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Query: UMLS:C0596131 (audiogenic seizure)
 315 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the expression of the sleep-inducing cytokine interleukin-1alpha (IL-1alpha) in the brains of audiogenic seizure-susceptible mice subsequent to the induction of sound-induced seizure. Animal models of epilepsy often require lesioning or trauma that may nonspecifically alter IL-1alpha expression. To avoid this, we employed the Frings mouse strain; a model of auditory-evoked reflex epilepsy. Frings mice were exposed to a high-intensity sound stimulus to induce a tonic extension seizure, and the expression of IL-1alpha transcripts in different brain regions was measured thereafter. Compared to control animals, IL-1alpha transcripts were elevated 6 to 8 h postseizure in the hypothalamus, but not hippocampus, by a dexamethasone-sensitive pathway. Similar results were obtained from the genetically distinct DBA/2J audiogenic seizure-susceptible mouse strain. These findings demonstrate that the expression of IL-1alpha is altered following generalized seizure activity, induced by noninvasive sensory stimulation, in a brain-region-specific manner.
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PMID:Interleukin-1alpha in the brain is induced by audiogenic seizure. 917 24

Frequent repetition of audiogenic seizure (AGS) ('AGS kindling') in the severe substrain of genetically epilepsy-prone rats (GEPR-9s) results in the appearance of cortical epileptiform electrographic activity, increases of seizure duration and additional convulsive behaviors. These findings suggest that the initial AGS network, which is located primarily in the brainstem, has undergone expansion to the forebrain. The medial geniculate body (MGB) is a thalamic structure that is the first major auditory nucleus efferent to the AGS-initiating site in the inferior colliculus. The MGB is not required for AGS induction, but it has been implicated in the expanded AGS network in GEPR-9s based on focal, pharmacological blockade experiments. The present study examined changes in acoustically evoked MGB neuronal responses in awake and behaving GEPR-9s and in anesthetized GEPR-9s after 14 repetitive AGS-inducing stimuli given daily. An elevated number of action potentials was observed in the MGB neuronal responses after AGS kindling in GEPR-9s. This increase of MGB neuronal responses was associated with a loss of habituation and lasted for at least 28 days after the 14th AGS. An increase in the incidence of sustained acoustic responses in MGB neurons was observed after repetitive AGS in GEPR-9s. Increases in the peak latency and threshold of MGB neuronal responses were also observed after AGS kindling. MGB neurons exhibited a rapid tonic firing during tonic seizures in behaving GEPR-9s, suggesting that the MGB may be implicated in the propagation of seizure activity. However, MGB neuronal firing was silent during post-tonic clonus, a behavior seen in GEPR-9s only after AGS repetition, suggesting that MGB does not play a direct role in the generation of this convulsive behavior. Thus, changes in neuronal firing in nuclei efferent to the MGB, in the expanded neuronal network for repetitive AGS, may be responsible for the generation of post-tonic clonus in GEPR-9s.
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PMID:Audiogenic kindling increases neuronal responses to acoustic stimuli in neurons of the medial geniculate body of the genetically epilepsy-prone rat. 925 19

The inferior colliculus (IC) central nucleus (ICc), is critical for audiogenic seizure (AGS) initiation in the genetically epilepsy-prone rat (GEPR). The ICc lacks direct motor outputs but sends a major projection to the external nucleus of IC (ICx), which does project to the sensorimotor integration nuclei within the AGS neuronal network. The present study compared acoustic responses of ICx neurons in the GEPR and normal anesthetized rat and evaluated whether the GEPR exhibits functional abnormalities in the pathway from ICc to ICx. There is a significantly greater incidence of sustained repetitive response patterns to the acoustic stimulus in GEPR ICx neurons (75%) than in normal ICx neurons (24%). Following unilateral microinjection of N-methyl-D-aspartate (NMDA) into the contralateral ICc, acoustically-evoked ICx excitation and inhibition were each increased in normal animals, which is consistent with the mixed projections previously reported in this pathway and observed with electrical stimulation in the present study. The NMDA-induced ICx firing increase may be relevant to AGS, since, in previous studies, bilateral focal microinjection of NMDA into the ICc induced AGS susceptibility in normal rats [23]. However, the incidence and degree of the ICx neuronal response changes after NMDA microinjection was not abnormal in the GEPR. These data suggest that the hyperresponsiveness of ICx neurons may not involve abnormal transmission between the ICc and ICx, despite the elevated ICx neuronal responses to acoustic stimuli. However, the ICx hyperresponsivess of the GEPR, which is likely due to the known decrease in effectiveness of GABA-mediated inhibition in GEPR neurons, may be a major mechanism subserving the critical role that this structure plays in the AGS network.
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PMID:Aberrant neuronal responsiveness in the genetically epilepsy-prone rat: acoustic responses and influences of the central nucleus upon the external nucleus of inferior colliculus. 925 25

An expanding body of data has indicated that the seizure prone state in genetically epilepsy-prone rats (GEPRs) is partially caused by deficits in central nervous system noradrenergic transmission. Several lines of evidence suggest that the noradrenergic terminals in the superior colliculus (SC) may act as determinants of seizure predisposition in the GEPR. In order to assess the role of the noradrenergic transmission in the SC in the regulation of seizure severity, several drugs with different mechanisms of enhancing noradrenergic transmission were bilaterally microinfused into the SC of GEPR-9s (severe seizure GEPRs). The rats were tested for audiogenic seizure intensity at 0.25, 1, 2, 3, and 4 h after treatments. Bilateral infusion of vehicle produced no reduction in the severity of the audiogenic seizure. Desipramine (2, 4, 8 micrograms/side), nisoxetine (2, 4, 8 micrograms/side), and idazoxan (0.25, 1, 4 micrograms/side) all decreased the seizure severity in a dose-dependent fashion. Significant decreases in the seizure severity were also observed after administration of methoxamine (0.15 microgram/side) or phenylephrine (0.15 microgram/side). Pretreatment with prazosin (1 microgram/side) significantly diminished the anticonvulsant effectiveness of methoxamine and nisoxetine while prazosin, by itself, had no effects on the seizure intensity. These results suggest that noradrenergic transmission in the SC may be involved in the seizure regulation in GEPR-9s, and that this regulation may be mediated, at least in part, through alpha 1 receptors.
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PMID:Anticonvulsant effect of enhancement of noradrenergic transmission in the superior colliculus in genetically epilepsy-prone rats (GEPRs): a microinjection study. 950 30

The ventrolateral periaqueductal gray is implicated as a component of the neuronal network for audiogenic seizure. This implication is based on immunocytochemical labeling of the proto-oncogene, c-fos, and microinjection studies in the severe substrain of genetically epilepsy-prone rats that exhibits tonic seizures. The present study examines changes in acoustically evoked neuronal responses within the periaqueductal gray in the awake and behaving genetically epilepsy-prone rat as compared to normal Sprague Dawley rats. Two populations of neuronal response were observed in the periaqueductal gray of both genetically epilepsy-prone and normal rats. Most of the neurons exhibited long latencies (>10 ms) and lower thresholds, and were more responsive to the acoustic stimulus. The remainder of the periaqueductal gray neurons exhibited short latencies (<10 ms) and higher thresholds, and exhibited minimal responsiveness to the acoustic stimulus. The mean threshold of periaqueductal gray acoustically evoked neuronal firing of short-latency neurons was significantly higher than normal in the genetically epilepsy-prone rat. The number of acoustically evoked action potentials was significantly elevated in the genetically epilepsy-prone rat, particularly at the highest acoustic intensity and at a repetition rate of 1/2 s. In the genetically epilepsy-prone rat, the number of action potentials exhibited adaptation (habituation) at 1/s as compared to 1/2 s across stimulus intensities. Habituation in normal rats was observed primarily at high intensities (95 dB sound pressure level or above). During wild running and tonic seizures in the genetically epilepsy-prone rat, periaqueductal gray neurons. which had diminished firing rates due to habituation, exhibited a tonic firing pattern. Just (1-5 s) prior to the onset of tonic convulsive behaviors, an increase in the rate of periaqueductal gray tonic firing was observed. These patterns of abnormal neuronal firing suggest that periaqueductal gray neurons may be involved in generation of the tonic seizure behavioral component of audiogenic seizure in the genetically epilepsy-prone rat, which will need confirmation in other audiogenic seizure models.
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PMID:Periaqueductal gray neurons exhibit increased responsiveness associated with audiogenic seizures in the genetically epilepsy-prone rat. 953 30

Frings audiogenic seizure-susceptible mice are a model for sensory-evoked reflex seizures. Their seizure phenotype is characterized by wild running, loss of righting reflex, tonic flexion, and tonic extension in response to high-intensity sound stimulation. The Frings mice represent an inbred colony that has not been genetically characterized. This investigation studied the mode of inheritance for audiogenic seizures by crossing the Frings mouse with the seizure-resistant C57BL/6J mouse. Among the backcross progeny generated by crossing (Frings x C57BL/6J)F1 mice with the Frings strain, 391 of the 836 N2 progeny were audiogenic seizure susceptible, a finding consistent with monogenic inheritance. Genetic mapping and linkage analysis of hybrid mice using MIT microsatellite marker sequences localized the seizure gene, named mass1 for monogenic audiogenic seizure susceptible, to an approximately 3.6 cM interval in the middle of mouse chromosome 13. Linkage of mass1 to chromosome 13 is an important step in identifying the gene associated with a monogenic seizure disorder in mice, which may ultimately lead to a better understanding of the pathophysiology of human seizure disorders.
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PMID:Genetic mapping of a locus (mass1) causing audiogenic seizures in mice. 959 5

Noda epileptic rat (NER) is a mutant rat, found in a Crj: Wistar colony, which exhibits a tonic clonic convulsion spontaneously about once per 30 h from 14 weeks of age. We performed modified acoustic priming, that is, repeated weekly sound stimulations from 3 weeks of age. In addition, characteristics of audiogenic seizure (AGS), and ictal/interictal electroencephalograms (EEGs) were examined. We also studied the effect of repeated weekly stimulations from 14 weeks of age on AGS susceptibility in another NER. From 9 weeks of age, the NER primed from 3 weeks of age had a high incidence (100%) of AGS: a typical seizure was composed of sudden wild running and/or jumping (WRJ) followed by clonic or tonic-clonic convulsion. The severity and the duration of the AGS were intensified and prolonged with an increase in age, respectively. By contrast, the NER repeatedly stimulated from the age of 14 weeks, rarely showed AGS (20-40(%). The majority of the seizures in this NER were WRJ. The cortical and hippocampal EEG during the tonic convulsion showed a low-voltage spike-wave (5-7 Hz). This evolved into a high-amplitude spike- or polyspike-waves associated with the clonic convulsion. Immediately after cessation of the seizures, the EEG showed a flattening or diffuse slowing. In interictal EEG analysis, sporadic spikes predominantly in the hippocampus and spike-wave bursts in both the cortex and hippocampus occurred from 11 and 20 weeks of age, respectively. These results indicate that AGS susceptibility in NER can be induced consistently by modified acoustic priming and this rat strain is a new genetic model useful for experimental studies of human epilepsy.
Epilepsy Res 1998 Apr
PMID:Induction of convulsive seizures by acoustic priming in a new genetically defined model of epilepsy (Noda epileptic rat: NER). 960 May 43

Patients with epilepsy and animals with experimental usually show behavioral changes such as increased anxiety. Audiogenic seizures (AS) are a model of generalized tonic-clonic limbic seizures induced by sound stimulation in genetically susceptible animals. The objective of this paper was to evaluate the exploratory activity of an inbred strain derived from Wistar progenitors that has been selected in our laboratory for AS susceptibility. The exploratory activity of audiogenic seizures susceptible (S) and resistant (R) Wistar rats was measured in two situations: an open arena and the elevated plus maze, an animal model of anxiety. S animals displayed a reduced exploration in both the open arena (reduced total distance moved) and the elevated plus maze (reduced number of enclosed-arm entries). In the latter there was also a decrease in open-arm exploration, particularly of the distal part of these arms. This effect persists even when the effect of a decreased number of enclosed-arm entries is removed by analysis of covariance. Therefore, the results indicate that audiogenic seizure genetically susceptible Wistar rats display a reduced exploration of novel environments. Moreover, the results with the elevated plus maze suggest that these animals are more anxious than AS resistant rats.
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PMID:Reduced exploratory activity of audiogenic seizures susceptible Wistar rats. 981 79

Both clinical and experimental studies suggest that the immature nervous system is unusually susceptible to seizures during critical periods in postnatal life. A late onset of gamma-aminobutyric acid (GABA)-mediated synaptic inhibition could conceivably play a contributing role in this phenomenon. Numerous studies have shown that neural systems that use GABA in the neonatal brain are different than those of adulthood. GABA is an excitatory neurotransmitter that likely plays a neurotrophic role in neuronal differentiation. Other reports suggest that unique, possibly transient, GABAergic interneuron populations exist in the embryonic and neonatal nervous system. At these early times in development, the immature nervous system is remarkably resistant to seizure generation. However, as the hippocampus and neocortex enter the critical period of enhanced seizure susceptibility, inhibitory GABA systems mature rapidly. At this time, blockade of GABA type A (GABAA) receptors produce unusually severe seizure discharges. In hippocampus, concurrent exuberant outgrowth of recurrent excitatory axon collaterals and synapses appear to play a role in the generation of these seizures. As the hippocampus matures, these axons are morphologically remodeled and nearly 50% of branches within arbors are pruned. This pruning of axon branches corresponds in time with the decrease in seizure susceptibility that characterizes adulthood. Developmental remodeling of neuronal connectivity is a common feature of most areas of the central nervous system. Results from an audiogenic seizure model of early onset epilepsy suggest that prevention of axon arbor remodeling by transient sensory deprivation can lead to a permanent overinnervation of target nuclei and chronic seizure susceptibility. Early life seizures may have a similar effect. Recent results in one model have shown that repeated seizures induced by intrahippocampal injections of tetanus toxin during a critical period results in a chronic epilepsy. Future studies should attempt to determine if the synchronized discharging of early-life seizures prevents the remodeling of neuronal connectivity that normally takes place during postnatal development and results in an overinnervated and chronically hyperexcitable hippocampus.
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PMID:Developmental neuroplasticity: roles in early life seizures and chronic epilepsy. 1051 15

1. Microinjection of manganese chloride (MnCl2) into the rat substantia nigra pars compacta (SNc) induces a neurodegenerative process manifested by apomorphine-induced rotational behavior. Manganese intoxication produces a parkinsonism-like phenotype in humans. 2. In addition to motor control the substantia nigra has also been proposed to be related to epilepsy and emotional behavior. 3. Although nitric oxide (NO) participation in neurodegenerative processes is still questioned, neurons stained for NAPDH-diaphorase, a marker of NO-producing cells, are spared in several experimental neuronal lesions. Additionally, NO has also been suggested to participate in motor control. 4. The objective of this study was to analyze the effects of MnCl2-induced nigral degeneration in audiogenic seizure susceptibility, anxiety and motor activity. We also analyzed if NO synthesis inhibition (N(G)-nitro-L-arginine 25 mg/Kg twice a day for 4 days) modifies MnCl2-induced neurodegenerative process. 5. MnCl2 (50 microg) microinjection into the SNc caused a statistical significant higher number of apomorphine (0.75 mg/kg s.c.)-induced rotations. No sensitization to audiogenic seizure was found but the lesion induced an increase of open arm exploration in the elevated plus maze, suggesting an anxiolytic effect. 6. The MnCl2-nigral lesion was accompanied by an increased number of NADPH-d positive neurons in the ipsilateral SNc and striatum (both sides). NO synthesis inhibition potentiated the MnCl2-nigral lesion and reversed the NADPH-d cell number increase. 7. The present results show that MnCl2-nigral lesion can influence emotional behavior and suggest that NO may modify the progression of manganese-induced degenerative process.
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PMID:Behavioral effects of intra-nigral microinjections of manganese chloride: interaction with nitric oxide. 1080 Jul 53


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