Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The level of norepinephrine in rat cerebellum was assayed after the administration of the convulsant 3-mercaptopropionic acid. Decrease in norepinephrine was observed after the onset of seizure. The results were compared with those of GABA which were diminished both during and after convulsions. The decrease of GABA was prior to that of norepinephrine.
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PMID:Levels of norepinephrine in rat cerebellum after administration of the convulsant 3-mercaptopropionic acid. 95 7

In rabbits epileptiform seizures were induced by systemic application of methoxypyridoxine, an antimetabolite of vitamin B6. The regional distribution of GABA was measured in 11 brain structures, before the onset of the seizure and during the generalized convulsions. In brain regions with a high GABA level the GABA content drops already preictally, in contrast to the GABA poor structures where no preictal decrease takes place. From this it is concluded that there exist two GABA pools, a functional one containing the GABA for chemical transmission, which is exhausted already preictally giving rise to the seizure discharges, and a metabolic one, which is utilized as an additional energy-source during the convulsions. Due to the decrease of the hippocampal GABA the endings of the dentate gyrus granule cells, the giant boutons contacting the apical dendrites of the pyramidal cells of CA3 and CA4, can discharge unrestrained. An ultrastructural correlate of the increased excitation is demonstrated. The dense-core vesicles of the giant boutons fuse in an omega-shaped form with the presynaptic membrane of the spines. This fusion-phenomenon is observed in ultrathin sections as well as in freeze-fractured replicas of this region.
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PMID:Antivitamin B6 induced ultrastructural changes in the hippocampus of the convulsant rabbit and its biochemical correlates. 99 35

Pretreatment of rats with hydrazine (100 mg/kg), a compound which raises brain gamma-aminobutyric acid (GAGA) 175 percent in 12 hr was not able to prevent the occurrence of seizures induced by monosodium L-glutamate (MSG). Pyridoxine (50 mg/kg) the cofactor essential in the conversion of glutamate to GABA, also failed to prevent convulsions induced by parenteral MSG administration. It is concluded that the mechanism of action of MSG-induced seizures is neither by decreasing brain GABA levels or interfering with the pyridoxine cofactor.
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PMID:Lack of protection by pyridoxine or hydrazine pretreatment against monosodium L-glutamate-induced seizures. 120 36

The convulsant profile of lindane was investigated in OF1 and NMRI mice lines in relation to other convulsants acting at the GABAA and NMDA receptor complexes. Thus, a specific GABA-gated chloride channel blocker, PTX, a GABAA receptor antagonist, PTZ, and an excitatory amino acid receptor agonist, NMDA, were used. Antagonism of the convulsant effects of each of these drugs was investigated with (+)MK-801, a blocker of the NMDA-operated cation channel, and with nifedipine, a voltage-dependent calcium channel antagonist. While no differences in potency for PTX or PTZ to induce seizures were observed between OF1 and NMRI mice, lindane was approximately 80 and 90% more potent in its ability to induce seizures and lethality, respectively, in OF1 than in NMRI mice. Brain lindane concentrations at the moment of convulsion, measured after ED100 doses of lindane (400 and 200 mg/kg for NMRI and OF1 mice, respectively), did not differ between OF1 and NMRI mice, suggesting that the different potency of lindane between these mouse lines is a consequence of pharmacokinetic factors. Furthermore, (+)MK-801 antagonized seizures induced by either lindane, PTX or PTZ with similar potencies in both mouse lines. These results, coupled with the different pharmacokinetics of lindane in OF1 and NMRI mice, suggest that the distinct effects of lindane in these mice are not mediated by different activities at either NMDA or GABAA receptor complexes. Nonetheless, nifedipine antagonized lindane-induced seizures with a three-fold higher potency in NMRI than in OF1 mice. In contrast, nifedipine failed to antagonize PTX and PTZ convulsions in both OF1 and NMRI mice. These results suggest that besides the GABAA receptor complex other mechanisms related to calcium mobilization may be involved in the convulsant action of lindane.
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PMID:Lindane-induced convulsions in NMRI and OF1 mice: antagonism with (+)MK-801 and voltage-dependent calcium channel blockers. 128 May 23

This paper reports the effect of acupuncturing "Renzhong" (GV26) and "Chengjiang" (GV24) points on OHP*-induced convulsion in mice. The results are as follows: 1. Convulsion induced by 6 ATA OHP were accompanied with a decrease in the brain GABA concentration. 2. When electro-acupuncture was applied for 15 minutes prior to exposure to hyperoxic chamber, the latency of convulsions was lengthened and the symptoms of seizures were alleviated. Besides, the brain GABA concentration was also elevated remarkably. 3. Administration of vitamin B6 enhanced the effect of acupuncture on convulsions and increased brain GABA concentration. 4. The latency of convulsions was well correlated with the GABA concentration of the brain (r = 0.9867). The above results indicate that acupuncture may elevate endogenous GABA levels in the brain and prevent the hyperbaric-oxygen-induced the decrease in the brain GABA content. Therefore. It is of protective effect against oxygen convulsions. Vitamin B6 may facilitate the effect of acupuncture by improving the GABA metabolism in the brain. In short, the effect of acupuncture against oxygen convulsions may be closely related to the increase in the brain GABA levels.
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PMID:[The effect of acupuncture on high oxygen pressure-induced convulsion and its relationship to the brain GABA concentration in mice]. 128 20

Past research has demonstrated brain opioid and GABA release in response to ejaculation. In the present study we evaluated the potential role of these neurotransmitters in the postictal behavioral depression (PBD), after-discharge (AD) duration, and seizure intensity in rats kindled in the medial preoptic area (MPOA) and amygdala (AMG). The PBD, the AD duration and the seizure intensity were measured after a standard kindling stimulus and after a standard kindling stimulus applied 2 min after ejaculation. The PBD was significantly increased when the animals were stimulated 2 min after ejaculation. This increase was found in MPOA- but not in AMG-kindled rats. Ejaculation had no effect on AD duration or seizure intensity. Naloxone administration before the initiation of sexual behavior completely blocked the increase in PBD in MPOA-kindled rats. It is suggested, by indirect evidence, that opioid release during sexual behavior is added to the release associated with kindled seizures, increasing the duration of the PBD. Since sexual behavior lacked effect on AD duration or seizure intensity, no evidence could be found suggesting that functionally relevant amounts of GABA are released during this behavior.
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PMID:Sexual behavior enhances postictal behavioral depression in kindled rats: opioid involvement. 129 97

A combination of fenbufen, a non-steroidal anti-inflammatory drug and the new quinolone produces a central stimulating action. To confirm the action, we used 6 kinds of new quinolones: enoxacin, norfloxacin, ofloxacin, ciprofloxacin, lomefloxacin and tosufloxacin in this experiment. The convulsive effects of these drugs were tested on the EEG recorded from the neocortex and subcortical regions of the rabbits. Animals treated with fenbufen (50-200 mg/kg, p.o.) tended to have a high amplitude slow wave in their EEG. Rabbits treated with the new quinolones at the dose of 100 mg/kg, p.o., with the exception of tosufloxacin, also tended to show a high amplitude slow wave in their EEG. Each new quinolone given 30 min after fenbufen (50 mg/kg, p.o.) elicited characteristic spikes on the EEG. Then, high-frequency-spikes and epileptiform seizure waves appeared for a long experimental period with this combination. The combination of fenbufen and tosufloxacin (100-400 mg/kg, p.o.) caused no changes in EEG and behavior. The spike and epileptiform wave could be suppressed only temporarily with diazepam (1-4 mg/kg, i.v.). These results suggest that combined use of fenbufen and one of the new quinolones, except for tosufloxacin, produces the seizure. Not only GABA but also several other mechanisms in the central nervous system may be involved in the convulsion.
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PMID:[Effects of the combination of new quinolones and a nonsteroidal anti-inflammatory drug, fenbufen, on the EEG of rabbits]. 131 78

One of ethanol's actions after acute exposure is anticonvulsant activity whereas withdrawal from chronic ethanol exposure increases convulsant activity. An increase in neuronal transmission in the GABAergic pathways from striatum to the substantia nigra (SN) and a decrease in GABAergic transmission from SN to superior colliculus (SC) both appear to play a major role in inhibiting seizure propagation. If this is the case, then the changes in seizure sensitivity caused by ethanol may be expected to affect GABAergic transmission in opposite ways in SN and SC. We measured the effects of in vitro ethanol on pre- and postsynaptic indices of GABA transmission using SN and SC tissue from both ethanol-naive rats and rats given ethanol in their drinking water for 24 days and then withdrawn for 24 hr, a treatment that decreases seizure latency. While ethanol inhibited 3H-GABA release from slices of SC at low concentrations (20-100 nM), much higher concentrations were required to inhibit release from SN (100-500 mM). In fact, release from SN was increased by low concentrations of ethanol. Ethanol in vitro (20-1000 mM) also inhibited specific binding of 35S-TBPS to the GABAA receptor but this effect was similar in both potency and efficacy in SC and SN. Next, the in vitro effects of ethanol were measured in rats that had consumed an average of 9.8 g ethanol/kg body weight/day and were then withdrawn for 24 hr. Ethanol inhibition of 3H-GABA release from SC was significantly less in ethanol-treated rats compared to controls whereas the inhibitory effect of ethanol was increased in SN from ethanol-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective changes in GABAergic transmission in substantia nigra and superior colliculus caused by ethanol and ethanol withdrawal. 131 35

Experimental absence seizures are characterized by the fact that they are exacerbated by both direct and indirect GABA agonists. To date most of the studies that have examined this phenomenon have utilized GABAA agonists. We assessed the effect of a GABAB agonist, baclofen and a specific GABAB antagonist in two pharmacological models of absence seizures in rodent after using either gamma-hydroxybutyrate or pentylenetetrazole to induce the bilaterally synchronous spike wave discharges that typify absence seizures in rodent. Baclofen markedly prolonged and the GABAB antagonist attenuated or blocked the experimental absence seizures in both models. These data suggest a role for GABAB-related mechanisms in the pathogenesis of generalized absence seizures and raise the possibility that GABAB antagonists may have therapeutic potential as antiabsence drugs.
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PMID:Evidence for GABAB-mediated mechanisms in experimental generalized absence seizures. 131 18

A system exerting inhibitory control over generalized epilepsies and involving neurons from the substantia nigra has been described by several authors in experimental models of convulsive seizures. In the present study, the existence of such a control system governing absence epilepsy was investigated using models of non-convulsive seizures in the rat. Activation of the GABAergic neurotransmission within the substantia nigra by local injection of GABA agonists (muscimol, THIP) or an inhibitor of GABA degradation (gamma-vinyl GABA) suppresses generalized non convulsive seizures, whether they are genetically determined or induced by systemic injections of gamma-butyrolactone (100 and 200 mg/kg), pentylenetetrazole (20 mg/kg) or THIP (7.5 mg/kg). The ascending dopaminergic nigral output or the GABAergic fibres to the ventromedial thalamus are not critically involved in this control system. By contrast, the GABAergic nigro-collicular pathway appears crucial: bilateral lesion of the superior colliculus abolishes the anti-epileptic effects of intranigral injection of muscimol and blockade of the GABAergic transmission within the superior colliculus results in a suppression of generalized non-convulsive seizures. Finally, activation of collicular cell bodies by low doses of kainic acid significantly suppresses absence seizures. These results suggest the existence of a control system inhibiting generalized non-convulsive seizures which is activated by the release of the tonic inhibition exerted by the nigral GABAergic fibres on collicular neurons. The similarities between this system and the control system described for convulsive seizures are discussed.
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PMID:The inhibitory control of the substantia nigra over generalized non-convulsive seizures in the rat. 132 77


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