Heterogeneous incidence and propagation of spreading depolarizations

Kaufmann, Dan; Theriot, Jeremy; Zyuzin, Jekaterina; Chang, Junbiao; Tang, Yujie; Bogdanov, Volodymyr B.; Multon, Sylvie; Schoenen, Jean; Ju, Y. Sungtaek; Brennan, KC

doi:10.1177/0271678x16659496

Cited by 41 publications

(55 citation statements)

References 53 publications

(101 reference statements)

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“…Another read-out to be taken as an indicator for the susceptibility of the nervous tissue to SD is the distance covered by SD before coming to a halt. Indeed, some SD events are gradually extinguished over their course of propagation, rather than traversing the entire cortical surface, as demonstrated by multimodal experimental imaging studies (Bere et al, 2014;Kaufmann et al, 2017;Menyhart et al, 2017a). Even though not documented so far, we observed that in old (18 months old) rats, experimentally triggered SDs are more likely to terminate after having propagated only a few millimeters away from the site of elicitation than in young (2 months old) rats.…”

Section: Sd Triggered Experimentallymentioning

confidence: 53%

Susceptibility of the cerebral cortex to spreading depolarization in neurological disease states: The impact of aging

Hertelendy

Varga

Menyhárt

et al. 2019

Neurochemistry International

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Secondary injury following acute brain insults significantly contributes to poorer neurological outcome. The spontaneous, recurrent occurrence of spreading depolarization events (SD) has been recognized as a potent secondary injury mechanism in subarachnoid hemorrhage, malignant ischemic stroke and traumatic brain injury. In addition, SD is the underlying mechanism of the aura symptoms of migraineurs. The susceptibility of the nervous tissue to SD is subject to the metabolic status of the tissue, the ionic composition of the extracellular space, and the functional status of ion pumps, voltage-gated and other cation channels, glutamate receptors and excitatory amino acid transporters. All these mechanisms tune the excitability of the nervous tissue. Aging has also been found to alter SD susceptibility, which appears to be highest at young adulthood, and decline over the aging process. The lower susceptibility of the cerebral gray matter to SD in the old brain may be caused by the age-related impairment of mechanisms implicated in ion translocations between the intra-and extracellular compartments, glutamate signaling and surplus potassium and glutamate clearance. Even though the aging nervous tissue is thus less able to sustain SD, the consequences of SD recurrence in the old brain have proven to be graver, possibly leading to accelerated lesion maturation. Taken that recurrent SDs may pose an increased burden in the aging injured brain, the benefit of therapeutic approaches to restrict SD generation and propagation may be particularly relevant for elderly patients.

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Section: Sd Triggered Experimentallymentioning

confidence: 53%

Susceptibility of the cerebral cortex to spreading depolarization in neurological disease states: The impact of aging

Hertelendy

Varga

Menyhárt

et al. 2019

Neurochemistry International

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“…22 Our findings are in agreement with easier induction and faster propagation of SD 7,29 and higher frequency of recurrent SDs 23 in the superficial cortical layers, and with preferential propagation of SD through the superficial layers in slices of the neocortex in vitro. 23,[30][31][32] In addition, we found that about half of SDs generated in superficial layers were arrested at the border between superficial and deep layers, whereas fully propagating SDs often slowed down at a depth of ~1000 μm (example shown in Figure 4A). This is in keeping with a kind of "barrier" for vertical SD propagation and segregation of SDs in the superficial and deep cortical layers previously reported for recurrent SDs evoked by continuous remote high potassium application.…”

Section: Discussionmentioning

confidence: 81%

Segregation of seizures and spreading depolarization across cortical layers

et al. 2019

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Objective: Cortical spreading depolarization (SD) and seizures are often co-occurring electrophysiological phenomena. However, the cross-layer dynamics of SD during seizures and the effect of SD on epileptic activity across cortical layers remain largely unknown. Methods: We explored the spatial-temporal dynamics of SD and epileptic activity across layers of the rat barrel cortex using direct current silicone probe recordings during flurothyl-induced seizures. Results: SD occurred in half of the flurothyl-evoked seizures. SD always started from the superficial layers and spread downward either through all cortical layers or stopping at the L4/L5 border. In cases without SD, seizures were characterized by synchronized population firing across all cortical layers throughout the entire seizure. However, when SD occurred, epileptic activity was transiently silenced in layers involved with SD but persisted in deeper layers. During partial SD, epileptiform activity persisted in deep layers throughout the entire seizure, with positive signals at the cortical surface reflecting passive sources of population spikes generated in deeper cortical layers. During full SD, the initial phase of SD propagation through the superficial layers was similar to partial SD, with suppression of activity at the superficial layers and segregation of seizures to deep layers. Further propagation of SD to deep layers resulted in a wave of transient suppression of epileptic activity through the entire cortical column. Thus, vertical propagation of SD through the cortical column creates dynamic network states during which epileptiform activity is restricted to layers without SD. Significance: Our results point to the importance of vertical SD spread in the SDrelated depression of epileptiform activity across cortical layers. K E Y W O R D Scortex, DC recordings, EEG, flurothyl, seizure, spreading depression

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“…A titanium omega bar was cemented to the interparietal bone, and exposed skull and scalp margins were sealed with cement. In a subset of experiments, the skull was thinned over the barrel cortex rather than removed (3 mm x 3 mm square) (Figures S1 and S2) (Kaufmann et al, 2017).…”

Section: Surgery For Awake Imagingmentioning

confidence: 99%