Electrically elicited seizures from the inferior colliculus: A potential site for the genesis of epilepsy?

McCown, Thomas J.; Greenwood, Robert; Frye, Gerald D.; Breese, George R.

doi:10.1016/0014-4886(84)90087-6

Cited by 147 publications

(42 citation statements)

References 6 publications

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“…However, the neuronal loss in the NRT does not seem to correlate with seizures because CA ischemia of less than a 5-min duration could be associated with severe NRT damage with out increased susceptibility to AGS. It is clear from the findings of the present study and from the work of other authors (McCown et al , 1984;Millan et al , 1986) that lesions of the IC cause initiation of AGS, and the mechanism is a loss of inhibitory function of this structure. To date, there is no experimental model that directly detects GABA-ergic recurrent inhibition in the IC.…”

Section: Paired Pulse Stimulationsupporting

confidence: 81%

“…The neuronal GABA-ergic alterations were primar ily evaluated by immunohistochemical assays for glutamic acid decarboxylase (GAD) reactivity. In view of a putative role of the inferior colliculus (IC) in the induction of AGS (Kesner, 1966;Wada et al , 1970;McCown et al, 1984;Bagri et al , 1989;Millan et al, 1986), evaluation of neuronal changes in this structure received special attention. Otherwise, to assess the functional status of the GABA-ergic ele ments, we used a physiologic test of feedback inhi bition that is mediated by GAB A-A receptors ap plying paired pulse stimulation (PPS) to the per forant path while measuring the evoked responses of the granule cells of the dentate gyrus in the hip pocampal formation.…”

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confidence: 99%

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Development of Susceptibility to Audiogenic Seizures following Cardiac Arrest Cerebral Ischemia in Rats

Kawai

Penix

Kawahara

et al. 1995

J Cereb Blood Flow Metab

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Summary: Susceptibility to aUdiogenic seizures (AGS) was investigated in Sprague-Dawley rats subjected to cardiac arrest cerebral ischemia (CAC!), produced by compression of the major cardiac vessels. The onset of AGS was regularly observed 1 day after CACI of >5 min duration. The duration of postischemic susceptibility to AGS was directly related to the density of cerebral isch emia, with 50% of more severely ischemic animals still showing AGS susceptibility 8 weeks after CAC!. Lesion ing of the inferior colliculi (IC) abolished the onset of AGS; no such effect was observed after lesioning the me dial geniculate (MG), Glutamic acid decarboxylase (GAD) immunochemistry revealed �50% loss of GAD-

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Section: Paired Pulse Stimulationsupporting

confidence: 81%

mentioning

confidence: 99%

Development of Susceptibility to Audiogenic Seizures following Cardiac Arrest Cerebral Ischemia in Rats

Kawai

Penix

Kawahara

et al. 1995

J Cereb Blood Flow Metab

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“…The central nucleus of the inferior colliculus (CNIC), in particular, has been proposed to be involved in AGS initiation (Willott and Lu, 1980) while the external cortex (ECIC), which receives a dense projection from the ipsilateral CNIC (Coleman and Clerici, 1987), is implicated in the propagation of the seizures (Willott and Lu, 1980;Chakravarty and Faingold, 1996). In several genetic models of AGS, the ECIC mediates the seizure output pathway in the neuronal network for AGS (Le Gal La Salle and Naquet, 1990;McCown et al, 1984) through its connections with the superior colliculus (SC) (Van Buskirk, 1983;Garcia-Cairasco et al, 1993). The mammalian SC is a laminated, midbrain structure that can be functionally divided into superficial and deep laminae (for review, see Stein and Meredith, 1993).…”

Section: Introductionmentioning

confidence: 99%

Morphologic and neurochemical alterations in the superior colliculus of the genetically epilepsy-prone hamster (GPG/Vall)

et al. 2007

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SummaryThe GPG/Vall hamster is an animal model that exhibits seizures in response to sound stimulation. Since the superior colliculus (SC) is implicated in the neuronal network of audiogenic seizures (AGS) in other forms of AGS, this study evaluated seizure-related anatomical or neurochemical abnormalities in the SC of the GPG/Vall hamster. This involved calbindin (CB) and parvalbumin (PV) immunohistochemistry, densitometric analysis and high performance liquid chromatography in the superficial and deep layers of the SC in control and epileptic animals. Compared to control animals, a reduction in SC volume and a hypertrophy of neurons located in the deep layers of the SC were observed in the epileptic hamster. Although, analysis of CB-immunohistochemistry in the superficial layers did not show differences between groups, analysis of PV-immunostaining in the deep SC revealed an increase in the mean gray level within immunostained neurons as well as a decreased immunostained neuropil in the GPG/Vall hamster as compared to control animals. These alterations were accompanied by a decrease in the levels of GABA and increased levels of taurine in the epileptic animal. These data indicate that the deep SC of the GPG/Vall hamster is structurally abnormal; suggesting its involvement in the neuronal network for AGS.

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“…Due to degen en(tion of cochlear hairs, strong acoustic stimuli in duce an abnormal response within the inferior col liculus accompanied by wild running episodes (Portman et al , 197 1;Penny et al , 1983). Spread of the abnormal response epileptic activity to the su perior colliculus, the brain-stem reticular forma tion, and the substantia nigra results in the tonic phase (Kesner, 1966;Willot and Lu, 1980;Jobe, 198 1;McCown et al , 1984;Browning et al , 1985). The hippocampus, amygdala, and most forebrain structures are not implicated in the audiogenic sei zures network (Browning, 1986;Faingold, 1988;Millan, 1988).…”

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confidence: 99%

Mapping of Cerebral Blood Flow Changes during Audiogenic Seizures in Wistar Rats: Effect of Kindling

Nehlig

Vergnes²,

Hirsch³

et al. 1995

J Cereb Blood Flow Metab

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Summary: The quantitative autoradiographic [14C]iodoantipyrine technique was applied to the measurement of rates of local cerebral blood flow (LCBF) during audio genic seizures in Wi star AS rats belonging to a genetic strain selected at the Centre de Neurochimie (Strasbourg, France) for their sensitivity to sound. Seizures were elic ited in naive rats never exposed to sound (single audio genic seizures) or in rats previously exposed to l�O seizure-inducing sound stimulations until generalization of the seizure to forebrain areas (referred to as "kindled animals"). During single audiogenic seizures, rates of LCBF increased over control values in all areas but the genu of the corpus callosum. The highest increases in LCBF (180-388%) were recorded in the inferior and su perior colliculus, reticular formation, monoaminergic cell groupings, especially the substantia nigra, posterior veg etative nuclei, and many thalamic and hypothalamic re gions. The lowest increases were seen in forebrain limbic regions and cortical areas. In kindled animals, LCBF rates increased over control levels in 67 areas of the 75In the breeding colony of our laboratory (Centre de Neurochimie, Strasbourg, France), we have se lected a strain of Wistar rats susceptible to audio genic seizures (Wistar AS) (Marescaux et aI., 1987). In these rats, the exposure to an intense sound stim ulus induces an epileptic seizure characterized by one or two wild running episodes lasting for about 10-30 s, followed by a tonic phase with dorsal hy perextension, the forelimbs stretched out forward and the hindlimbs flexed. This seizure is followed 9studied. LCBF increases were generally of a lower am plitude in kindled than in naive rats. Differences between the two groups of seizing rats were located mostly in brain-stem regions, mainly the inferior colliculus, reticu lar formation, substantia nigra, and posterior vegetative nuclei. Conversely, rates of LCBF were similar in fore brain areas of naive and kindled animals. In conclusion, the present data show that there is a good correlation between the structures known to be involved in the ex pression of audiogenic seizures (inferior col\iculus, retic ular formation, substantia nigra mainly) and the large in crease in LCBF during single audiogenic seizures, while rates of LCBF increase to a lesser extent in forebrain areas not involved in this type of seizures. The circula tory adaptation to kindled seizures is rather a decreased response in brain-stem regions and no change in the fore brain, although the kindling process induces a generaliza tion of the seizure from brain-stem to anterior regions.

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Electrically elicited seizures from the inferior colliculus: A potential site for the genesis of epilepsy?

Cited by 147 publications

References 6 publications

Development of Susceptibility to Audiogenic Seizures following Cardiac Arrest Cerebral Ischemia in Rats

Development of Susceptibility to Audiogenic Seizures following Cardiac Arrest Cerebral Ischemia in Rats

Morphologic and neurochemical alterations in the superior colliculus of the genetically epilepsy-prone hamster (GPG/Vall)

Mapping of Cerebral Blood Flow Changes during Audiogenic Seizures in Wistar Rats: Effect of Kindling

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