scholarly journals Periaxonal and nodal plasticities modulate action potential conduction in the adult mouse brain

Cell Reports ◽  
2021 ◽  
Vol 34 (3) ◽  
pp. 108641 ◽  
Author(s):  
Carlie L. Cullen ◽  
Renee E. Pepper ◽  
Mackenzie T. Clutterbuck ◽  
Kimberley A. Pitman ◽  
Viola Oorschot ◽  
...  
Keyword(s):  
Action Potential ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Adult Mouse Brain

scholarly journals Periaxonal and nodal plasticity modulate action potential conduction in the adult mouse brain

2019 ◽  
Author(s):  
Carlie L Cullen ◽  
Renee E Pepper ◽  
Mackenzie T Clutterbuck ◽  
Kimberley A Pitman ◽  
Viola Oorschot ◽  
...  
Keyword(s):  
Action Potential ◽  
Conduction Velocity ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Brain Regions ◽  
Adult Mouse Brain ◽  
Arrival Times ◽  
Structural Modifications ◽  
Periaxonal Space

SummaryCentral nervous system myelination increases action potential conduction velocity, however, it is unclear how myelination is coordinated to ensure the temporally precise arrival of action potentials, and facilitate information processing within cortical and associative circuits. Here, we show that mature myelin remains plastic in the adult mouse brain and can undergo subtle structural modifications to influence action potential arrival times. Repetitive transcranial magnetic stimulation and spatial learning, two stimuli that modify neuronal activity, alter the length of the nodes of Ranvier and the size of the periaxonal space within active brain regions. This change in the axon-glial configuration is independent of oligodendrogenesis and tunes conduction velocity to increase the synchronicity of action potential transit.

Corrigendum to “Localization and fate of Fgf10-expressing cells in the adult mouse brain implicate Fgf10 in control of neurogenesis” [Mol. Cell. Neurosci. 37 (2008) 857–868]

2010 ◽  
Vol 43 (2) ◽  
pp. 259
Author(s):  
Mohammad K. Hajihosseini ◽  
Stijn De Langhe ◽  
Eva Lana-Elola ◽  
Harris Morrison ◽  
Neil Sparshott ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Adult Mouse Brain

scholarly journals Comparative Analysis of the Frequency and Distribution of Stem and Progenitor Cells in the Adult Mouse Brain

Stem Cells ◽  
2008 ◽  
Vol 26 (4) ◽  
pp. 979-987 ◽  
Author(s):  
Mohammad G. Golmohammadi ◽  
Daniel G. Blackmore ◽  
Beatrice Large ◽  
Hassan Azari ◽  
Ebrahim Esfandiary ◽  
...  
Keyword(s):  
Comparative Analysis ◽  
Progenitor Cells ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Adult Mouse Brain ◽  
Stem And Progenitor Cells

scholarly journals Embryonic Cerebrospinal Fluid Activates Neurogenesis of Neural Precursors within the Subventricular Zone of the Adult Mouse Brain

2013 ◽  
Vol 198 (5) ◽  
pp. 398-404 ◽  
Author(s):  
E. Carnicero ◽  
M.I. Alonso ◽  
R. Carretero ◽  
F. Lamus ◽  
J.A. Moro ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Mouse Brain ◽  
Subventricular Zone ◽  
Adult Mouse ◽  
Adult Mouse Brain ◽  
Neural Precursors

scholarly journals MicroRNA-210 overexpression induces angiogenesis and neurogenesis in the normal adult mouse brain

Gene Therapy ◽  
2013 ◽  
Vol 21 (1) ◽  
pp. 37-43 ◽  
Author(s):  
L Zeng ◽  
X He ◽  
Y Wang ◽  
Y Tang ◽  
C Zheng ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Normal Adult ◽  
Adult Mouse Brain

Abstract 3153: Endoglin Deficiency in Bone Marrow is Sufficient to Cause Vascular Dysplasia in the Adult Mouse Brain After VEGF Stimulation

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Eun-Jung Choi ◽  
Espen J. Walker ◽  
Kristine Jun ◽  
Robert Kuo ◽  
Hua Su ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Viral Vector ◽  
Vascular Density ◽  
Index Number ◽  
Adult Mouse Brain ◽  
Healthy Human ◽  
Angiogenic Response ◽  
The Mean

Background and Objective: We have previously demonstrated that VEGF overexpression in the brain of adult Eng+/- mice causes vascular abnormalities. We also found that bone marrow-derived cells (BMDCs) home to vascular endothelial growth factor (VEGF)-induced angiogenic foci in the adult mouse brain and contribute to angiogenesis. Impaired angiogenesis in infarcted myocardium of Eng+/- mice was rescued using treatment with healthy human BMDCs but not with BMDCs from Hereditary Hemorrhagic Telangiectasia (HHT1) patients carrying ENG mutations. We hypothesized that ENG-haploinsufficiency in BMDCs can cause cerebrovascular dysplasia in the adult mouse after VEGF stimulation. Methods: WT or Eng+/- BM (2×106 cells) were transplanted to lethally irradiated C57BL/6 recipient mice (8-10 weeks old) via tail vein injection. After 4 weeks of BM transplantation, adeno-associated viral vector expressing VEGF (AAV-VEGF, 2×109 genome copies) was stereotactically injected into the basal ganglia. Brain sections were collected at 4 weeks after virus injection. The vascular density (vessels per 20× objective field) and dysplasia index (number of vessels >15µm in diameter per 200 vessels) were quantified on lectin-stained brain sections. Results: To examine the angiogenic response to VEGF, the vascular density around the AAV-VEGF injection site was analyzed. The mean vascular density increased in all mice with VEGF stimulation. Mice transplanted with Eng+/- BM showed less vascular density compared to mice transplanted with WT BM. The mean vascular densities were167 ± 21 (Eng+/-BM, n=4) and 202 ± 15 (WT BM, n=5) (P<0.01). Further, mice with WT BM had angiogenesis with normal vascular morphology. In contrast, mice with Eng+/- BM had markedly enlarged and dysmorphic vessels. To assess the degree of the dysplastic response, dysplasia index was analyzed. Mice with Eng+/- BM had several fold-higher dysplasia index than mice with WT BM: 2.6 ± 1.4 (Eng+/- BM) versus 0.7 ± 0.4 (WT BM) (P<0.01). Conclusions: In the adult mouse after VEGF stimulation, ENG-deficiency in BM (1) caused a 17% reduction in brain angiogenic response, and (2) increased cerebrovascular dysplasia, compared to control animals. These data support the possibility that cerebrovascular malformations resulting from VEGF stimulation with ENG-haploinsufficiency is attributable to impaired cell-autonomous monocyte/macrophage function, in contrast to the view that ENG dysfunction is primarily an endothelial phenomenon.

Sign in / Sign up

Export Citation Format

Share Document