Topic
Tonic Convulsion
About: Tonic Convulsion is a research topic. Over the lifetime, 66 publications have been published within this topic receiving 985 citations.
Papers published on a yearly basis
Papers
Journal Article•
TL;DR: The patterns of maximal seizures evoked in mice by the intravenous injection of 38 mgm./kgm.
Abstract: The patterns of maximal seizures evoked in mice by the intravenous injection of 38 mgm./kgm. Metrazol and by supramaximal electroshock have been compared. In addition, eight clinically useful antiepileptic drugs were tested for their ability to prevent the characteristic hindleg tonic extensor component of maximal Metrazol seizures (M.M.S.) and maximal electroshock seizures (M.E.S.). The results were as follows: (1) The M.M.S. and M.E.S. patterns in mice are similar in that the major feature is a tonic convulsion characterized by initial flexion and subsequent extension of the hindlegs; the duration of the tonic components of the two types of seizures is remarkably similar. However, there are important differences in the M.M.S. and M.E.S. The M.M.S. is clonic-tonic whereas the M.E.S. is tonic-clonic. Postictal relaxation supervenes after the tonic component of the M.M.S. whereas a clonic component of long duration follows the tonic component of the M.E.S. Recurrent seizures frequently occur after intravenous Metrazol, but are never observed after supramaximal electroshock of brief duration. The mortality rate from M.M.S. is about ten times higher than that from M.E.S. Explanations have been advanced for these similarities and differences in the two types of seizure pattern. (2) Tridione, Paradione, phenobarbital, Mebaral and Phenurone are much more potent in modifying M.M.S. than M.E.S.; in sharp contrast, the three hydantoin derivatives—Dilantin, Mesantoin and Thiantoin—are much more potent in modifying M.E.S. than M.M.S. A probable explanation for the division of the drugs into these two classes is found in the fact that the hydantoin derivatives excel in the inhibition of seizure spread but are relatively ineffective in elevating seizure threshold; in contrast, all the other drugs tested possess both mechanisms of anticonvulsant action. Inhibition of seizure spread is probably paramount for the drug-induced modification of M.E.S. whereas a large component of chemoshock threshold elevation is important for the drug-induced modification of M.M.S. Certain features of the maximal seizure and its sequelae are dependent on the nature of the stimulus initiating the convulsion; however, the tonic extensor component is constant in its character and time course and is independent of the stimulus evoking it. The M.M.S. test is not suitable as a routine anticonvulsant assay procedure, but a study of its properties has contributed to the understanding of maximal seizures and of the mechanism and the spectrum of action of anticonvulsant drugs.
111 citations
TL;DR: The results suggest that the histaminergic neuron system is important in inhibition of the duration of clonic convulsion on electrically induced seizure in mice.
Abstract: The purpose of this study was to investigate the possible role of the central histaminergic neuron system in electrically-induced seizure in mice. For this purpose, we examined the effects of intraperitoneal (i. p.) injections of histaminergic agents, such as l-histidine, metoprine, and α-fluoromethylhistidine (FMH), on electrically-induced seizure. l-Histidine decreased the duration of clonic convulsion in electrically-induced seizure, but not affected that of tonic convulsion. This effect of l-histidine was antagonized by pretreatment with FMH, indicating that it was due to histamine formed by decarboxylation of l-histidine in the central nervous system. The anticonvulsive effect of l-histidine was also reduced by the H1-antagonist pyrilamine, but not by the H2-antagonist zolantidine, indicating that the effect on electrically-induced seizure is mediated through central H1-receptors. Metoprine, which increased the histamine levels in the cerebral cortex, diencephalon and midbrain of mice, decreased the duration of clonic convulsions dose-dependently. Conversely, FMH, which decreased the brain histamine levels, increased the duration of clonic convulsions. Good inverse correlations were found between the duration of clonic convulsions and brain histamine levels, especially in the diencephalon: the histamine levels were inversely proportional to the duration of clonic convulsions. No correlation was found between the duration of tonic convulsions and brain histamine levels. These results suggest that the histaminergic neuron system is important in inhibition of the duration of clonic convulsion on electrically induced seizure in mice.
91 citations
TL;DR: The effects of two Rho‐kinase inhibitors, Y‐27632 and fasudil, on seizures induced by pentylenetetrazole (PTZ) or maximal electroconvulsive shock (MES) are determined.
Abstract: Background and purpose:
Rho/Rho-kinase signalling is involved in many cellular events, including some in the CNS. However, the role of this pathway in epilepsy has not yet been assessed. Therefore, we determined the effects of two Rho-kinase inhibitors, Y-27632 and fasudil, on seizures induced by pentylenetetrazole (PTZ) or maximal electroconvulsive shock (MES).
Experimental approach:
Effects of Y-27632 (5–10 mg kg−1) and fasudil (5–25 mg kg−1) on duration of myoclonic jerks, clonic and tonic convulsions, tonic hindlimb extensions and percentage of tonic convulsion index, as well as recovery latency for righting reflex were investigated in mice stimulated with PTZ (65 mg kg−1) or MES (50 Hz, 50 mA and 0.4 s). These inhibitors were also tested on a model of kindling induced by PTZ (35 mg kg−1, for 11 days). Membrane and cytosolic levels of RhoA protein were measured in brain homogenates from kindled mice.
Key results:
Y-27632 and fasudil diminished onset of myoclonic jerks, clonic convulsions and tonic hindlimb extensions in mice given PTZ. These inhibitors suppressed the percentage of tonic convulsion index and recovery latency for righting reflex in the mice excited with MES. Western blotting demonstrated that Rho translocation to plasma membrane increased in the brain homogenates obtained from PTZ-kindled mice. However, the Rho-kinase inhibitors at the given doses did not change motor coordination of the mice.
Conclusions and implications:
Rho/Rho-kinase signalling may play a role in epilepsy induced by PTZ and MES. Furthermore, Rho-kinase inhibitors could be novel important antiepileptic agents.
British Journal of Pharmacology (2008) 155, 44–51; doi:10.1038/bjp.2008.225; published online 9 June 2008
70 citations
TL;DR: The notion that NO does not directly induce a clonic convulsion, but may be generated as a consequence of onset of seizure is supported.
Abstract: The role of nitric oxide (NO) in epileptogenesis was studied in pentylenetetrazole (PTZ)-treated animals using in vivo and ex vivo EPR spectroscopy. NO generation was measured directly in the brain of a PTZ-induced mouse in vivo by an L-band EPR spectrometer. An elevation in NO production in the brain was observed during convulsions, and more NO was generated in the tonic seizure vs. the clonic seizure. NO content in several brain tissues (including the cerebral cortex (CR), cerebellum (CL), olfactory bulb (OB), hippocampus (HI), and hypothalamus (HT)) of PTZ-doped rats was analyzed quantitatively ex vivo by X-band EPR. To test the involvement of NO in seizure development, pharmacological analyses were performed using the NO synthase (NOS) inhibitors N(G)-nitro-L-arginine (L-NNA), N(G)-monomethyl-L-arginine (L-NMMA), and 3-bromo-7-nitroindazole (3Br-7NI). All of these inhibitors suppressed the convulsions, holding them at the clonic level, and prevented development of a tonic convulsion in rats doped with up to 80 mg/kg PTZ. 3Br-7NI completely inhibited NO production, but L-NNA and L-NMMA showed only 70% inhibition of NO production in PTZ-doped rats. In order to examine the contributions of NO in convulsions, rats were treated with anticonvulsants (phenytoin and diazepam) before PTZ treatment. Both drugs completely suppressed tonic convulsion in PTZ-doped rats at doses up to 80 mg/kg, but NO levels were similar to those detected in a clonic convulsion. These results support the notion that NO does not directly induce a clonic convulsion, but may be generated as a consequence of onset of seizure.
68 citations
TL;DR: Electroshock seizures have been studied in young rats and guinea pigs, and a correlation has been demonstrated between the developmental pattern and threshold of the induced seizures and the level of carbonic anhydrase activity in the brain.
Abstract: SummaryElectroshock seizures have been studied in young rats and guinea pigs, and a correlation has been demonstrated between the developmental pattern and threshold of the induced seizures and the level of carbonic anhydrase activity in the brain. In young rats aged 20 to 35 days, the seizures were mainly tonic in pattern, whereas the clonic type of seizure predominated in rats aged 10 to 20 days. Failure to induce convulsions in the newborn rat was associated with a low level of carbonic anhydrase activity in the brain. The degree of maturation of the newborn guinea pig was equivalent to that of the 15-day-old rat, both with regard to the type of seizure response and the level of brain carbonic anhydrase activity. That brain carbonic anhydrase is of functional significance in the generalized spread of the seizure discharge and in the production of a maximal tonic convulsion is suggested by these data and by observations of the anticonvulsant activity of acetazolamide.
57 citations
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Performance Metrics
| Year | Papers |
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| 2021 | 2 |
| 2019 | 1 |
| 2017 | 1 |
| 2016 | 4 |
| 2014 | 3 |
| 2013 | 1 |