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Merck

Active shrinkage protects neurons following axonal transection.

iScience (2023-09-13)
Mehmet Şerif Aydın, Sadık Bay, Esra Nur Yiğit, Cemil Özgül, Elif Kaval Oğuz, Elçin Yenidünya Konuk, Neşe Ayşit, Nureddin Cengiz, Ender Erdoğan, Aydın Him, Mehmet Koçak, Emrah Eroglu, Gürkan Öztürk
초록

Trauma, vascular events, or neurodegenerative processes can lead to axonal injury and eventual transection (axotomy). Neurons can survive axotomy, yet the underlying mechanisms are not fully understood. Excessive water entry into injured neurons poses a particular risk due to swelling and subsequent death. Using in vitro and in vivo neurotrauma model systems based on laser transection and surgical nerve cut, we demonstrated that axotomy triggers actomyosin contraction coupled with calpain activity. As a consequence, neurons shrink acutely to force water out through aquaporin channels preventing swelling and bursting. Inhibiting shrinkage increased the probability of neuronal cell death by about 3-fold. These studies reveal a previously unrecognized cytoprotective response mechanism to neurotrauma and offer a fresh perspective on pathophysiological processes in the nervous system.

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Sigma-Aldrich
(−)-Blebbistatin, solid, synthetic
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Nifedipine, Relatively selective blocker of L-type Ca2+ channels.
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2,3-Butanedione monoxime, ≥98%
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Mibefradil dihydrochloride hydrate, ≥98% (HPLC), powder
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ROCK Inhibitor (Y-27632), The ROCK Inhibitor (Y-27632) is available in a 5 mg format & has been optimized & validated for cell culture & Neuroscience applications.
Sigma-Aldrich
PD 150606, A cell-permeable, non-competitive, selective non-peptide calpain inhibitor [Ki = 210 nM for calpain-1 and 370 nM for calpain-2.