Spreading depolarization induced by amygdala micro-injury prevents disruption of fear memory extinction in rats

Рысакова, М. П.; Павлова, И. В.; Vinogradova, Lyudmila V.

doi:10.1016/j.bbr.2021.113559

Cited by 2 publications

(2 citation statements)

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“…It has been previously shown that SD induced in the cortico-striatal system of rodents can non-synaptically propagate without detriment to all structures of the system. Cortical SD spreads to the amygdala and striatum [ 11 , 20 , 21 ]; striatal SD propagates to the amygdala and cortex [ 2 , 10 , 20 ]; SD induced by the amygdala injury always invades the cortex and striatum [ 6 , 7 ]. Striatal SD can propagate to the cortex via two different pathways—via rostral (more reliable) and temporal transit points due to minimal anatomical barriers at the interface regions [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recently we developed a method of SD induction via standard local micro-injury of the brain parenchyma [ 6 ]. Using the method, we found that a rather small volume of tissue damage (0.3 mm 3 ) was sufficient to trigger SD in the cortex and amygdala of unanesthetized rats [ 6 , 7 ]. However, the amygdala damage triggered SD with significantly lower probability than the identical damage of the cortex did [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Region-Specific Vulnerability of the Amygdala to Injury-Induced Spreading Depolarization

et al. 2022

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Spreading depolarization (SD), a self-propagated wave of transient depolarization, regularly occurs in the cortex after acute brain insults and is now referred as an important diagnostic and therapeutic target in patients with acute brain injury. Here, we show that the amygdala, the limbic structure responsible for post-injury neuropsychological symptoms, exhibits strong regional heterogeneity in vulnerability to SD with high susceptibility of its basolateral (BLA) region and resilience of its centromedial (CMA) region to triggering SD by acute focal damage. The BLA micro-injury elicited SD twice as often compared with identical injury of the CMA region (71% vs. 33%). Spatiotemporal features of SDs triggered in the amygdala indicated diverse patterns of the SD propagation to the cortex. Our results suggest that even relatively small cerebral structures can exhibit regional gradients in their susceptibility to SD and the heterogeneity may contribute to the generation of complex SD patterns in the injured brain.

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