Ictal electrographic pattern of focal subcortical seizures induced by sound in rats

Vinogradova, Lyudmila V.; Grinenko, Olesya

doi:10.1016/j.brainres.2016.01.027

Cited by 4 publications

(4 citation statements)

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“…In awake Wistar rats with innate hypersensitivity to acoustic stimulation (audiogenic epilepsy), repetitive acoustic stimulation reliably triggers SD in the hyperexcitable cerebral cortex (48,61). In these soundsusceptible rodents, short-lasting acoustic stimulation elicits brief (5-10 sec) mild epileptic activation of the brainstem, primarily of the inferior colliculus, the key site of the auditory processing network (61)(62)(63)(64)(65)(66). The minimal brainstem seizures usually have asymmetric pattern (66) and their repetition reliably triggers SD in the cortex of one hemisphere (48,61,62).…”

Section: Triggering Sd By Sensory Stimulationmentioning

confidence: 99%

“…In these soundsusceptible rodents, short-lasting acoustic stimulation elicits brief (5-10 sec) mild epileptic activation of the brainstem, primarily of the inferior colliculus, the key site of the auditory processing network (61)(62)(63)(64)(65)(66). The minimal brainstem seizures usually have asymmetric pattern (66) and their repetition reliably triggers SD in the cortex of one hemisphere (48,61,62). Lateralization of the unilateral cortical SD coincides with that of brainstem epileptic excitation, suggesting involvement of intra-hemispheric ascending pathways in triggering the unilateral cortical SD (51,62,66).…”

Section: Triggering Sd By Sensory Stimulationmentioning

confidence: 99%

“…The minimal brainstem seizures usually have asymmetric pattern (66) and their repetition reliably triggers SD in the cortex of one hemisphere (48,61,62). Lateralization of the unilateral cortical SD coincides with that of brainstem epileptic excitation, suggesting involvement of intra-hemispheric ascending pathways in triggering the unilateral cortical SD (51,62,66). Thus, sensory (acoustic) stimulation may produce asymmetric network hyperactivity, the only cortical manifestation of which is a unilateral SD.…”

Section: Triggering Sd By Sensory Stimulationmentioning

confidence: 99%

“…At the early kindling stages, when excitability of the cortex is only slightly increased and episodic brainstem excitation triggers cortical SD without seizure activation of the cortex, SD is always unilateral and appears in the fronto-parietal cortex after a significant time delay (1-2 min), indicating local triggering SD in a restricted cortical area of one hemisphere and its subsequent non-synaptic propagation (48,61). At the late kindling stages, acoustically-induced brainstem excitation triggers strong generalized seizures and multifocal bilateral short-latency SD in the highly hyperexcitable cortex (48,66,69).…”

Section: Triggering Sd By Sensory Stimulationmentioning

confidence: 99%

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Initiation of spreading depression by synaptic and network hyperactivity: Insights into trigger mechanisms of migraine aura

Vinogradova

2017

Cephalalgia

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Background Cortical spreading depression (SD) is thought to underlie migraine aura but mechanisms of triggering SD in the structurally normal, well-nourished cortex of migraine patients remain unknown. Synaptic and network dysfunctions appear to underlie episodic neurological disorders, including migraine. The narrative review summarizes old and recent experimental evidence for triggering SD by synaptic/network mechanisms and discusses the relevance of the data to migraine pathogenesis. Our hypothesis is that under some conditions synaptic/network hyperactivity may reliably ignite SD, and this mechanism may underlie triggering migraine aura in patients. Findings High-frequency tetanic stimulation of the cortex reliably triggers SD in synaptically connected regions; SD is a reliable cortical response to acute hyperexcitability (epileptic seizures), though chronic epilepsy prevents triggering SD; in the hyperexcitable cortex, SD may be triggered by sensory stimulation; compromised glutamatergic transmission plays the critical role in triggering SD. Conclusion SD may be triggered by dynamic network instability produced by dysfunction of calcium-dependent glutamate release. Synaptic drive from subcortical sensory processing structures (brainstem and/or thalamocortical networks) is able to evoke depolarization of hyperexcitable cortical neurons sufficient to initiate the regenerative SD process. Studying SD initiation by synaptic/network hyperexcitability may provide insights into basic mechanisms underlying SD generation in migraine brain.

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