Transient immunohistochemical labelling of rat retinal axons during Wallerian degeneration by a monoclonal antibody to neurofilaments
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Cited by (26)
Late onset neuropathy with spontaneous clinical remission in mice lacking the POZ domain of the transcription factor Myc-interacting zinc finger protein 1 (Miz1) in Schwann cells
2015, Journal of Biological ChemistryCitation Excerpt :The corresponding axon appeared darker and less granular, most likely due to changes of the neurofilament and microtubule cytoskeleton. Therefore, we co-stained sciatic nerves from P90 Miz1ΔPOZ and control mice with an antibody against unphosphorylated neurofilament-H from the SMI-32 clone and against neurofilament-M. SMI-32 positivity is a marker for degenerating axons, whereas the neurofilament-M antibody recognizes neurofilaments independently of the phosphorylation status (41, 42). Morphometric quantifications uncovered no significant increase in SMI-32 signal intensity in Miz1ΔPOZ compared with control mice (Fig. 8A).
The mechanism of axonal degeneration after perikaryal excitotoxic injury to the retina
2012, Experimental NeurologyCitation Excerpt :Early axonal injury in Wlds and wild-type SD rats was quantitatively assessed by immunolabeling for SMI-32, an antibody that recognizes the non-phosphorylated chain of neurofilament heavy. SMI-32 has been consistently demonstrated to be a highly sensitive, marker of axonal cytoskeleton disruption, (Chidlow et al., 2011; Meller et al., 1994) owing to the labile nature of non-phosphorylated neurofilament heavy chain and its susceptibility to degradation by calpain. Microglial status in Wlds and wild-type SD rats was quantitatively assessed by immunolabeling for Iba1, ED1 and OX-6.
Immunoelectron microscopy reveals the presence of neurofilament proteins in retinal terminals undergoing dark degeneration
2008, Brain ResearchCitation Excerpt :Excessive activation of calpains after injury has been proposed as a contributing factor in axonal degeneration, myelin breakdown, death of cells, and apoptosis (Couto et al., 2004; Paquet-Durand, 2007). In intact terminals, the continuous influx of calcium during depolarization is thought to stimulate calpains, disassembling NFs (Roots, 1983; Meller et al., 1994), whereas the pathophysiological mechanisms of TD probably involve a decreased enzymatic breakdown, due to decreased depolarization by the disconnection of the axon from the cell body, and increased influx of NF proteins from the distal segments of the axons by continuous axonal transport. Another interesting point addressed here is the comparison of the temporal pattern of optic nerve degeneration and retinal fiber terminal degeneration.
Hypoxic injury of isolated axons is independent of ionotropic glutamate receptors
2007, Neurobiology of DiseaseCitation Excerpt :SMI31 recognizes phosphorylated neurofilaments. An increase in non-phosphorylated neurofilaments may indicate the early stages of injury (Meller et al., 1994). Immunoreactivity for non-phosphorylated neurofilaments recognized by SMI32 was not detected in OGD treated axons at 1, 6 and 24 h after the initial injury (data not shown).
Injury to axons and oligodendrocytes following endothelin-1-induced middle cerebral artery occlusion in conscious rats
2006, Brain ResearchCitation Excerpt :Assessments of axonal injury using APP antiserum are however limited as immunostaining is restricted mainly to the margins of the ischemic lesion, and hence is largely absent from the ischemic core (Yam et al., 1997). SMI32 immunohistochemistry has been used to characterize axonal injury in several pathologies including optic nerve transection in rats (Meller et al., 1994), experimental autoimmune encephalomyelitis in mice (Jackson et al., 2005), and focal thrombotic cortical lesions in mice (Bidmon et al., 1997). To our knowledge, however, SMI32 immunohistochemistry has not been used to characterize axonal injury following middle cerebral artery occlusion (MCAO) in rats.
This study was supported by grants of the Deutsche Forschungsgemeinschaft (DFG EY 8/13-2; Schm 776/4-1, Heisenberg-Programm).
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The authors are indebted to Ms. U. Neubacher for excellent help in the laboratory, and to Ms. D. Strehler for photographic work.