Acquired neuroprotection is a synaptic-activity-dependent form of adaptation in the nervous system that renders neurons more resistant to harmful conditions. The term was coined by Hilmar Bading.[1] This use-dependent enhancement of cellular survival activity requires changes in gene expression triggered by neuronal activity and nuclear calcium signaling. In rodents, components of the neuroprotective gene program can reduce brain damage caused by seizure-like activity or by a stroke.[1][2][3] In acute and chronic neurodegenerative diseases, gene regulatory events important for acquired neuroprotection are antagonized by extrasynaptic NMDA receptor signaling leading to increased vulnerability, loss of structural integrity, and bioenergetics dysfunction.[4][5]

References

  1. 1 2 Zhang, Sheng-Jia; Zou, Ming; Lu, Li; Lau, David; Ditzel, Désirée A. W.; Delucinge-Vivier, Celine; Aso, Yoshinori; Descombes, Patrick; Bading, Hilmar (2009-08-01). "Nuclear calcium signaling controls expression of a large gene pool: identification of a gene program for acquired neuroprotection induced by synaptic activity". PLOS Genetics. 5 (8): e1000604. doi:10.1371/journal.pgen.1000604. ISSN 1553-7404. PMC 2718706. PMID 19680447.
  2. ↑ Zhang, Sheng-Jia; Buchthal, Bettina; Lau, David; Hayer, Stefanie; Dick, Oliver; Schwaninger, Markus; Veltkamp, Roland; Zou, Ming; Weiss, Ursula (2011-03-30). "A signaling cascade of nuclear calcium-CREB-ATF3 activated by synaptic NMDA receptors defines a gene repression module that protects against extrasynaptic NMDA receptor-induced neuronal cell death and ischemic brain damage". The Journal of Neuroscience. 31 (13): 4978–4990. doi:10.1523/JNEUROSCI.2672-10.2011. ISSN 1529-2401. PMC 6622995. PMID 21451036.
  3. ↑ Lau, David; Bengtson, C. Peter; Buchthal, Bettina; Bading, Hilmar (2015-08-25). "BDNF Reduces Toxic Extrasynaptic NMDA Receptor Signaling via Synaptic NMDA Receptors and Nuclear-Calcium-Induced Transcription of inhba/Activin A". Cell Reports. 12 (8): 1353–1366. doi:10.1016/j.celrep.2015.07.038. ISSN 2211-1247. PMID 26279570.
  4. ↑ Hardingham, G. E.; Fukunaga, Y.; Bading, H. (2002-05-01). "Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways". Nature Neuroscience. 5 (5): 405–414. doi:10.1038/nn835. ISSN 1097-6256. PMID 11953750. S2CID 659716.
  5. ↑ Hardingham, Giles E.; Bading, Hilmar (2010-10-01). "Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders". Nature Reviews. Neuroscience. 11 (10): 682–696. doi:10.1038/nrn2911. ISSN 1471-0048. PMC 2948541. PMID 20842175.
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