Active shrinkage protects neurons following axonal transection
Creators
- 1. Istanbul Medipol Univ, Res Inst Hlth Sci & Technol SABITA, Regenerat & Restorat Med Res Ctr REMER, TR-34810 Istanbul, Turkiye
- 2. Yuzuncu Yil Univ, Fac Educ, Dept Sci Educ, TR-65080 Van, Turkiye
- 3. Bakircay Univ, Sch Med, Dept Med Biol, TR-35665 Izmir, Turkiye
- 4. Bandirma Onyedi Eylul Univ, Sch Med, Dept Histol & Embryol, TR-10200 Balikesir, Turkiye
- 5. Selcuk Univ, Sch Med, Dept Histol & Embryol, TR-42130 Konya, Turkiye
- 6. Bolu Abant Izzet Baysal Univ, Sch Med, Dept Physiol, TR-14030 Bolu, Turkiye
Description
Trauma, vascular events, or neurodegenerative processes can lead to axonal injury and eventual transec(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, 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 fresh perspective on pathophysiological processes in the nervous system.
Files
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Files
(245 Bytes)
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