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PubMed2004

Receptor mechanisms involved in the anticonvulsant effect of melatonin in maximal electroshock seizures.

The present study investigates the mechanisms involved in the anticonvulsant effect of melatonin in maximum electroshock (MES) seizures. Melatonin (25-100 mg/kg) dose-dependently decreased the duration of tonic hindlimb extension (THLE). The anticonvulsant effect of melatonin was blocked by bicuculline, a GABA(A) receptor antagonist, and luzindole, an ML(1) receptor antagonist, while prazosin, an ML(2) receptor antagonist, enhanced the anticonvulsant actions of melatonin in this seizure model. Administration of serotonergic agents, mianserin and ondansetron, along with melatonin, increased the antiseizurogenic activity of melatonin, while buspirone had no effect. Pretreating the animals with diazepam, carbamazepine or lamotrigine enhanced the anticonvulsant effect of melatonin. Melatonin thus appears to be an effective anticonvulsant, and melatonin ML(1) receptors, GABAergic and serotonergic mechanisms may play an important role in mediating the anticonvulsant activity of melatonin in electroshock seizures.

Animals↗
PubMed1999

Role of nitric oxide in electroshock and pentylenetetrazole seizure threshold in rats.

There are contradictory reports on whether nitric oxide (NO) is a proconvulsant or anticonvulsant. Hence a study was designed to investigate the effect of NO donor l-Arginine and NO synthesis inhibitor N omega-nitro-L-arginine (NOARG) on electroshock- and pentylenetetrazole (PTZ)-induced seizure threshold in rats. L-arginine was tested in three doses (75, 150 and 300 mg/kg), and NOARG was administered in doses of 4, 8 and 16 mg/kg. L-Arginine increased the intensity of current required to produce a threshold seizure, whereas NOARG had the opposite effect. In PTZ-induced seizures, L-arginine significantly decreased the dose of PTZ required to produce a threshold seizure, while NOARG increased it. Hence, it was concluded that NO synthase inhibition had the opposite effect in electroshock- and PTZ-induced seizures, meriting further studies on the mechanism of effect.

Animals↗
PubMed2002

Influence of several convulsants on the protective activity of a non-competitive AMPA/kainate antagonist, LY 300164, and lamotrigine against maximal electroshock in mice.

Aminophylline (50-100 mg/kg) and strychnine (0.125-0.5 mg/kg) significantly raised the ED50 values of LY 300164 against maximal electroshock in mice, from 4 to 8 mg/kg (aminophylline 100 mg/kg) and from 3.6 to 11.5 mg/kg (strychnine 0.5 mg/kg). Also, aminophylline (25-50 mg/kg) and strychnine (0.125-0.25 mg/kg) increased the ED50 value of lamotrigine in this test, for instance from 5.5 to 8.0 mg/kg (aminophylline 50 mg/kg) and from 5.2 to 8.9 mg/kg (strychnine 0.25 mg/kg). Moreover, the ED50S values of aminophylline and strychnine for the reduction of the anticonvulsant effect of LY 300164 (7 mg/kg, the dose equal to its ED97 value against maximal electroshock) were 79.9 and 0.2 mg/kg, respectively. The respective ED50 values for the inhibition of the antiseizure action of lamotrigine were 40.9 and 0.2 mg/kg. Neither bicuculline nor picrotoxin affected the protective action of LY 300164 or lamotrigine. Strychnine significantly lowered the plasma concentrations of LY 300164 and this my point to a pharmacokinetic mechanism of the observed interaction. Aminophylline did not affect the plasma concentrations of the studied anticonvulsant drugs and strychnine - that of lamotrigine, so a pharmacokinetic interaction does not seem probable. The present results indicate that the potential of aminophylline and strychnine to attenuate the anticonvulsant activity of conventional antiepileptics is extended to LY 300164 and lamotrigine.

Aminophylline↗
PubMed2006

Effect of cyclooxygenase-2 (COX-2) inhibitors in various animal models (bicuculline, picrotoxin, maximal electroshock-induced convulsions) of epilepsy with possible mechanism of action.

Enzyme cyclooxygenase (COX) is reported to play a significant role in neurodegeneration and may play a significant role in the pathogenesis of epilepsy. Bicuculline (4 mg/kg; ip), picrotoxin (8 mg/kg; ip) and electroshock (60 mA for 0.2 sec) significantly induced convulsions in male Laka mice. COX-inhibitors viz. nimesulide (2.5 mg/kg; ip) and rofecoxib (2 mg/kg, ip) administered 45 minutes prior to an epileptic challenge prolonged mean onset time of convulsions, decreased duration of clonus and decreased % mortality rate against bicuculline- and picrotoxin-induced convulsions in mice. COX-2 inhibitors were ineffective towards maximal electroshock-induced convulsions. Nimesulide (1 mg/kg) and rofecoxib (1 mg/kg) also enhanced the effect of subprotective dose of muscimol against picrotoxin-induced convulsions. The result of the present study strongly suggests for a possible role of cyclooxygenase isoenzymes particularly, COX-2 in the pathophysiology of epilepsy and its GABAergic modulation.

Animals↗
PubMed1978

[Activity of Na, K-ATPase and the enzymes of intermediate metabolism in the brains of rats exposed to electroshock].

Activity of Na, K -ATPase, acetylcholinesterase (AChE) and glutamic acid decarboxylase (GAD) in the fractions of the rat brain and spinal cord tissue were studied in rats during a single electroshock (ES) and 5 and 30 minutes after it. GAD activity of the synaptosome fraction was shown to decrease insignificantly, but activity of AChE, Na, K -ATPase and possibly of proteolytic enzymes increased 5 minutes after electroshock and became normal in 30 minutes. It is supposed that the revealed inhibition of Na, K -ATPase activity in the "synaptosomes" of the rat brain cortex could be of pathogenetic significance in the origination of the convulsive process.

Acetylcholinesterase↗
PubMed1979

[Na, K-ATPase activity of the meninges in electroshock and the action of the anticonvulsant agent, diazepam].

It was shown that the phenomenon of inactivation of Na, K-ATPase of the non-purified fraction of the rat cortical synaptosomes under electroshock may be related to "modification" of the potassium active center of the enzyme. The anticonvulsant diazepam injected intramuscularly also inhibits Na, K-ATPase of the cerebral membranes. However, in subsequent electrical stimulation of the brain the drug activates Na, K-ATPase as compared to controls. Diazepam also abolishes clonic convulsions induced by electrical stimulation of the brain. At the same time it does not eliminate compensatory shifts in the activity of acetyl-cholinesterase of the rat cerebral and spinal synaptosomes, characteristic of electroshock. The results are discussed from the standpoint that inhibition of the activity of Na, K-ATPase of the nerve endings membranes may underlie the pathogenetic mechanism of the convulsive activity.

Acetylcholinesterase↗
PubMed1989

The effect of propranolol on maximal electroshock seizures in mice.

The aim of this study was to determine the possible effect of propranolol, a beta-adrenoceptor blocker, on maximal electroshock seizures (MES) in mice. It was found that doses of 5, 10 and 20 mg/kg propranolol caused an increase in the convulsion threshold of maximal electroshock seizures (MES) proportional to the dose and, that the mode of the anticonvulsant action of propranolol used doses in this study is related to membrane stabilization.

Animals↗
PubMed1979

Anticonvulsant effects of benzhydryl piperazines on maximal electroshock seizures in rats.

The anticonvulsant effects of four benzhydryl piperazines, SC-13504 (ropizine, an anticonvulsant), hydroxyzine (HDX, an anxiolytic), chlorcyclizine (CCZ, an antihistaminic) and buclizine (BUC, an antihistaminic), were investigated utilizing a modified maximal electroshock seizure test in rats. In addition to detecting the presence or absence of tonic hindlimb extension, the modified method quantified various phases of the seizure. All four benzhydryl piperazines exhibited anticonvulsant activity in maximal electroshock seizure, but SC-13504 was similar in efficacy to phenobarbital and phenytoin, and much more effective than HDX, CCZ or BUC. Additionally, SC-13504 possessed a therapeutic index much greater than any of the compounds tested. The duration of action of the benzhydryl piperazines, in hours was: SC-13504, 0.5 to 8; HDX, 0.5 to 2; CCZ, 0.5 to 16; and BUC, 2 to 8. Buc and CCZ are postulated to be converted to active anticonvulsant metabolites.

Animals↗
PubMedDate not supplied

Protective effects of different beta-blocking agents against electroshock lethality in mice.

The protective effect of phenytoin against an electroshock lethal dose (ELD), was compared with that of three different beta-blocking agents. These compounds were propranolol with quinidine-like activity (QLA) but no intrinsic sympathomimetic activity (ISA), practolol with ISA but no QLA and metoprolol with no ISA but some QLA. Phenytoin (15 mg/kg) and propranolol (70 mg/kg) protected all the animals. Metoprolol was only effective at higher concentrations (130 mg/kg). Practolol afforded some degree of protection at low doses (20 mg/kg) but at higher doses its ISA can be deleterious by decreasing the ELD threshold. These results suggest that QLA is more important than beta-blocking activity for protection against electroshock lethality.

Adrenergic beta-Antagonists↗
PubMed1993

An immediate morphopathologic response of neurons to electroshock; a reliable model for producing "dark" neurons in experimental neuropathology.

Ninety rats were electroshocked by a single condenser discharge 1 min. prior to perfusion fixation and delayed autopsy. Voltage and capacity of the condenser as well as surface area and position of the electrodes were varied between 125 and 1250 V, 20 and 200 microF, 2 and 24 mm2, and frontal to posterior, respectively. Within these ranges the electroshock rendered a varying number of brain neurons together with their dendritic arborization stainable by a special silver method. In toluidine blue preparations both somata and nuclei of these neurons appeared markedly shrunken and hyperchromatic, indicating morphological damage ("dark" neuron). A 250-V shock damaged only granule neurons of the hippocampal dentate gyrus. After a 750-V shock it was the substantia nigra, the lateral septal nucleus, the anterior amygdaloid area, and the lateral preoptic area that consistently contained electrically damaged neurons, without other kinds of parenchymal damage.

Animals↗
PubMed1993

Effect of piracetam on electroshock induced amnesia and decrease in brain acetylcholine in rats.

Piracetam, a prototype of a new class of psychotropic agents, the nootropic agents, which improve learning ability and memory retention, was found to induce a dose-related prevention of disruption of acquisition of a passive avoidance response produced by electroshock application. The amnesia attenuating effect of piracetam was accompanied by prevention of the decrease in acetylcholine concentrations of rat brain induced by electroshock. The study indicates that the cognition enhancing effect of piracetam may be due to a facilitatory effect on cholinergic transmission.

Acetylcholine↗
PubMed1983

Long-term effect of electroshock treatment on the entry of calcium into the cerebroventricular fluid in the rat.

The rate of appearance (Ra) of calcium (Ca) in the cerebroventricular compartment of urethane-anesthesized rats was determined by two methods: one is measurement of isotope dilution during ventricular-cisternal perfusion with artificial cerebrospinal fluid (CSF) containing 45Ca, the other is estimation of the rate of entry of 45Ca from plasma after rapid injection of tracer 45CaCl2 intravenously. Electroshock treatment (EST) for 3 successive days resulted in a marked increase in the rate of entry of calcium from blood to CSF. The effect of EST on the permeability of the blood-CSF barrier to Ca could be observed even 24 hr after the generalized seizure induced by electroshock has terminated.

Animals↗
PubMed1982

Electroshock afterdischarges are related to neuronal oscillability: neuronal models of Aplysia.

Identifiable giant neurons of Aplysia explored intracellularly behave differently at the offset of an intracellular electroshock (IES) or after a synaptic 'tetanization', according to their functional type: neurons of the stable type depolarize and fire at the offset of the IES, anodal or cathodal, thus eliciting an afterdischarge (AD). The threshold of this AD is lowered if the neuron is destabilized, i.e. converted from the stable to an oscillatory type (for instance by decalcification). Neurons normally of the tonic type are more sensitive to an IES, eliciting a longer afterdischarge than the stable neurons. Extracellular electroshock (EES) anodal or cathodal, applied directly on desheathed somata of Helix give long-lasting afterdischarges at the offset. In addition, EES stimulating presynaptic terminals or axons leads to a high frequency synaptic input on remote neurons. At the offset of this input either prolonged synaptic afterdischarges or postsynaptic rebounds of the membrane potential sustaining bursts of decreasing amplitude denote apparent oscillatory properties of the synaptically activated neuron. Finally, any conversion by convulsants of tonic neurons to oscillators highly facilitates the elicitation of afterdischarges of axons simultaneous to paroxysmal depolarization shifts of the homologous somata. These results indicate that afterdischarge elicitation is highly facilitated (low threshold) in normal oscillatory neurons and/or chemically destabilized neurons.

Animals↗
PubMed1981

Electroshock seizures in mice: effect on brain adenosine and its metabolites.

Adenosine and its immediate metabolites, inosine and hypoxanthine, were measured in mouse brain following the induction of electroshock seizures and after a subconvulsive series of electric shocks. Electroshock seizures resulted in a marked and prolonged rise in inosine, with maximal values at 5 min. Hypoxanthine increased more slowly but reached high levels by 10 min. Adenosine was unchanged. Phenytoin and to a lesser extent phenobarbital reduced these effects. Following the subconvulsive stimulus, 15 single shocks over an interval of 5 sec, inosine increased rapidly, adenosine rose slightly, and hypoxanthine did not change. Both phenytoin and phenobarbital blocked these increases in adenosine and inosine. Early elevations in inosine may play some role in seizure generation and propagation. The high levels of inosine and hypoxanthine found after recovery may be involved in the termination of epileptic activity, possibly by interacting with the benzodiazepine receptor for which they are ligands.

Adenosine↗
PubMed1975

[Electroshocks, antidepressive agents, and anesthesia].

During 12 years, we have effected 6,982 electroshocks with anesthesia and celocurine (N.D.) on 713 patients, i.e. 7.25% of the total hospitalized patients. 62% of them (440) were all this time under antidepressant drugs and 38% (273) were not. We observed 16 minor incidents ten (2.27%) among those under treatment and six (2.19%) among the others; of these 16 incidents, 11 led to an interruption of the treatment for safety. The association of antidepressant drugs with electroshock under anesthesia and celocurine (N.D.) does not present any real danger.

Adolescent↗
PubMed2002

Electroshock: a crime against the spirit.

Since its introduction in 1938, electroshock (electroconvulsive treatment, ECT) has been to its proponents a blessing and to its critics a curse. The author, himself an insulin coma-electroshock survivor, sides with the critics arguing that ECT is inherently harmful and dehumanizing. To support his views, he cites findings and comments from the professional literature in four areas: brain damage, memory loss, death, and brainwashing. The author also presents seven reasons for the continuing use of ECT, including profitability, value as a reinforcer of the biological model of mental illness, the absence of informed consent, the procedure's function as a "treatment of next resort," government and media support, and the public's failure to hold psychiatrists accountable for their conduct. The author concludes the article with his poem "Aftermath."

Brain Damage, Chronic↗
PubMed1981

[The role of high-dosage neuroleptic therapy and electroshock in the treatment of the acute phase of schizophrenia].

The authors studied the effectiveness of neuroleptic high-dosage therapy in comparison to the electroshock treatment in the acute phase of systematic and unsystematic schizophrenia in a total of 75 patients. The results obtained show that the neuroleptic high-dosage therapy exceeds the effectiveness of the electroshock treatment mainly in the group of unsystematic schizophrenia.

Adult↗
PubMedDate not supplied

[Bencyclane in memory disorders. Treatment of memory disorders caused by electroshock in a group of depressed patients].

Subjects treated with electroshock and subjected simultaneously to bencyclan at a dose of 00 mg (2 ampoules) i.v. and 100 mg (1 pill) per os pro die did not present dysmnesia either during the intervals between one electroshock treatment and another, nor at the conclusion of treatment (on average 12 sessions in about 40 days), while a control group treated at the same rhythm and with the same number of sessions, but without bencyclan, presented considerable memory lapses which disappeared only after a lengthy period of this latter treatment. Memory disturbances have been evaluated with a memorization test to which all patients were subjected. This test belongs to the group of intellectual efficiency reactive tests used in the psychology laboratory of the Catholic University of Milan; it consists of a group of 12 figures of common objects which, once observed, have to be recalled exactly immediately and some time later by the patient, who has to indicate the name and position of the objects represented in the chart.

Adult↗