Literature DB >> 30811255

Spreading depolarization and neuronal damage or survival in mouse neocortical brain slices immediately and 12 hours following middle cerebral artery occlusion.

Dylan Petrin1, Peter J Gagolewicz1, Rasha H Mehder1, Brian M Bennett1, Albert Y Jin1, R David Andrew1.   

Abstract

Whereas many studies have examined the properties of the compromised neocortex in the first several days following ischemia, there is less information regarding the initial 12 h poststroke. In this study we examined live mouse neocortical slices harvested immediately and 12 h after a 30-min middle cerebral artery occlusion (MCAo). We compared nonischemic and ischemic hemispheres with regard to the propensity for tissue swelling and for generating spreading depolarization (SD), as well as evoked synaptic responses and single pyramidal neuron electrophysiological properties. We observed spontaneous SD in 7% of slices on the nonstroked side and 25% in the stroked side following the 30-min MCAo. Spontaneous SD was rare in 12-h recovery slices. The region of the ischemic core and surround in slices was not susceptible to SD induced by oxygen and glucose deprivation. At the neuronal level, neocortical gray matter is surprisingly unaltered in brain slices harvested immediately poststroke. However, by 12 h, the fields of pyramidal and striatal neurons that comprise the infarcted core are electrophysiologically silent because the majority are morphologically devastated. Yet, there remains a subset of diffusely distributed "healthy" pyramidal neurons in the core at 12 h post-MCAo that persist for days poststroke. Their intact electrophysiology and dendritic morphology indicate a surprisingly selective resilience to stroke at the neuronal level. NEW & NOTEWORTHY It is generally accepted that the injured core region of the brain resulting from a focal stroke contains no functioning neurons. Our study shows that some neurons, although surrounded by devastated neighbors, can maintain their structure and electrical activity. This surprising finding raises the possibility of discovering how these neurons are protected to pinpoint new strategies for reducing stroke injury.

Entities:  

Keywords:  whole cell recording; ATPase; Na-K pump; hypothalamus; neuroprotection; pyramidal; spreading depolarization; spreading depression; stroke; traumatic brain injury

Mesh:

Year:  2019        PMID: 30811255      PMCID: PMC6589712          DOI: 10.1152/jn.00670.2018

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  58 in total

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Journal:  J Neurophysiol       Date:  1985-10       Impact factor: 2.714

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Journal:  J Cereb Blood Flow Metab       Date:  1996-11       Impact factor: 6.200

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Authors:  M Nedergaard; A J Hansen
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Authors:  J P Dreier; K Körner; N Ebert; A Görner; I Rubin; T Back; U Lindauer; T Wolf; A Villringer; K M Einhäupl; M Lauritzen; U Dirnagl
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2.  Transient Hypoperfusion to Ischemic/Anoxic Spreading Depolarization is Related to Autoregulatory Failure in the Rat Cerebral Cortex.

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3.  Neuronal Swelling: A Non-osmotic Consequence of Spreading Depolarization.

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4.  Reappraisal of anoxic spreading depolarization as a terminal event during oxygen-glucose deprivation in brain slices in vitro.

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