Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to test the GABA hypothesis of kindling, GABA-complex antagonists were administered in a dose-response paradigm to rats that had been implanted with indwelling forebrain electrodes, but not kindled. Focal seizures were then elicited from either the cortex or the amygdala to see whether kindling-like secondary generalization would occur. Norharmane, a benzodiazepine inverse agonist, failed to promote secondary generalization from either the cortex or the amygdala. Bicuculline, a GABAA receptor antagonist, and picrotoxin, a chloride ionophore antagonist, enhanced generalization from both sites and, in amygdala-implanted subjects, appeared to produce a significant acceleration of kindling as well. Aminophylline, an adenosine antagonist tested for purposes of comparison, also enhanced secondary generalization from both sites, and in amygdala-implanted subjects produced long electrographic discharges which sometimes developed into status epilepticus.
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PMID:Secondary generalization in non-kindled rats following acute administration of GABA-complex and adenosine antagonists. 169 79

Aminophylline (A) is a proconvulsant in adult rats. We studied the effect of A on amygdala kindling in 15-day-old rat pups. Production of generalized seizures was significantly promoted by A at doses ranging from 10 to 100 mg/kg. Terminal status epilepticus (TSE) was produced in 33% of pups receiving 25 mg/kg A, 75% of pups receiving 50 mg/kg A, and 100% of pups receiving 100 mg/kg A. The number of stimuli needed to produce a stage 4-5 generalized seizure was significantly smaller in animals receiving 10 mg/kg A (5.7 +/- 3.4), 25 mg/kg A (3.4 +/- 2.4), 50 mg/kg A (1.9 +/- 1.4), or 100 mg/kg A (1.9 +/- 1.6) than in saline-treated controls (12.3 +/- 3.7) (P less than 0.001). In addition, 16% of pups receiving 50 mg/kg and 33% of pups receiving 100 mg/kg A and never stimulated developed TSE. These seizure-promoting effects of A in rat pups undergoing amygdala kindling are far more dramatic and occur at far lower doses than those previously reported in adults.
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PMID:Proconvulsant effects of aminophylline during amygdala kindling in developing rats. 272 Sep 53

Adenosine is an endogenous neuromodulator that suppresses excitatory neurotransmission. We postulated that adenosine-mediated mechanisms resist status epilepticus (SE) entry and limit SE severity. In the first experiment rats were given an adenosine agonist (2-chloroadenosine), an adenosine antagonist (aminophylline), or saline vehicle, prior to SE induction with pulsed-train current delivered to amygdala in successive 5-min current-on sessions. Saline-treated animals entered limbic SE, with predominantly exploratory behavior, after 6.0 +/- 0.9 current-on sessions. Aminophylline increased major convulsive activity during stimulation and resulted in entry into convulsive SE after only 2.1 +/- 0.1 sessions. 2-Chloroadenosine, in contrast, suppressed major convulsive activity during stimulation, and blocked (in 3/7) or delayed (4/7) SE entry, with successes requiring 12.8 +/- 0.9 stimulation sessions. In a second experiment, animals already in exploratory SE were administered a single injection of saline vehicle, aminophylline, or 2-chloroadenosine. Aminophylline converted exploratory SE into lethally severe convulsive SE. 2-Chloroadenosine suppressed SE behaviorally and electrographically, and protected recipients from the seizure-associated cerebral damage seen in saline-administered SE controls. These results support the hypothesis that endogenous adenosine mechanisms resist SE entry, modulate the severity of ongoing SE, and limit the anatomic spread of seizure activity.
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PMID:Effect of an adenosine antagonist and an adenosine agonist on status entry and severity in a model of limbic status epilepticus. 808 55