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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurotoxin, 6-hydroxydopamine, when injected intraperitoneally, protected mice from seizures induced by pentylenetetrazol (Metrazol) and altered the nature of the convulsive response induced by an auditory stimulus. Conversely, the indenopyrrole, eboracin, protected mice from seizures induced by auditory stimulation and altered the response to Metrazol. In each case the altered response was characterized by a marked prolongation of the clonic component without progression to the generalized tonic phase. It appeared, therefore, that 6-hydroxydopamine raised the threshold to tonus in audiogenic seizures, and eboracin raised it in Metrazol seizures. Eboracin raised threshold to clonic phase in audiogenic seizures whereas 6-hydroxydopamine raised it in Metrazol seizures. Our findings showed that in Metrazol and audiogenic seizures thresholds to clonus and progression to the tonic phase were mediated by different biochemical mechanisms and suggested that agents controlling induction of clonic manifestations in one seizure model may be those involved in controlling seizure spread in the other.
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PMID:Convulsive thresholds in mice: action of 6-hydroxydopamine and eboracin. 392 44

A bilateral mechanical lesion of the midbrain and pontine tegmentum was found to abolish completely the tonic components of sound-induced seizures in genetically epilepsy-prone rats (GEPR) that display tonic-clonic seizures. Correlations between varied lesions placements and effects on maximal audiogenic seizures provided evidence that damage to the nucleus reticularis pontis oralis (RPO) of the midbrain and pontine reticular formation (RF) was responsible for the seizure-attenuating effects. Moreover, electrolytic lesions of the pontine RF involving the RPO nucleus were found to abolish the tonic components of the maximal audiogenic seizure. Additionally, bilateral mechanical lesions involving the RPO nucleus were found to attenuate the clonic components of sound-induced seizures in GEPR that display only running seizures and clonus. These findings are consistent with previous studies showing that pontine tegmental lesions attenuate the tonic components of maximal electroshock- and pentylenetetrazol-induced seizures, and lend further support to the hypothesis that all generalized tonic seizures share a common neural substrate. The role of the brainstem RF in tonic versus clonic convulsions is discussed in light of the present findings.
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PMID:Effect of midbrain and pontine tegmental lesions on audiogenic seizures in genetically epilepsy-prone rats. 398 48

Male Long-Evans rats were kindled via daily electrical stimulation of the left prepyriform cortex. The animals were then used in two experiments which examined the pharmacological basis of cocaine's effects on three mutually exclusive components of the kindled seizure, which were the following: (a) latency to clonus, (b) clonus duration, and (c) duration of AD outlasting clonus. The first experiment compared the effects produced by cocaine HCl (20 mg/kg, IP), lidocaine HCl (20 mg/kg, IP), and amphetamine sulfate (2.5 mg/kg, IP). The results indicated that both cocaine and lidocaine reduced the duration of kindled AD, latency to clonus, and duration of AD persisting beyond clonus, thus suggesting that these cocaine effects are mediated by local anesthetic mechanisms. Only cocaine reduced clonus duration, which suggests that this cocaine effect is not produced by a local anesthetic action. The second experiment examined the effects of cocaine following the administration of three dose levels of the monoamine antagonists haloperidol, prazosin, yohimbine, propranolol, or metergoline (selected for their ability to block dopamine, alpha-1-norepinephrine, alpha-2-norepinephrine, beta-norepinephrine, and serotonin receptors, respectively). The results of this experiment found no support for a monoaminergic contribution to cocaine's effect on clonus latency or AD after clonus. However, results for prazosin, which reduced clonus duration and exhibited an additive effect with cocaine on this variable, suggest that cocaine's norepinephrine action (especially on the alpha-norepinephrine systems) may modulate clonus duration.
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PMID:Monoaminergic and local anesthetic components of cocaine's effects on kindled seizure expression. 399 58

Rats were either given 80 escapable shocks, yoked inescapable shocks, restraint or given no treatment. Two hours later all subjects received i.p. injection of bicuculline (4, 6 or 8 mg/kg) and were immediately tested for latency to initial myoclonic jerk and clonus. The latency to clonic convulsion was dramatically affected by prior shock treatment, and the direction of this change depended upon the escapability/inescapability of the shock. Subjects that were given escapable shock showed a delay of onset to seizure, while subjects inescapably shocked demonstrated a decreased latency to clonus in comparison to restrained and naive controls. It was also demonstrated that if the subjects were tested immediately following a stress experience, both the 80 escapable and inescapable shock condition protected against bicuculline-induced seizures in comparison to the control condition. Finally Experiment 2 confirmed a previous finding that less stress, i.e., 20 inescapable shocks, protects against seizures when the animals are challenged with bicuculline either immediately or 2 h later. Our suggestion is that control over stress may facilitate GABAergic transmission, and this may be the mechanism whereby coping protects against the behavioral and physiological disruption produced by exposure to a stressor.
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PMID:Coping and seizure susceptibility: control over shock protects against bicuculline-induced seizures. 404 19

The anticonvulsant properties of adenosine were tested pharmacologically on amygdala-kindled seizure activity in rats. The adenosine analogue 2-chloroadenosine and the adenosine uptake blocker papaverine both increased the latency to behavioral clonus as well as reduced the duration and severity of the clonic motor convulsion. Both drugs, however, failed to alter the postkindling afterdischarge (AD) threshold. Theophylline, an adenosine antagonist, had the opposite effects, prolonging the AD and motor seizure durations and facilitating partially kindled seizures, but again not altering the prekindling or postkindling AD thresholds of amygdala-elicited seizures. In contrast, carbamazepine raised AD thresholds, suggesting that it does not produce its anticonvulsant effects through adenosine systems. Since endogenous adenosine can impede seizure spread and seizure continuation, but does not affect seizure initiation from the amygdala, perhaps endogenous adenosine has the special property of being brought into play as an anticonvulsant only by the seizure itself.
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PMID:Is adenosine an endogenous anticonvulsant? 404 18

Although most laboratories employ transcorneal stimulation as a means of producing electroshock seizures, transauricular stimulation is also used by many investigators. The present study shows that seizures produced with transcorneal electroshock differ from those produced by transauricular electroshock in several ways: transauricular stimulation is more effective at eliciting tonic convulsions; the threshold for clonus is lower when transcorneal electrodes are used; and the face and forelimb clonus produced by transcorneal stimulation cannot be produced with transauricular stimulation at any current. The present findings are consistent with the hypothesis that tonic seizures are more easily triggered with transauricular stimulation because they originate in the brainstem and because this brain region is preferentially activated when ear-clip electrodes are used.
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PMID:Variation in threshold and pattern of electroshock-induced seizures in rats depending on site of stimulation. 406 1

Electrographic and behavioral seizures were induced in rats by repeated electrical stimulation of the dorsal hippocampus for three consecutive days. Animals were killed in the following groups: Control group; group killed during the clonus phase of a convulsion in the third stimulating session; group killed 10 minutes after the termination of a convulsion in the third stimulating session. Membrane ATPase activity was shown to be significantly increased in the group killed during the clonic phase compared to that of the control group and was significantly reduced post-convulsively, compared to both the control group and the group killed during the convulsion. The results suggest a modification of enzyme activity which may be important in the initiation and maintenance of seizure activity.
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PMID:Epilepsy and membrane Na+K+ATPase: changes in activity using an experimental model of epilepsy. 610 Sep 44

Phenytoin antagonized the electroshock-induced increase in levels of cyclic adenosine 3',5'-monophosphate (cAMP) and cyclic guanosine 3',5'-monophosphate (cGMP) in cerebrum and cerebellum, respectively, from CF-1 mice. However, the effective dose range of phenytoin for significant reduction of the elevated levels of cAMP and cGMP was 2 to 5 times higher than that for prevention of tonic hindlimb extension in 95% of mice. The effective dose range of phenytoin for alteration of cyclic nucleotide levels was nearer to that for preventing tonic flexion and clonus; endpoints which are less relevant to anticonvulsant efficacy than is prevention of tonic hindlimb extension. Also , the greatest reduction in cyclic nucleotide levels occurred at a dose (100 mg/kg) which produced toxic signs in mice. Quaking mice (qk/qk), a mutant strain which exhibits spontaneous seizures, did not have abnormal levels of cAMP or cGMP in cerebrum or cerebellum, and a dose of phenytoin (15 mg/kg) which abolished all seizure activity did not alter levels of these cyclic nucleotides. In frogs, the electroshock-associated increase in levels of cAMP in the central nervous system was not altered by phenytoin even when the doses administered were up to twice the ED95 for prevention of tonic hindlimb extension. Because these data from mice and frogs show that the anticonvulsant effect of phenytoin is dissociated, by dose, from effects on central nervous system cyclic nucleotide levels, it is doubtful that the alteration of cyclic nucleotide levels is a mechanism by which phenytoin exerts its anticonvulsant effect
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PMID:Phenytoin antagonism of electrically induced maximal seizures in frogs and mice and effects on central nervous system levels of adenosine 3',5'-monophosphate and guanosine 3',5'-monophosphate. 627 34

The relative anticonvulsant potential of the gamma-aminobutyric acid (GABA) agonist, muscimol, was compared after microinjection into either the inferior colliculus, substantia nigra or medial septum of ethanol-dependent rats. Bilateral microinjection of muscimol (10-30 ng) into the inferior colliculus 15 to 60 min before testing suppressed all sound-induced seizure components (wild running, clonus and tonus) in rats withdrawn from ethanol for 6.5 to 8.5 hr. However, forelimb tremors were not altered. Audiogenic seizures were suppressed for at least 3 hr after muscimol (30 ng). In the medial septum and substantia nigra, microinjection of muscimol (30-100 ng) only partially reduced the tonic component of audiogenic seizures and exerted no effect on the frequency of wild running or clonus. GABA (10 micrograms) and two other GABA agonists [4,5,6,7-tetrahydroisoxazolo[5, 40c]pyridin-3-ol (THIP), 300 ng and chlordiazepoxide, 10-30 micrograms], microinjected into the inferior colliculus, also reduced audiogenic seizure susceptibility. However, 1, 3-butanediol, which suppresses ethanol withdrawal seizures after peripheral administration in rats, was inactive. The relative proconvulsant potential of the GABA antagonist, bicuculline methiodide, also was compared after microinjection into either the inferior colliculus, substantia nigra or medial septum of ethanol naive rats. In each animal, audiogenic seizure-like wild running, clonus and tonus were evoked by microinjecting bicuculline methiodide into the inferior colliculus at the rate of 6.0 ng/6 min. However, these reactions did not occur when bicuculline methiodide was applied at a slower rate (1.8 ng/6 min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of susceptibility to audiogenic seizures in ethanol-dependent rats after microinjection of gamma-aminobutyric acid (GABA) agonists into the inferior colliculus, substantia nigra or medial septum. 631 42

From the results obtained with the experimental series CORASIN (fast compression with He-N2-O2), a method of compression has been developed for the baboon (Papio papio) to dive deeper than 600 m. This method utilizes an exponential compression profile with stages of 40 min every 100 m and with the introduction of N2 before each stage from 200 m onward to maintain a concentration of 5.5%. Between 0 and 800 m, this procedure did not produce myoclonus or epileptic seizures; tremor appeared beyond 400 m (578 +/- 109 m) but remained slight. If N2 was not introduced, the tremor appeared earlier (266 +/- 52 m) and became severe; between 600 and 800 m, muscular hypertonus, myoclonus, and muscular cramps occurred. The modifications of the electroencephalogram were slight; the increase in slow activity did not exceed 300% with or without N2. Beyond 800 m, the compression procedure with N2 injections revealed new phenomena. There was a general depression of EEG activity starting at 800 m; from 1,000 m and deeper, there were periods of motor disturbances (hypertonus, spasms, and shaking), palpebral clonus, and eye movements associated with peak EEG activities localized in the posterior region of the skull that sometimes evolved toward an epileptic seizure localized in this region. These symptoms differed from the classical description of high-pressure nervous syndrome, which comprises an increase in tremor followed by convulsions. These differences may perhaps be linked to our compression procedure using N2 injection, to the effect of the pressure itself, or to a combination of the two.
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PMID:HPNS of baboons during helium-nitrogen-oxygen slow exponential compressions. 646 4


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