Cell adhesion protein that is required for normal responses to cell-cell contacts in brain and in the peripheral nervous system. Plays a role in neurite outgrowth in response to contactin binding (PubMed:11564762). Plays a role in mediating cell-cell contacts between Schwann cells and axons (PubMed:20188654). Plays a role in the formation and maintenance of the nodes of Ranvier on myelinated axons. Nodes of Ranvier contain clustered sodium channels that are crucial for the saltatory propagation of action potentials along myelinated axons. During development, nodes of Ranvier are formed by the fusion of two heminodes. Required for normal clustering of sodium channels at heminodes; not required for the formation of mature nodes with normal sodium channel clusters (PubMed:14602817, PubMed:20188654). Required, together with GLDN, for maintaining NFASC and sodium channel clusters at mature nodes of Ranvier (PubMed:24719088). Constituent of a NFASC/NRCAM/ankyrin-G complex (Probable). Detected in a complex with CNTN1 and PTPRB (PubMed:11564762). Interacts with GLDN/gliomedin and MYOC (PubMed:16039564, PubMed:23897819). Detected at nodes of Ranvier (PubMed:14602817, PubMed:20188654, PubMed:24719088). Detected in sciatic nerve (PubMed:14602817, PubMed:20188654, PubMed:24719088). Detected in brain, especially in the cerebellum Purkinje cell layer, inner granule cell layer and molecular layer (at protein level) (PubMed:11564762). Detected in neurons and Schwann cells (PubMed:20188654). Mice are born at the expected Mendelian rate, are viable and fertile. They present no obvious phenotype excepting subtle size differences of cerebellar lobes IV and V. Contrary to wild-type, cerebellar cells do not form neurites when plated on a surface coated with contactin (in vitro) (PubMed:11564762). Neonates present delayed formation of sodium channel clusters at developing nodes of Ranvier, but are indistiguishable from wild-type at 10 days after birth (PubMed:14602817, PubMed:20188654). Mice lacking both Gldn and Nrcam are born at the expected Mendelian rate, but are smaller than control littermates and display important neurological impairments, in spite of seemingly normal nerve myelination. Motor abnormalities vary between individuals, ranging from ataxia, uncoordinated movements and premature death to weakness of the hind limbs, hypomotility, strongly impaired ability to hang from a horizontal bar with their forelimbs and a tendency to stumble. The motor defects correlate with decreased velocity of nerve conduction and slower propagation of action potentials. Most mice die within 60 days after birth, and none are fertile. Mutant mice display delayed formation of mature nodes of Ranvier; 15 days after birth about 20% of the nodes lack detectable sodium channel clusters. Sodium channel clustering and nerve conduction appear normal 60 and 75 days after birth, but subsequently a gradual disintegration of the nodal protein complexes is seen. About 70% of the mutant nodes present high-density sodium channel clustering at 120 days after birth, as opposed to nearly 100% for wild-type. Contrary to wild-type, in adult nodes of Ranvier the sodium channels are often clustered near the paranode border with an empty gap in the middle. At nodes of Ranvier, Schwann cell microvilli are sparse or absent and show defects in their orientation, resulting in various structural abnormalities at the node and the paranode border (PubMed:24719088). Belongs to the immunoglobulin superfamily. L1/neurofascin/NgCAM family.