on separate days, received 1, 2, 4, 6, or 8 mg/kg of phenytoin by iv injection. Electroshock was applied 15 min later, the percentage of animals protected from seizure by each dose was determined, and drug concentrations in serum, serum water, brain, and CSF were measured by gas chromatography. The relationship between anticonvulsant activity and drug concentration could be described by a Hill-type equation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Microinjection of muscimol into entopeduncular nucleus suppresses pilocarpine but not maximal electroshock seizures in rats.

Microinjection of muscimol (406 pmol) into the rat entopeduncular nucleus, the analogue of the primate globus pallidus pars interna, significantly suppressed pilocarpine but not maximal electroshock seizures in a spatially specific manner. In contrast to its lack of efficacy in the entopeduncular nucleus, microinjection of muscimol into the substantia nigra suppressed maximal electroshock seizures. These findings suggest that the neural networks and/or the neurotransmitters that subserve the propagation of pilocarpine and maximal electroshock seizures differ with regard to the entopeduncular nucleus. The data also underscore the powerful regulatory role of the substantia nigra in diverse models of seizures.

Animals↗
PubMed1988

The influence of electroshock on adrenoceptor function in rat brain cerebral cortex: selectivity for the alpha-adrenoceptor site.

The present study was undertaken to examine the effect of electroshock on adrenoceptor-mediated cAMP and inositol phosphate accumulation in rat brain cerebral cortical slices. Under the conditions of these experiments, isoproterenol-induced cAMP accumulation was unaltered by electroshock, although there was a significant reduction in the norepinephrine- and isoproterenol + 6-fluoronorepinephrine-stimulated responses. No change in alpha-adrenoceptor-mediated inositol phosphate accumulation was noted. The results indicate that electroshock selectively modifies an alpha-adrenoceptor system in brain that differs from that associated with inositol phosphate accumulation.

Animals↗
PubMed1986

Modification of electroshock and pentylenetetrazol seizure patterns in rats after precollicular transections.

Rats with precollicular transections leaving the brain stem intact were subjected to electroshock or pentylenetetrazol-induced convulsions. Animals with transections failed to display the face and forelimb clonus (with or without rearing) typically seen in sham-operated rats subjected to pentylenetetrazol- or minimal electroshock-induced convulsions elicited with corneal electrodes. Moreover, rats with transections exhibited all other components of pentylenetetrazol- and electroshock-induced seizures. These findings support the hypothesis that tonic and some types of clonic convulsions can occur independently of seizure discharge in forebrain structures, whereas clonus restricted to the face and forelimbs depends on seizure discharge emanating from structures within the forebrain for expression.

Animals↗
PubMed1988

Anticonvulsant and antiepileptogenic actions of MK-801 in the kindling and electroshock models.

The actions of MK-801, a noncompetitive antagonist at the N-methyl-d-aspartate subtype of excitatory amino acid receptor, were investigated on the development of kindling and on seizures in the electroshock and kindling models. The drug MK-801 potently and effectively suppressed the tonic hindlimb extension component of electroshock-induced seizures; it also suppressed both the electrophysiological and behavioral manifestations of the development of kindling. In contrast to its effects on electroshock-induced seizures and the development of kindling, MK-801 only partly reduced the duration of seizures in fully kindled animals and did not elevate the threshold for afterdischarge despite the use of a large dose, associated with profound untoward behavioral effects. Together with previous findings, these results support the idea that noncompetitive blockade of NMDA receptors markedly inhibits the development of kindling. The diminished effectiveness of MK-801 against kindled seizures suggests that MK-801 will not be a clinically-useful anticonvulsant against complex partial seizures.

Amygdala↗
PubMed1992

Antiparkinsonian drugs memantine and trihexyphenidyl potentiate the anticonvulsant activity of valproate against maximal electroshock-induced seizures.

Memantine increased the threshold for electroconvulsions, when administered at 1.0-6.0 mg/kg (i.p.) and given in subthreshold doses of 0.0156, 0.0625, 0.125 and 0.5 mg/kg (i.p.) potentiated the protective efficacy of valproate, against maximal electroshock (50 mA)-induced seizures in mice, lowering the ED50 from 235 to 197, 172, 164 and 130 mg/kg, respectively. Trihexyphenidyl, applied in doses of 30 and 50 mg/kg (i.p.), did not influence the electroconvulsive threshold per se but when combined with valproate, strongly enhanced its anticonvulsant activity against maximal electroshock-induced seizures lowering the ED50 from 206 to 103 and 46 mg/kg, respectively. The chimney test and retention testing in mice revealed that administration of memantine at 0.5 mg/kg (i.p.) or trihexyphenidyl at 30 mg/kg (i.p.) together with valproate in doses of 130 or 103 mg/kg (i.p.), respectively, resulted in motor impairment and caused impairment of long-term memory, similar to the effects of valproate alone, when applied at its ED50 against maximal electroshock. Neither memantine nor trihexyphenidyl altered the total level of valproate in plasma. It may be concluded that the potentiation of the anticonvulsant activity of valproate, by memantine and trihexyphenidyl, is not associated with a pharmacokinetic interaction.

Animals↗
PubMed1991

Interaction of felbamate and diazepam against maximal electroshock seizures and chemoconvulsants in mice.

The anticonvulsant effects of felbamate alone or in combination with diazepam were investigated against maximal electroshock-, pentylenetetrazol-, isoniazid- and bicuculline-induced seizures in mice. A single subprotective dose of felbamate, a dose which offers no protection to animals when combined with diazepam, enhanced the protective effects of diazepam against seizures induced by electroshock, pentylenetetrazol and isoniazid, as measured by significant reduction of ED50 values. However, felbamate failed to significantly affect the protective action of diazepam against bicuculline. Felbamate does not interact directly with the GABA-benzodiazepine-ionophore complex. Thus the enhancement of anticonvulsant activity of diazepam by felbamate against maximal electroshock and pentylenetetrazol may involve an indirect effect at benzodiazepine receptors. The anticonvulsant action of felbamate against isoniazid does not seem to involve benzodiazepine receptors and may be due to reversing the inhibitory effect of isoniazid on glutamate decarboxylase (GAD) activity. The interaction between felbamate and diazepam may also involve other mechanisms.

Animals↗
PubMed1991

Effects of cold-restraint and swim stress on convulsions induced by pentylenetetrazol and electroshock: influence of naloxone pretreatment.

The influence of two stressogenic conditions, restraint at 4 degrees C for 30 min (cold-restraint stress; CRS) or swimming at 20 degrees C for 3 min (swim stress; SS), on nociception and on convulsions triggered by different agents was assessed in mice. In saline-pretreated mice CRS and SS caused analgesia (hot-plate test, 56 degrees C), delayed the onset of convulsions induced by pentylenetetrazol (PTZ, 100 mg/kg, IP) and aggravated convulsions elicited by maximal transcorneal electroshock (150 mA pulses at 60 Hz for 0.2 s). Pretreatment with naloxone (10 mg/kg, SC, 30 min prior to testing), which did not affect the responsiveness of nonstressed mice to the hot plate or to the convulsant treatments, attenuated the development of analgesia following CRS, but not SS, and further prolonged the latency to onset of PTZ-induced convulsions in both stressed groups. Thus the extent to which CRS and SS can each delay the onset of PTZ-triggered convulsion appears to be limited by activation of a proconvulsant opioid system. In contrast, naloxone pretreatment did not modify the effects of CRS or SS on the severity of electroshock-induced seizures. In conclusion, CRS and SS can each, simultaneously, exert anticonvulsant and proconvulsant influences on responsiveness to PTZ and electroshock, respectively. Also, both forms of stress can activate an opioid system modulating the onset of PTZ-induced seizures, which is distinct from that controlling nociception. These findings, together with those of other stress, convulsions and opioid systems, which depends on the characteristics of the stressogenic condition, species, convulsant agent and parameter considered.

Analgesia↗