Nogo Receptor mRNA Expression in Intact and Regenerating CNS Neurons

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

“…A more likely explanation, however, is that while the levels of Nogo-A are decreased in the necrotic lesion, they are concurrently increased in selected perilesional tissue and the total levels of Nogo-A remain unchanged or show only a modest increase. The changes in Nogo-A observed in the present study are in contrast to the relatively minor changes observed in models of experimental spinal cord injury (SCI; Josephson et al, 2001;Huber et al, 2002;Hunt et al, 2002bHunt et al, , 2003Wang et al, 2002b). However, in other models of CNS injury such as hippocampal deafferentation, global ischemia and kainic acid lesions, a marked increase of Nogo-A mRNA was observed (Zhou et al, 2003;Meier et al, 2003;Mingorance et al, 2004).…”

“…Although the expression of Nogo-A in neurons under normal conditions has previously been described (Grandpre et al, 2000;Josephson et al, 2001;Huber et al, 2002;Hunt et al, 2002b;Liu et al, 2002b;Wang et al, 2002b;Jin et al, 2003;Mingorance et al, 2004), the function of neuronal Nogo-A remains unclear. However, as a member of the reticulon family of genes (Oertle and Schwab, 2003), Nogo (RTN-4) has been suggested to play a role in cellular physiology and protein trafficking (van de Velde et al, 1994;Grandpre et al, 2000;Teng et al, 2004).…”

“…Part of the increased neuronal immunoreactivity for Nogo-A observed in these regions may be explained by impaired anterograde transport of Nogo-A due to posttraumatic axonal damage, since Nogo-A is detected at the synaptic level under normal physiological conditions and has been observed in growing axons of the developing CNS (Tozaki et al, 2002). However, Nogo-66 and Nogo-A mRNA expression may be upregulated in neurons with a preserved capacity for axonal regeneration, implying that Nogo-A may even be a growth-promoting gene when present in neurons (Hunt et al, 2003), such as intrinsic neurons in the reticular thalamus, a region with relatively high capacity for axonal regeneration showing marked upregulation of growth-related genes following axotomy (Anderson et al, 1998;Hunt et al, 2002bHunt et al, , 2003. In the present report, we also observed increased Nogo-A expression in dendritic processes with yet unclear functional significance.…”

Blockade of Nogo-66, Myelin-Associated Glycoprotein, and Oligodendrocyte Myelin Glycoprotein by Soluble Nogo-66 Receptor Promotes Axonal Sprouting and Recovery after Spinal Injury

“…The NgR protein is widely expressed in the adult brain with most, but not all, neurons expressing the protein (Hunt et al, 2002;Josephson et al, 2002Josephson et al, , 2003X. Wang et al, 2002c).…”

Intrathecally infused antibodies against Nogo-A penetrate the CNS and downregulate the endogenous neurite growth inhibitor Nogo-A

“…CNS targets for therapeutic antibodies in animal experiments or human trials are currently mainly Alzheimer's disease (Gelinas et al, 2004;Hock et al, 2003), neuroinflammatory diseases Goldman et al, 1997;Warrington et al, 2000), tumors (Papanastassiou et al, 1995), spinal cord injury (Schwab, 2004), and stroke (During et al, 2000;Papadopoulos et al, 2002;Wiessner et al, 2003). Nogo-A is a potent neurite growth inhibitory protein present in oligodendrocyte and CNS myelin membranes of the adult CNS and, to a lower degree, on membranes of subpopulations of neurons (Dodd et al, 2005;Huber et al, 2002;Hunt et al, 2002;Josephson et al, 2001;Oertle et al, 2003;Wang et al, 2002a,b). Antibodies against Nogo-A applied to the adult CNS via the cerebrospinal fluid (CSF) lead to enhanced regrowth of lesioned axons as well as enhanced compensatory sprouting after spinal cord injury and stroke in adult rats (Schwab, 2004).…”