Cortical spreading depression reversibly disrupts convulsive motor seizure expression in amygdala-kindled rats

Kelly, Mary Ellen; Battye, Roy; McIntyre, Dan C.

doi:10.1016/s0306-4522(98)00656-3

Cited by 33 publications

(25 citation statements)

References 35 publications

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“…Cortical regions send abundant projections to the hippocampus, STN and amygdala and are essential for the manifestation of motor seizures (Braak et al, 1996;McDonald 1998;Hamani et al, 2004). Kelly et al (1999) used cortical spread depression, a reversible lesion method to inactivate frontal motor cortex, and found that it could block the convulsive expression of amygdala kindled seizures. The authors emphasized that the cortex mediates a crucial role in clonic motor seizures by transferring the ictal discharges to the brain stem and spinal cord.…”

Section: Discussionmentioning

confidence: 99%

“…Injection of GABA agonists into the STN significantly reduced motor seizures, probably due to decreased excitatory input to the SNr (Veliskova et al, 1996;Deransart et al, 1998). And, finally, the frontal cortex is believed to be the route seizures take from subcortical limbic structures to the brainstem and spinal cord, where the convulsive components are manifested (Corcoran et al, 1975;Kelly et al 1999;McIntyre and Gilby, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Temporal sequence of ictal discharges propagation in the corticolimbic basal ganglia system during amygdala kindled seizures in freely moving rats

Shi

Luo

Woodward³

et al. 2007

Epilepsy Research

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We used a multiple channel, single unit recording technique to investigate the neural activity in different corticolimbic and basal ganglia regions in freely moving rats before and during generalized amygdala kindled seizures. Neural activity was recorded simultaneously in the sensorimotor cortex (Ctx), hippocampus, amygdala, substantia nigra pars reticulata (SNr) and the subthalamic nucleus (STN). We observed massive synchronized activity among neurons of different brain regions during seizure episodes. Neurons in the kindled amygdala led other regions in synchronized firing, revealed by time lags of neurons in other regions in crosscorrelogram analysis. While there was no obvious time lag between Ctx and SNr, the STN and hippocampus did lag behind the Ctx and SNr in correlated firing. Activity in the amygdala and SNr contralateral to the kindling stimulation site lagged behind their ipsilateral counterparts. However no time lag was found between the kindling and contralateral sides of Ctx, hippocampus and STN. Our data confirm that the amygdala is an epileptic focus that emits ictal discharges to other brain regions. The observed temporal pattern indicates that ictal discharges from the amygdala arrive first at Ctx and SNr, and then spread to the hippocampus and STN. The simultaneous activation of both sides of the Ctx suggests that the neocortex participates in kindled seizures as a unisonant entity to provoke the clonic motor seizures. Early activation of the SNr (before the STN and hippocampus) points to an important role of the SNr in amygdala kindled seizures and supports the view that different SNr manipulations may be effective ways to control seizures.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Temporal sequence of ictal discharges propagation in the corticolimbic basal ganglia system during amygdala kindled seizures in freely moving rats

Shi

Luo

Woodward³

et al. 2007

Epilepsy Research

View full text Add to dashboard Cite

show abstract

“…The motor cortex is presumably the source of the behavioral responses (clonus) seen in the animals upon stimulation (Kelly et al, 1999). Synaptic changes here could underlie the lowered threshold for seizure recruitment and convulsive expression.…”

Section: Regional Spread Of Activin ␤A Mrna Inductionmentioning

confidence: 94%

Activin mRNA induced during amygdala kindling shows a spatiotemporal progression that tracks the spread of seizures

Foster

Puchowicz

McIntyre

et al. 2004

J of Comparative Neurology

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The progressive development of seizures in rats by amygdala kindling, which models temporal lobe epilepsy, allows the study of molecular regulators of enduring synaptic changes. Neurotrophins play important roles in synaptic plasticity and neuroprotection. Activin, a member of the transforming growth factor-␤ superfamily of growth and differentiation factors, has recently been added to the list of candidate synaptic regulators. We mapped the induction of activin ␤A mRNA in amygdala and cortex at several stages of seizure development. Strong induction, measured 2 hours after the first stage 2 (partial) seizure, appeared in neurons of the ipsilateral amygdala (confined to the lateral, basal, and posterior cortical nuclei) and insular, piriform, orbital, and infralimbic cortices. Activin ␤A mRNA induction, after the first stage 5 (generalized) seizure, had spread to the contralateral amygdala (same nuclear distribution) and cortex, and the induced labeling covered much of the convexity of neocortex as well as piriform, perirhinal, and entorhinal cortices in a nearly bilaterally symmetrical pattern. This pattern had filled in by the sixth stage 5 seizure. Induced labeling in cortical neurons was confined mainly to layer II. A similar temporal and spatial pattern of increased mRNA expression of brain-derived neurotrophic factor (BDNF) was found in the amygdala and cortex. Activin ␤A and BDNF expression patterns were similar at 1, 2, and 6 hours after the last seizure, subsiding at 24 hours; in contrast, c-fos mRNA induction appeared only at 1 hour throughout cortex and then subsided. In double-label studies, activin ␤A mRNA-positive neurons were also BDNF mRNA positive, and they did not colocalize with GAD67 mRNA (a marker of ␥-aminobutyric acidergic neurons). The data suggest that activin and BDNF transcriptional activities accurately mark excitatory neurons participating in seizure-induced synaptic alterations and may contribute to the enduring changes that underlie the kindled state.

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“…In addition, the seizure initially became bilateral through homotopic corpus callosal projections to the contralateral motor cortex. This suggestion was derived from the observation that bisection of the anterior half of the corpus callosum lateralized the forelimb clonus of an amygdala triggered convulsion, producing a hemi-convulsion identical to that observed following unilateral CSD of the hemisphere contralateral to a kindled amygdala site (41,58,59). …”

Section: Kindling (Dr D C Mcintyre)mentioning

confidence: 97%

“…If CSD was provoked in the hemisphere contralateral to the kindled amygdala, a hemi-convulsion occurred with strong clonus unilaterally in the limbs associated with the kindled hemisphere. If the CSD was induced in the motor cortex of the kindled hemisphere (ie, ipsilateral to the focus), the convulsion was blocked and the focal AD truncated (41). These observations suggested that kindled amygdala AD most likely recruited the ipsilateral networks, including the frontal cortices, to drive the convulsion.…”

Section: Kindling (Dr D C Mcintyre)mentioning

confidence: 99%

Animal Models of Limbic Epilepsies: What Can They Tell Us?

2002

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Cortical spreading depression reversibly disrupts convulsive motor seizure expression in amygdala-kindled rats

Cited by 33 publications

References 35 publications

Temporal sequence of ictal discharges propagation in the corticolimbic basal ganglia system during amygdala kindled seizures in freely moving rats

Temporal sequence of ictal discharges propagation in the corticolimbic basal ganglia system during amygdala kindled seizures in freely moving rats

Activin mRNA induced during amygdala kindling shows a spatiotemporal progression that tracks the spread of seizures

Animal Models of Limbic Epilepsies: What Can They Tell Us?

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