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PubMed1984

Regulatory effects of neurotransmitters on electroshock and pentylenetetrazol seizures.

Evidence that biogenic amines and a neuroactive purine are involved in pathophysiological mechanisms of experimental seizures produced by electroshock or pentylenetetrazol is reviewed. Diminishing the influence of norepinephrine (NE) in the brain by depleting its content or by blockade of beta adrenoreceptors enhances seizure activity, and increasing its influence may suppress seizures. Serotonin appears to have action similar to that of NE, but dopamine has little effect in these seizure models. Adenosine also appears to suppress seizure activity. Thus NE, serotonin, and adenosine may be natural, endogenous substances that inhibit or confine seizure activity in the brain.

Adenosine↗
PubMed1982

Correlation of lithium effect on electroshock-induced seizure in rats with its concentration in brain and plasma.

Effects of graded doses of lithium chloride (2.5, 5.0 and 7.5 mEq/kg, i.p.) on electroshock-induced seizure threshold, recovery time and concentration of lithium (Li) ion in plasma and brain tissue of albino rats, at different post injection intervals, were investigated. A significant decrease in seizure susceptibility corresponded with high Li ion concentration at 4 to 8 hr post injection period in the rat brain tissue.

Animals↗
PubMed1993

[Effect of sodium valproate, phenobarbital and diazepam during their combined use on convulsions induced by electroshock in mice].

Complex pathogenetic therapy (CPT) of epilepsy in the form of combined action of drugs enhancing GABA-mediated inhibition was carried out. The anticonvulsant potency of drugs and of their combinations was determined by a maximal electroshock seizure test in mice. Combined anticonvulsant effects were evaluated by the isobolographic method, various doses of drugs were compared in proportion to their ED 50. It was shown that synergistic effects of potentiation type were in all cases of combined use of drugs. ED 50 of each drug could be decreased in combinations of sodium valproate with diazepam by 7 times, phenobarbital with sodium valproate--by 12 times, phenobarbital with diazepam--by 14 times and sodium valproate with phenobarbital and diazepam--by 26 times. Thus, these results suggest that complex use of drugs acting on different mechanisms of GABA-mediated inhibitory control lead to a marked potentiation of the end effect. The obtained data allow to conclude that CPT of epilepsy which can provide potentiation of effects of each drug and a significant reduction of their doses is reasonable to be used.

Animals↗
PubMed1994

Effect of GABA analogues on various components of maximum electroshock-induced seizures in mice.

Out of fourteen compounds reported here only four [N-valproyl GABA (V.GABA), N-phthaloyl GABA (P.GABA), gamma-phthalimido N-amyl butyramide (PGA) and gamma-phthalimido N-phenyl butyramide (PGP)] gave significant protection to all the four components of maximal electroshock-induced seizures (MES) in mice. It appeared that substitution of either amino or carboxylic or both groups of gamma-aminobutyric acid (GABA) with bulkier groups like aliphatic or aromatic carbons usually produced effective anticonvulsant GABA derivatives. V.GABA and P.GABA were the most effective anticonvulsant GABA derivatives in protecting all the components of MES-induced seizures. They were 2.3 and 1.5 times potent than sodium valproate in molar ratio, but P.GABA has low therapeutic index when compared to V.GABA. The observed anticonvulsant activity may be due to enhanced GABA concentration in the CNS. Probably, the active compound (V.GABA) crossed the blood brain barrier and hydrolysed to GABA and valproic acid to bring about its anticonvulsant action.

Animals↗
PubMedDate not supplied

The influence of ethanol on pentetrazol-induced seizures and anticonvulsant activity of phenobarbital and valproate against maximal electroshock in mice.

The effect of acute (1, 2, and 3 g/kg) and chronic (2 g/kg) ethanol administration and ethanol withdrawal on pentetrazol-induced seizures and influence of ethanol in a dose of 2 g/kg upon the protective efficacy of valproate and phenobarbital against maximal electroshock-induced seizures was investigated. In the acute study ethanol increased, in the chronic study ethanol had no effect on ED50 values for pentetrazol. During withdrawal the ED50 was reduced. In the acute study ethanol reduced ED50 values for valproate and phenobarbital, in the chronic study had no effect. During withdrawal ED50 values for phenobarbital were elevated.

Animals↗
PubMed1994

Involvement of adenosine in postictal events in rats given electroshock.

The effect of a selective adenosine antagonist, 8-cyclopentyl 1,3-dimethylxanthine (8-CPT) was used to examine involvement of adenosine in ictal and postictal events in rats subjected to maximal electroshock (MES). MES induces the ictal event of hindlimb tonic extension (HLTE) followed by postictal depression (PID). 8-CPT 10 mg/kg, ip produced maximal significant reduction of PID without affecting HLTE, further confirming involvement of adenosine in PID. Carbamazepine and sodium valproate were studied independently and were coadministered with 8-CPT to determine if their anticonvulsant activity was modulated by adenosine and if they altered PID. 8-CPT did not antagonize the seizure protection afforded by CBZ or SV. CBZ significantly reduced postictal events whereas SV had no significant effect. These observations further confirm a role for adenosine in postictal phenomena.

Adenosine↗
PubMedDate not supplied

The convulsive action of pentylenetetrazol and electroshock in irradiated rats.

Convulsive activity of pentylenetetrazol and electroshock was measured in rats irradiated 24 hr earlier with 800 R of X rays. At this time the content of "free" acetylcholine (ACh) was increased in the cerebral cortex, and the content of "bound" ACh was depressed in the brain stem. Irradiation facilitated the action of convulsogenic agents. Atropine did not prevent convulsions but facilitated them. An increase in the endogenous pool of ACh by eserine similarly to atropine facilitated the action of convulsogenic agents in control rats. In irradiated rats eserine shortened the duration of electrogenic convulsions, but it did not change significantly the latency of pentylenetetrazol convulsions. A causal relationship between the effects observed and post-irradiation modification of the content of "free" and "bound" ACh in the cerebral cortex and brain stem is discussed.

Acetylcholine↗
PubMed1998

Additive anticonvulsant effect of flunarizine and sodium valproate on electroshock and chemoshock induced seizures in mice.

The efficacy of Flunarizine (FLU), a calcium channel blocker, in combination with conventional antiepileptic drugs, phenytoin (PHT), carbamazepine (CBZ), sodium valproate (VPA), and ethosuximide (ESM), at ED50 doses, were examined for protective effects against maximal electroshock seizures (MES) and pentylenetetrazol (PTZ) induced seizures in mice. In both models, only VPA and FLU showed significantly enhanced protection, which was additive ie. 100% protection. In the MES test, though FLU combined with PHT did show a slightly enhanced protection (66.6%), with CBZ there was no enhancement as compared to either drug alone. In the PTZ test, FLU with ESM showed 83% protection this however was not statistically significant. The findings of this study in mice suggest that FLU would be a suitable candidate for add-on therapy with VPA for clinical epilepsy.

Animals↗
PubMed1998

Tramadol, a centrally acting opioid: anticonvulsant effect against maximal electroshock seizure in mice.

The present study was designed to investigate the pro- or anticonvulsant effect of tramadol using maximal electroshock (MES) test. An attempt was also made to determine the possible opioid receptor mechanism involved. MES seizures were induced through transauricular electrodes (60 mA, 0.2s) and the seizure severity was assessed by the duration of tonic hindlimb extensor phase. Intraperitoneal (i.p.) administration of tramadol resulted in a dose-dependent anticonvulsant action; the ED50 for the effect was 33 mg/kg. The anti-MES effect of tramadol was antagonized by the low doses (0.05 and 0.1 mg/kg, s.c.) of MR 2266, a selective kappa receptor antagonist and also by the high doses (1.0 and 5.0 mg/kg, i.p.) but not the low doses (0.1 and 0.25 mg/kg) of naloxone. The results suggest that the anti-MES effect of tramadol is mediated by kappa receptors, since MR 2266 and naloxone (in high doses) are known to block these receptors.

Animals↗
PubMed1987

Functional anatomy of pentylenetetrazol and electroshock seizures in the rat brainstem.

The ability of discrete brainstem injections of gamma-vinyl-gamma-aminobutyric acid (GVG), an irreversible inhibitor of gamma-aminobutyric acid transaminase, to prevent pentylenetetrazol (PTZ) seizures and maximal electroshock seizures (MES) was studied and compared in rats. PTZ seizures were prevented by GVG injections in the anterior thalamus, the caudal hypothalamus, the superior colliculus, cerebellar nuclei, and in a large area of the medial medullary, pontine, and mesencephalic tegmentum encompassing the vestibular nuclei, the reticular formation, and portions of the central gray. GVG injections in the substantia nigra did not protect against PTZ seizures. In contrast, tonic hindlimb extension in MES was prevented consistently by injections in the substantia nigra. A minority of injections in the vestibular nuclei, cerebellar nuclei, and parts of the reticular formation also protected against tonic hindlimb extension of MES. These results indicate a striking difference in the functional anatomy of PTZ-induced seizures and MES. PTZ seizures appear to be mediated by an extensive system involving the reticular formation, diencephalic regions in the vicinity of the anterior medial thalamus and caudal hypothalamus, and bulbar regions which give rise to descending motor pathways to the spinal cord. In contrast to PTZ seizures, MES appears to be mediated by a different neuroanatomical substrate with the present data implicating only the substantia nigra definitely in that process.

Aminocaproates↗
PubMed2002

Mouse strain variation in maximal electroshock seizure threshold.

Maximal electroshock seizure threshold (MEST) is a classical measure of seizure sensitivity with a wide range of experimental applications. We determined MEST in nine inbred mouse strains and one congenic strain using a procedure in which mice are given one shock per day with an incremental (1 mA) current increase in each successive trial until a maximal seizure (tonic hindlimb extension) is elicited. C57BL/6J and DBA/2J mice exhibited the highest and lowest MEST, respectively, with the values of other strains falling between these two extremes. The relative rank order of MEST values by inbred strain (highest to lowest) is as follows: C57BL/6J > CBA/J = C3H/HeJ > A/J > Balb/cJ = 129/SvIMJ = 129/SvJ > AKR/J > DBA/2J. Results of experiments involving a single electroconvulsive shock given to separate groups of mice at different current intensities suggest that determination of MEST by the method used is not affected by repeated sub-maximal seizures. Overall, results document a distinctive mouse strain distribution pattern for MEST. Additionally, low within strain variability suggests that environmental factors which affect quantification of MEST are readily controlled under the conditions of this study. We conclude that MEST represents a useful tool for dissecting the multifactorial nature of seizure sensitivity in mice.

Animals↗
PubMed1993

Anticonvulsant activities of some arylsemicarbazones displaying potent oral activity in the maximal electroshock screen in rats accompanied by high protection indices.

Various semicarbazones derived from aryl aldehydes, phenylalkyl aldehydes, and phenylalkyl ketones as well as some related compounds were evaluated for anticonvulsant activity. Most of the compounds displayed anticonvulsant activity in the maximal electroshock (MES) and subcutaneous pentylenetetrazole (scPTZ) screens accompanied by neurotoxicity when given to mice by the intraperitoneal route. However quantitative data revealed protection indices (TD50/ED50) of less than 4 in general. Oral administration of the compounds to rats led to excellent potency in the MES screen accompanied by high protection indices while virtually no activity in the scPTZ test was displayed. These observations support the theory that one large hydrophobic group (in this case the aryl ring) and two electron donor atoms (present in the semicarbazono group) are requirements for protection in the MES screen. In general, the semicarbazones had rapid onsets of action, and one of the ways in which these compounds displayed their anticonvulsant activity is likely to be interaction with chloride channels. Empirical and semiempirical conformational calculations indicated that certain molecular fragments and hydrophobicity of these molecules affect bioactivity.

Administration, Oral↗
PubMed1979

Sparing of metabolic stress in Purkinje cells after maximal electroshock.

Experimental seizures were induced in mice by application of 50 mA for 0.2 sec via corneal electrodes. The reproducible conclusive behavior was characterized by a sequence of 2 sec of tonic flexion, 13 sec of tonic extension, and 8 sec of clonus followed by a postictal depressive stage. The animals were frozen and tissues were prepared for analysis according to Lowry and Passonneau [Lowry, O. H. & Passonneau, J. V. (1972) A Flexible System of Enzymatic Analysis (Academic, New York)]. Freeze-dried samples (1-10 ng) of pyramidal cell bodies and adjacent neuropil from the parietal cortex and of Purkinje cell bodies and adjacent neuropil from the cerebellum were analyzed for glucose, ATP, and P-creatine (0.01-0.05 pmol). There were marked decreases in these energy stores after the maximal electroshock in three of the areas examined. In the Purkinje cell bodies, however, the metabolic stress was dampened; glucose concentrations decreased, but the levels of ATP were maintained and, to a lesser extent, those of P-creatine. The results indicate that the output from the Purkinje cells is less than in the other regions examined in the excitable stages of the convulsion. The lesser energy debt probably reflects lower energy demand as well as a lower discharge intensity. The fact that Purkinje cells are spared from the metabolic stress imposed on other regions may be a partial explanation of the seizure activity. A diminished output from the Purkinje cells could be a situation that permits cortical convulsive activity.

Adenosine Triphosphate↗
PubMed1978

Electroshock therapy: myths and realities.

The methodology of the 1940s provided the data base for the myths that grew up around electroshock therapy. Since then indications have been refined and techniques drastically revised--as with many other medical treatments. When administered for carefully defined indications, in the proper setting by an experienced team, and with appropriate safeguards, EST is safe, effective, and often the treatment of choice.

Affective Symptoms↗
PubMed1998

A lasting change in trazodone response after non-convulsive electroshock therapy for medication-resistant senile depression.

A senile patient showed a dramatic recovery from medication-resistant depression after non-convulsive electroshock therapy (nc-EST), with a lasting change in response to trazodone, which mainly acts as a serotonin re-uptake inhibitor. This result suggests that a change in the serotonin reuptake mechanism may be involved in the effect of nc-EST on depression.

Aged↗
PubMed1992

Effects of postnatal electroshock convulsions on epileptogenesis of the amygdala and hippocampus in adult rats.

Adult rats which received repeated electroshock convulsions (ESCs) during postnatal development underwent electrical kindling of the amygdala (AM) and hippocampus (HIPP). Completion of kindling, especially AM kindling, was significantly faster in the groups with ESCs from the neonatal to late infantile age than in the control group. It is discussed that especially the late infantile age in the postnatal development was supposed to play an important role in the faster kindling brought about by postnatal convulsions and that the faster kindling was due in part to abbreviation of the partial seizure process. However, the neonatal ESC group showed significantly delayed completion of HIPP kindling.

Amygdala↗
PubMed1994

[Efficacy and safety of electroshock therapy without convulsions under general anesthesia in senile depression].

We examined the efficacy and safety of electroshock therapy (EST) under general anesthesia in 26 depressed patients (9 males, 17 females, age range 55-79). The scores of the Hamilton Psychiatric Rating Scale for depression were significantly decreased after EST and clinical symptoms such as depressive mood. psychomotor retardation, anxiety, agitation, suicidal tendencies, hypochondria and sleeplessness improved in all of the patients. Complications included amnesia (16/26), delirium (3/26) and transient arrhythmia (1/26) after EST, but neither lethal nor lasting complications were observed. In summary, EST was an effective and convenient method of treatment for senile depression.

Aged↗
PubMed1995

Chronic mild stress-induced anhedonia model of depression; sleep abnormalities and curative effects of electroshock treatment.

A core symptom of human depressive disorder is anhedonia, the loss of interest or pleasure in daily activities. Anhedonia, measured as subsensitivity to reward, can be induced in rats by a regimen of repeated, mild, unpredictable stressors. Here, the hedonic state of rats was assessed using an intracranial self-stimulation (ICSS) procedure. The ICSS frequency threshold was determined before, during and after a period of exposure to the stress regimens. After 13 days of repeated mild stress, the ICSS threshold was significantly increased, suggesting a gradual decrease of sensitivity to reward. This anhedonic state lasted throughout the stress period. When stressed anhedonic animals were given electroshock treatment, the stress-induced increase in ICSS threshold was rapidly and completely reversed. Moreover, biological markers of human depression such as reduced latency to the first REM sleep episode or increased time spent in REM sleep were also found in electroencephalographic recordings of chronically stressed animals. These sleep abnormalities were observed beginning in the second week of a three-week stress regimen and progressively disappeared after termination of stress. In conclusion, these data provide further evidence supporting stress-induced anhedonia in rats as a unique animal model of human depression combining convergent elements of biological, etiological, symptomatological and therapeutic validity.

Journal Article↗