Polysialic acid-induced plasticity reduces neuropathic insult to the central nervous system.
Under chronic conditions of neuropathic pain, nociceptive C terminals are lost from their target region in spinal lamina II, leading to reduced thermal hyperalgesia. This region of the spinal cord expresses high levels of polysialic acid (PSA), a cell surface carbohydrate known to weaken cell-cell interactions and promote plasticity. Experimental removal of PSA from the spinal cord exacerbates hyperalgesia and results in retention of C terminals, whereas it has no effect on plasticity of touch Abeta fibers and allodynia. We propose that expression of PSA at this stress pathway relay point could serve to protect central circuitry from chronic sensory overload.
El Maarouf
Abderrahman
A
Department of Cell Biology, Cellular and Developmental Neuroscience, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.
Kolesnikov
Yuri
Y
Pasternak
Gavril
G
Rutishauser
Urs
U
D000704:Analysis of Variance; D000818:Animals; D006026:Glycoside Hydrolases / Q000494:pharmacology; D006652:Histological Techniques; D006930:Hyperalgesia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D036421:Nerve Fibers, Unmyelinated / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology*; D010146:Pain / Q000378:metabolism / Q000503:physiopathology*; D020671:Posterior Horn Cells / Q000378:metabolism*; D012794:Sialic Acids / Q000172:deficiency / Q000378:metabolism*
D012794:Sialic Acids; C021319:polysialic acid; D006026:Glycoside Hydrolases; C090534:endo-alpha-sialidase