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

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

A new audiogenic seizure (AGS)-susceptible strain of rats (P77PMC) was evaluated as a possible model of human febrile seizures. The long-term effects of experimental febrile seizures were observed. All 30-day-old rat pups exhibited clonic seizures during exposure to an ambient temperature of 45 +/- 0.5 degree C. The mean latency from the beginning of the hyperthermic stimulus to the onset of convulsion was 16.9 +/- 2.2 min. The rats survived this hyperthermic seizure, developed a resistance to acoustic stimulations, but were more susceptible at the age of 50 to 60 days to kainate-induced limbic seizures than controls. The results of this study imply that febrile seizures of developing P77PMC rats can change later seizure susceptibility, and there may be some correlation between febrile convulsion and temporal lobe epilepsy.
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PMID:Long-term effects of febrile convulsion on seizure susceptibility in P77PMC rat--resistant to acoustic stimuli but susceptible to kainate-induced seizures. 399 15

Twenty rats of an audiogenic seizure (AGS)-susceptible stock were exposed to four different sound stimuli and seizure severity and seizure-latency were registered. Two sounds with harmonic spectra, one pure tone and band noise were used. The harmonic spectra were found to be significantly (P less than 0.005) more effective than the other stimuli in inducing AGS when seizure-latency was taken as a parameter. Connections from the auditory pathway to the reticular formation seem to be of importance in the triggering of these seizures. AGS-susceptible rats may offer a useful tool for experimental hearing research.
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PMID:Sounds with harmonic spectra are more effective than pure tones in inducing audiogenic seizure in rats. 399 86

A kindling-like effect was produced by exposing 30-day-old rats to repeated hyperthermia-induced seizures. Naive audiogenic seizure (AGS)-susceptible rats (P77PMC) were easier to be kindled than AGS-resistant rats (Wistar). This hyperthermic kindling model may be used to study the outcome and mechanisms of human febrile seizures. The mechanisms underlying hyperthermic kindling remain to be investigated.
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PMID:Kindling phenomenon of hyperthermic seizures in the epilepsy-prone versus the epilepsy-resistant rat. 407 29

Benzodiazepine receptors were investigated in the cerebral cortex, the hippocampus, the brainstem, and the cerebellum of audiogenic seizure (AGS)-susceptible and seizure-resistant (ER) control rats. In AGS-susceptible rats of Sprague-Dawley descent, muscimol (10-6 M and 3 x 10-5 M) activated the binding of 3H-diazepam (0.4 nM) significantly less than in ER-rats. This finding may be strain selective, since it was not observed in AGS-susceptible rats of Wistar descent. Specific binding of the convulsant benzodiazepine receptor ligand methyl 6,7-dimethoxy-4-ethyl carboline-3-carboxylate (3H-DMCM), the benzodiazepine receptor ligand 3H-diazepam and the chloride channel directed cage convulsant t-butylbicyclophosphorothionate 35S-TBPS were not significantly changed in AGS-susceptible as compared to control rats. Our findings indicate that a disturbance at the level of the benzodiazepine receptor/GABA receptor/chloride channel complex is not a likely general aetiological factor for audigenic seizures in rats.
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PMID:A study on benzodiazepine receptor binding in audiogenic seizure-susceptible rats. 609 92

Benzodiazepine receptors appear to be pharmacologically important as the modulator of anxiolytic, anticonvulsant, and muscle relaxant activities in the central nervous system. The acute effects of valproic acid (VPA), diazepam (DZ), phenobarbital (PB), and phenytoin (PHT) on benzodiazepine receptor binding as measured by 3H-flunitrazepam were studied in Sprague Dawley (S/D) rat cerebral cortices. The acute effects of seizures were also studied in both S/D rats and audiogenic seizure rats. In the VPA (100 mg/kg, IP) treated rats, there was a 11% increase in benzodiazepine receptor density (Bmax). This effect appear to be dose dependent as higher doses of VPA (200-500 mg/kg) resulted in more increase in Bmax. No significant change occurred in Kd after acute VPA treatment. However, acute PB (100 mg/kg), PHT (100-200 mg/kg), or DZ (50 mg/kg) did not produce any changes in Bmax or dissociation constants (Kd). In S/D rats, significant increases in Bmax were observed 30 minutes after seizures induced by electroshock or pentylenetetrazol (50 mg/kg) IP injection. However, audiogenic seizure rats had higher Bmax prior to the induction of seizures when compared to normal S/D rats, and no changes in Bmax occurred after seizures in audiogenic seizure rats. No changes in Kd were seen in either S/D rats or audiogenic seizure rats before and after seizures. These data suggest that an increase in benzodiazepine receptor density might correlate with the mechanism of anticonvulsant action of VPA, and that a possible disorder of the GABA/benzodiazepine receptor complex may be involved in the seizure susceptibility in audiogenic seizure rats.
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PMID:Effects of seizures and antiepileptic drugs on benzodiazepine receptors in rat brain. 609 63

The preferential alpha-2 noradrenergic agonists, clonidine (0.2--0.4 mg/kg), oxymetazoline (2.5--10.0 mg/kg) and UK 14,304 (0.6 mg/kg), when given i.p., reduce the severity of audiogenic seizures in 19- to 26-day-old DBA/2 mice. This protective effect can be diminished or reversed by alpha-2 noradrenergic antagonists such as yohimbine (2.5 mg/kg) or piperoxan (20--50 mg/kg) given i.p. or phentoalamine (100 micrograms) given intracerebroventricularly. It is not reversed by the preferential alpha-1 noradrenergic antagonist phenoxybenzamine (5 mg/kg) given i.p. Yohimbine, (1--2.5 mg/kg), piperoxan (20--50 mg/kg) or phenoxybenzamine (5 mg/kg) given i.p. alone did not change the severity of audiogenic seizure responses. Phentolamine (10--100 micrograms) or prazosin (10--50 micrograms) given intracerebroventricularly induced spontaneous limb myoclonus in some mice. Audiogenic seizure responses were unchanged after phentolamine (10--100 micrograms) but were reduced after prazosin (25--50 micrograms). Activation of a receptor pharmacologically similar to the peripheral alpha-2 noradrenergic receptor protects against seizures in this epilepsy model.
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PMID:Noradrenergic influences on sound-induced seizures. 610 28

The anticonvulsive effects of GABA, taurine, and glycine were investigated on several chemically-induced and genetic seizure models. Intravenous injections of either GABA, taurine, or glycine provided protection against 3-mercaptopropionic acid (MPA)-induced convulsions in adult Swiss mice. GABA was partially effective against isonicotinic acid hydrazide and was without effect against bicuculline-induced convulsions. Prolonged administration of glycine prevented MPA-induced convulsions but not electrically induced seizures or seizures induced by strychnine or metrazol. Intragastric glycine protected young audiogenic seizure-susceptible DBA/2 mice against all three phases of sound-induced convulsions (wild running, clonic and tonic seizure), but GABA and taurine provided little or no protection. With increase of glycine, the cerebral levels of glutamine and serine also increased, but that of glutamic acid decreased. The endogenous glutamic and glycine levels were slightly higher in the brains of the audiogenic seizure-susceptible DBA/2 mice than in that of the resistant BALB/Cy strain.
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PMID:Anticonvulsant effects of some inhibitory neurotransmitter amino acids. 613 43

In this study we have investigated the possible role played by dopaminergic mesocorticolimbic neurons in ethanol withdrawal syndrome in rats. 6-hydroxydopamine-induced bilateral lesions of A10 nucleus resulted in selective fall in forebrain dopamine content accompanied by enhanced motor activity and audiogenic seizure intensity when measured during withdrawal period. Opposite changes, hypolocomotion and lower seizures intensity, were observed after metoclopramide injection. Pimozide also diminished seizure intensity but at higher dose (0.4 mg/kg) produced an increase in locomotor activity. Bromocriptine, an agonist of dopaminergic receptors, depressed both locomotor activity and audiogenic seizure intensity. It is concluded that mesolimbic dopaminergic neurons may be involved in the mechanism of ethanol withdrawal syndrome.
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PMID:Effects of 6-hydroxydopamine-induced lesions of A10 dopaminergic neurons and neuroleptic or bromocriptine treatment on ethanol withdrawal syndrome in rats. 614 54

A growing body of evidence supports a pathophysiological role for norepinephrine (NE) and serotonin in the regulation of seizures in the genetically epilepsy-prone rat (GEPR). Other evidence indicates that gamma-aminobutyric acid (GABA) and taurine may also participate in the seizure regulation process. Innate deficits in NE and serotonin appear to be causes of the genetically determined seizure-prone states of the GEPR, whereas abnormalities in GABAergic systems and taurine metabolism may represent inadequate attempts of the central nervous system to compensate for the seizure-prone state in these rats. In audiogenic seizure-susceptible (AGS) mice, evidence suggests a role for dopamine as well as GABA and possibly serotonin. NE may contribute to the regulation of seizures in AGS mice, but consistent evidence for a primary role for this monoamine is lacking. It is suggested that there is no single common neurotransmitter abnormality underlying genetic seizure disorders in humans or other animals and that the GEPR and the AGS mouse may both serve as good models for study of the neurochemical abnormalities that underlie the different human epilepsies.
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PMID:Neurotransmitter abnormalities in genetically epileptic rodents. 614 25


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