Cell surface receptor that plays a functionally redundant role in postnatal brain development and in regulating axon regeneration in the adult central nervous system (PubMed:22406547, PubMed:27339102). Contributes to normal axon migration across the brain midline and normal formation of the corpus callosum (PubMed:27339102). Protects motoneurons against apoptosis; protection against apoptosis is probably mediated by MAG (PubMed:26335717). Plays a role in inhibiting neurite outgrowth and axon regeneration via its binding to neuronal chondroitin sulfate proteoglycans (PubMed:22406547). Binds heparin (PubMed:22406547). Like other family members, plays a role in restricting the number dendritic spines and the number of synapses that are formed during brain development (PubMed:22325200). Signaling mediates activation of Rho and downstream reorganization of the actin cytoskeleton (PubMed:22325200). Identified in a complex that contains RTN4R, RTN4RL1 and NGFR; the interaction depends on the presence of chondroitin sulfate proteoglycans (PubMed:22406547). Does not interact with MAG, OMG and RTN4 (PubMed:12839991). Localized to the surface of neurons, including axons. Detected in brain (at protein level) (PubMed:22406547). Detected in retina ganglion cell layer and inner nuclear layer (PubMed:22406547). At 13.5 dpc, strongly expressed in PNS ganglia and developing heart, and weakly expressed in brain and spinal cord. By postnatal day 1, strongly expressed in dorsal root ganglia and in dorsal and gray matter areas of spinal cord. Expressed in various adult brain structures including the amygdala, caudate putamen, cerebellum, cerebral cortex, hippocampus, olfactory bulb and thalamus. No visible phenotype (PubMed:22406547). Mice are born at the expected Mendelian rate, are viable and fertile (PubMed:22406547). Compared to wild-type littermates, cultured hippocampus neurons from mutant mice display an increased number of excitatory synapses (PubMed:22325200). Likewise, mice with a triple gene disruption that lack Rtn4r, Rtn4rl1 and Rtn4rl2 have no visible phenotype, are healthy and viable (PubMed:22406547, PubMed:22325200). Mice with a triple gene disruption that lack Rtn4r, Rtn4rl1 and Rtn4rl2 have normal brain size and grossly normal brain anatomy, but display defects of medial brain structures, including an absence of the fasciola cinereum, corpus callosum agenesis and formation of bilateral Probst bundles indicative of the failure of callosally projecting neurons to extend across the midline (PubMed:27339102). Mice with a triple gene disruption of Rtn4r, Rtn4rl1 and Rtn4rl2 display impaired ability to stay on a rotarod and increased spontaneous locomotion (PubMed:27339102). These mice display an increased number of excitatory synapses in the apical dendritic regions of hippocampus neurons, an increase in the complexity of dendrite structure and increased total dendrite length (PubMed:22325200). One month after birth, mice with a triple gene disruption that lack Rtn4r, Rtn4rl1 and Rtn4rl2 show a significant reduction in the survival of motoneurons (PubMed:26335717). Compared to wild-type or single mutants, cerebellar granule cells from mice lacking Rtn4r, Rtn4rl1 and Rtn4rl2 show decreased myelin-mediated inhibition of neurite outgrowth, an inhibition that is strongly decreased on myelin deficient in Mag, Rtn4 and Omg (PubMed:22406547). Mice lacking both Rtn4r and Rtn4rl1 show increased axon regeneration after injury; the same effect is observed when Rtn4r, Rtn4rl1 and Rtn4rl2 are disrupted (PubMed:22406547). Combined disruption of Rtn4r, Rtn4rl1 and Ptprs further increases axon regeneration after injury (PubMed:22406547). Single gene disruption of Rtn4r, Rtn4rl1 and Rtn4rl2 and combined disruption of Rtn4r and Rtn4rl2 have no effect on axon regeneration (PubMed:22406547). Belongs to the Nogo receptor family.