Stroke Produces Dysfunctional Brain Cells

Summary: Researchers report that following a stroke, the production of new neurons in the hippocampus fail to develop correctly. However, intervening in the production of these neurons could help mitigate memory problems experienced by those who suffer a stroke.

Source: SfN.

Mice produce new neurons in the hippocampus following a stroke that fail to develop properly, finds new research published in Journal of Neuroscience. Intervening in the production of these cells may help to mitigate stroke-induced memory impairments.

Stroke has long been known to increase adult neurogenesis. Despite the proliferation of new cells in a brain region critical for memory, previous stroke research in animals shows this process is accompanied by deficits on tasks that depend on the hippocampus. These observations led Albrecht Kunze and colleagues to investigate how newborn cells mature and integrate into the existing hippocampal network after stroke.

By temporarily cutting off blood supply to the brains of male and female mice, the researchers demonstrate the neurons generated as a result of this stroke model develop into hyperexcitable cells that may contribute to hippocampal dysfunction. This finding begins to uncover the cellular mechanisms underlying post-stroke neuropsychiatric disorders.

Uncoupled intrinsic and synaptic excitability in DCX+ ABGCs after stroke. image is credited to Ceanga et al., JNeurosci (2019).
About this neuroscience research article

Funding: This work was supported by the Interdisciplinary Center for Clinical Research Jena, German Ministry of Education and Research, Deutsche Forschungsgemeinschaft.

Source: David Barnstone – SfN
Publisher: Organized by
Image Source: image is credited to Ceanga et al., JNeurosci (2019).
Original Research: Abstract for “Stroke accelerates and uncouples intrinsic and synaptic excitability maturation of mouse hippocampal DCX+ adult-born granule cells” by Mihai Ceanga, Silke Keiner, Benedikt Grünewald, Holger Haselmann, Christiane Frahm, Sebastien Couillard-Després, Otto W. Witte, Christoph Redecker, Christian Geis and Albrecht Kunze in Journal of Neuroscience. Published January 7 2019.

Cite This Article

[cbtabs][cbtab title=”MLA”]SfN “Stroke Produces Dysfunctional Brain Cells.” NeuroscienceNews. NeuroscienceNews, 13 January 2019.
<>.[/cbtab][cbtab title=”APA”]SfN(2019, January 13). Stroke Produces Dysfunctional Brain Cells. NeuroscienceNews. Retrieved January 13, 2019 from[/cbtab][cbtab title=”Chicago”]SfN “Stroke Produces Dysfunctional Brain Cells.” (accessed January 13, 2019).[/cbtab][/cbtabs]


Stroke accelerates and uncouples intrinsic and synaptic excitability maturation of mouse hippocampal DCX+ adult-born granule cells

Stroke robustly stimulates adult neurogenesis in the hippocampal dentate gyrus. It is currently unknown if this process induces beneficial or maladaptive effects, but morphological and behavioral studies have reported aberrant neurogenesis and impaired hippocampal-dependent memory following stroke. However, the intrinsic function and network incorporation of adult-born granule cells (ABGCs) after ischemia is unclear.

Using patch-clamp electrophysiology we evaluated doublecortin positive (DCX+) ABGCs as well as DCX- dentate gyrus granule cells two weeks after a stroke or sham operation in DCX/DsRed transgenic mice of either sex. The developmental status, intrinsic excitability, and synaptic excitability of ABGCs were accelerated following stroke, while dendritic morphology was not aberrant. Regression analysis revealed uncoupled development of intrinsic and network excitability, resulting in young, intrinsically hyperexcitable ABGCs receiving disproportionately large glutamatergic inputs. This aberrant functional maturation in the subgroup of ABGCs in the hippocampus may contribute to defective hippocampal function and increased seizure susceptibility following stroke.


Stroke increases hippocampal neurogenesis but the functional consequences of the postlesional response is mostly unclear. Our findings provide novel evidence of aberrant functional maturation of newly generated neurons following stroke. We demonstrate that stroke not only causes an accelerated maturation of the intrinsic and synaptic parameters of doublecortin positive, new granule cells in the hippocampus, but that this accelerated development does not follow physiological dynamics due to uncoupled intrinsic and synaptic maturation. Hyperexcitable immature neurons may contribute to disrupted network integration following stroke.

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