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Persistent astroglial swelling accompanies rapid reversible dendritic injury during stroke-induced spreading depolarizations

  • W. Christopher Risher
    ,
  • Deborah Croom
    ,
  • Sergei A. Kirov(corresponding author)
*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

Spreading depolarizations are a key event in the pathophysiology of stroke, resulting in rapid dendritic beading, which represents acute damage to synaptic circuitry. The impact of spreading depolarizations on the real-time injury of astrocytes during ischemia is less clear. We used simultaneous in vivo 2-photon imaging and electrophysiological recordings in adult mouse somatosensory cortex to examine spreading depolarization-induced astroglial structural changes concurrently with signs of neuronal injury in the early periods of focal and global ischemia. Astrocytes in the metabolically compromised ischemic penumbra-like area showed a long lasting swelling response to spontaneous spreading depolarizations despite rapid dendritic recovery in a photothrombotic occlusion model of focal stroke. Astroglial swelling was often facilitated by recurrent depolarizations and the magnitude of swelling strongly correlated with the total duration of depolarization. In contrast, spreading depolarization-induced astroglial swelling was transient in normoxic healthy tissue. In a model of transient global ischemia, the occurrence of a single spreading depolarization elicited by a bilateral common carotid artery occlusion coincided with astroglial swelling alongside dendritic beading. With immediate reperfusion, dendritic beading subsides. Astroglial swelling was either transient during short ischemic periods distinguished by a short-lasting spreading depolarization, or persistent during severe ischemia characterized by a long-lasting depolarization with the ultraslow negative voltage component. We propose that persistent astroglial swelling is initiated and exacerbated during spreading depolarization in brain tissue with moderate to severe energy deficits, disrupting astroglial maintenance of normal homeostatic function thus contributing to the negative outcome of ischemic stroke as astrocytes fail to provide neuronal support.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 1709-1720 (12 pages)

Journal (Volume, Issue Number)

Glia (Volume 60, Issue 11)

Publication milestones

  • Published - 11/2012

Publication status

Published - 11/2012

ISSN

0894-1491

Publication IDs

  • Scopus: 84865860670
  • PubMed: 22821441

Publication metrics

Metrics

SciVal
FWCI
1.42
SciVal
Author count
3
SciVal
citations
54
SciVal
Paper percentile
93
SciVal
Top percentile
10
Scopus
citations
Fractional count
1
Fractional count
0.33
Fractional count
2
Fractional count
0.67
Fractional count
1
Fractional count
1

PlumX, opens in new tab

Captures
72
Citation count
80

Funding Details

FunderFunding number
NINDS
F31NS064753