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

The convulsive thresholds for bicuculline and electroshock seizures were studied in audiogenic seizure (AGS)-susceptible and control rats. Electroshock seizure thresholds, determined as the amperage necessary to cause tonic extension of the hindlegs in 50% of the rats (CC50 = convulsive current fifty) were markedly lowered in rats of two stocks, bred for AGS susceptibility. During the clonic phase of electroshock seizure the bicuculline threshold was slightly lowered but started to rise after the convulsion had ceased. After 5 min, the threshold was significantly elevated and the maximal increase was reached in 15 min. In control rats the level normalized curvilinearly within an hour, but in AGS rats it decreased more slowly and was still elevated after 90 min. After an audiogenic seizure, the threshold for bicuculline-induced seizures in AGS rats also rose significantly but declined rapidly after having reached a maximum at 15 min. This rise in seizure threshold for bicuculline might indicate a postictal change in GABAergic transmission.
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PMID:Seizure thresholds and their postictal changes in audiogenic seizure (AGS)-susceptible rats. 649 19

An apparatus for pure tone stimulation of audiogenic seizure (AGS)-susceptible rats is described, and the effect of change in sound pressure level and frequency on AGS response in Uaz:AGS (SD) rats is shown. By use of pure tone stimulation, the prevalence of AGS response in rats of this strain, which have been bred for seizure-susceptibility, is 77%. With increasing frequency, the intensity-response curves show a shift to lower sound pressure levels, the ED50 for 20 kHz (83.8 dB) being significantly lower than the ED50 for 5 (110.5 dB) and 10 kHz (97.5 dB). Repeated exposure to seizure-inducing sound at weekly intervals leads to more severe seizures in individual rats. This should be taken into consideration as one possible confounding factor when using this method for assaying the efficacy of anticonvulsant drugs.
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PMID:The effect of changes in sound pressure level and frequency on the seizure response of audiogenic seizure susceptible rats. 673 83

Allophenic mice composed of cells from a strain (DBA/2) susceptible to sound-induced seizures and cells from a strain (C57BL/6) resistant to them were produced by embryo aggregation techniques. Twenty-eight allophenic mice were tested for audiogenic seizure susceptibility. The results were compared with the genotypic composition of the coat melanocytes. For those animals with a predominance of one genotype or the other in the coat, their seizure phenotype was the same as that of the strain most represented in the coat. In contrast, those animals with major contributions of both genotypes in the coat demonstrated the entire spectrum of susceptibility phenotypes. Such results are likely to be a manifestation of a relatively small target tissue for the genes influencing the development of audiogenic seizure susceptibility.
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PMID:Audiogenic seizure susceptibility of C57BL/6 in equilibrium DBA/2 allophenic mice. 712 85

The short-latency auditory-evoked response was recorded from adult (over 8 wk) and young (16-22 day) mice of the audiogenic seizure-prone DBA/2J (D2) and seizure-resistant C57BL/6J (C6) strains. An auditory complex made up of eleven peaks and troughs was found within the first 20 ms after click stimuli. The latencies of the potentials tended to be shorter in the C6 mice and in the adults of both strains. The ratio of amplitude differences of late to early peaks ('amplitude index') was much larger (P less than 0.01) in D2 mice. The data are consistent with greater neuronal recruitment to acoustic stimuli in the higher-order auditory centers of D2 mice.
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PMID:A comparison of short-latency auditory-evoked potentials in two strains of mice: possible neurophysiological correlates of susceptibility to audiogenic seizures? 728 63

In audiogenic seizure (AGS) susceptible rats, the acute (intraperitoneal and intravenous) dose-response effects of (--)-cannabidiol (CBD) for preventing AGS and for causing rototod neurotoxicity (ROT) were determined. Also, the anti-AGS and ROT effects of 10 CBD analogs, given in intravenous doses equivalent to the AGS-ED50 (15 mg/kg) and ROT-ID50 (31 mg/kg) of CBD, were ascertained. Compared to CBD, (--)-CBD diacetate and (--)-4-(2'-olivetyl)-alpha-pinene were equally effective whereas (--)-CBD monomethyl ether, (--)-CBD dimethyl ether, (--)-3'-acetyl-CBD monoacetate, (+)-4-(2'-olivetyl)-alpha-pinene, (--)-and (+)-4-(6'-olivetyl)-alpha-pinene, (+/-)-AF-11, and olivetol were less effective anticonvulsants. Except for (--)- and (+)-4-(2'-olivetyl)-alpha-pinene and olivetol, all analogs showed less ROT than CBD. Also, CBD and all analogs were not active in tetrahydrocannabinol seizure-susceptible rabbits, the latter a putative model of cannabinoid psychoactivity in humans. These data suggest anticonvulsant requirements of 2 free phenolic hydroxyl groups, exact positioning of the terpinoid moiety in the resorcinol system and correct stereochemistry. Moreover, findings of separation of anticonvulsant from neurotoxic and psychoactive activities, notably with CBD diacetate, suggest that additional structural modifications of CBD may yield novel antiepileptic drugs.
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PMID:Antiepileptic potential of cannabidiol analogs. 729 73

The cochleae from 3 lines of mice, selectively bred for differential susceptibility to priming-induced audiogenic seizures, were examined following acoustic priming and retest or kanamycin treatment, and the degree of cochlear damage was assessed. After 60 sec of acoustic priming, animals from the high and unselected lines which had subsequently developed audiogenic seizure susceptibility exhibited severe cochlear damage limited to the outer hair cells. Low line mice, which had been selected for resistance to acoustic priming-induced audiogenic seizures and were not seizure susceptible, exhibited no cochlear pathology following acoustic priming. Following kanamycin treatment, all 3 lines developed subsequent audiogenic seizure susceptibility. Histological examination of cochleae from mice so treated revealed a pattern of damage similar to that caused by acoustic priming, except that the cochleae of priming-induced audiogenic seizure resistant low line mice revealed a significant amount of outer hair cell damage. The results are discussed with respect to the physiological mechanism underlying a selectively bred behavioral phenotype in terms of a possible instance of damage/disuse-supersensitivity in the central nervous system.
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PMID:Acoustic priming and kanamycin-induced chochlear damage. 735 78

Whole brain levels of 5-HT and NE in audiogenic seizure susceptible DBA mice were compared with those of the nonsusceptible C57BL/6 strain at different ages and in two separate laboratories that used different assay procedures. Contrary to previous reports, there were not significant differences between the susceptible and nonsusceptible animals in whole brain levels of either amine at the age of peak seizure susceptibility. Differential stress associated with capturing the susceptible mice had no effect on brain levels of NE. The data question the suggestion that deficits in brain monoamine transmission capable of being indexed by lower whole brain levels of NE and/or 5-HT play a role in genetically determined susceptibility to audiogenic seizures.
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PMID:Inverse relationship between whole brain monoamine levels and audiogenic seizure susceptibility in mice: failure to replicate. 739 36

The specific acitivity of cerebral histamine N-methyltransferase (HMT) was significantly lower in the audiogenic seizure-susceptible (SS) 21-day old DBA/2J mouse when compared to the non-susceptible 70-day old DBA/2J mouse but not when compared to the seizure resistant (SR) C57B1/6J mouse at 21 days of age. There was no significant difference between the two strains at 70 days of age. The lower HMT specific activity was also observed in a SS mutant of the deermouse Peromyuscus maniculatus, relative to the SR, wild-type animal. The activity of cerebral catechol-O-methyltransferase (COMT) was significantly lower in the DBA/2J mice relative to the C57B1/6J at 21 and 70 days while, in Peromyscus, it was higher in the SS mutant than in the SR animal. The activity of MAO, B was lower in the 21-day old, relative to the 70-day old DBA/2J and the 21-day old C57B1/6J mice. There were no differences in MAO A or B between SS and SR Peromyscus. The findings raise the possibility that cerebral methylation may operate at characteristic rates in SS animals.
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PMID:Differences in activity in cerebral methyltransferases and monoamine oxidases between audiogenic seizure susceptible and resistant mice and deermice. 743 89

The incidence of febrile convulsions was determined in six inbred strains of mice at four ages. Febrile convulsions were elicited by placing the mice in a cylinder with the air temperature raised to 51 +/- 2 degrees C; this elevated the mouse's body and brain temperature to between 40 and 46 degrees C. The strains used were DBA/2Bg, DBA/1Bg, DBA/1Bg-ras, C57BL/10Bg, C57BL/6Bg, and C57BL/6Bg-Gad-1 alpha; the ages were 21 +/- 1, 29 +/- 1, 59 +/- 1, and 119 +/- 1 days of age. DBA/2Bg, DBA/1Bg, and C57BL/6Bg-Gad 1 alpha are audiogenic seizure susceptible at 21 +/- 1 and 29 +/- 1 days of age, but not at 59 +/- 1 and 119 +/- 1 days of age; whereas C57BL/10Bg, C57BL/6Bg, and DBA/1Bg-ras are audiogenic seizure resistant at all ages. Mice of both sexes, all strains, and all ages had a febrile convulsion and died. Thus, in inbred mice, there does not appear to be either a genetic or developmental correlation between audiogenic seizures and febrile convulsions. This finding may be contrasted with that in other studies showing a correlation between susceptibility to audiogenic seizures and to either electroshock convulsions or chemoconvulsions. However, there are subtle strain and age variants in susceptibility to febrile convulsions of these mice.
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PMID:Febrile convulsions in inbred strains of mice susceptible and resistant to audiogenic seizures. 743 31

Amino acid and monoamine concentrations were examined in tissue extracts of caudate nucleus of genetic substrains of BALB/c mice susceptible or resistant to audiogenic seizures. Amino acids [aspartate, glutamate, glycine, taurine, serine, gamma-aminobutyric acid (GABA)], monoamines, and related metabolites were separated by isocratic reverse-phase chromatography and detected by a coulometric electrode array system. In situ activity of tyrosine hydroxylase and tryptophan hydroxylase were determined by measuring the accumulation of L-DOPA and 5-hydroxytryptophan after administration of the decarboxylase inhibitor NSD-1015. Highly significant decreases in concentrations of both excitatory (glutamate and aspartate) and inhibitory amino acids (GABA and taurine) were observed in extracts of caudate nucleus of seizure-prone mice. Substantial decreases in concentrations of dopamine (DA) and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, were also noted. Decreased accumulation of L-DOPA after NSD-1015 administration provided evidence for decreased tyrosine hydroxylase activity and decreased DA synthesis in striatum of seizure-prone mice compared with seizure-resistant mice. Decreased concentrations of the DA metabolite 3-methoxytyramine (after NSD-1015 administration) suggested that DA release was also compromised in seizure-prone mice. No significant difference in 5-hydroxytryptophan accumulation in striatum of seizure-prone and seizure-resistant mice suggested that tryptophan hydroxylase activity and serotonin synthesis were not affected. The data suggest that seizure-prone BALB/c mice have a deficiency in intracellular content of both excitatory and inhibitory amino acids. The data also raise the issue of whether GABAergic interactions with the nigrostriatal DA system are important in the regulation of audiogenic seizure susceptibility.
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PMID:Determination of amino acids and monoamine neurotransmitters in caudate nucleus of seizure-resistant and seizure-prone BALB/c mice. 768 Nov


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