Sodium-dependent lysophosphatidylcholine (LPC) symporter, which plays an essential role for blood-brain barrier formation and function (PubMed:18694395, PubMed:23209793, PubMed:24828044, PubMed:24828040, PubMed:34349262). Specifically expressed in endothelium of the blood-brain barrier of micro-vessels and transports LPC into the brain (PubMed:24828044, PubMed:24828040, PubMed:34349262). Transport of LPC is essential because it constitutes the major mechanism by which docosahexaenoic acid (DHA), an omega-3 fatty acid that is essential for normal brain growth and cognitive function, enters the brain (PubMed:24828044, PubMed:24828040, PubMed:34349262). Transports LPC carrying long-chain fatty acids such LPC oleate and LPC palmitate with a minimum acyl chain length of 14 carbons (PubMed:24828044, PubMed:34349262). Does not transport docosahexaenoic acid in unesterified fatty acid (PubMed:24828044). Not required for central nervous system vascular morphogenesis (PubMed:24828040). a 1-acyl-sn-glycero-3-phosphocholine(in) + Na(+)(in) = a 1-acyl-sn-glycero-3-phosphocholine(out) + Na(+)(out) 1-(4Z,7Z,10Z,13Z,16Z,19Z-docosahexaenoyl)-sn-glycero-3-phosphocholine(in) + Na(+)(in) = 1-(4Z,7Z,10Z,13Z,16Z,19Z-docosahexaenoyl)-sn-glycero-3-phosphocholine(out) + Na(+)(out) 1-(9Z-octadecenoyl)-sn-glycero-3-phosphocholine(in) + Na(+)(in) = 1-(9Z-octadecenoyl)-sn-glycero-3-phosphocholine(out) + Na(+)(out) 1-hexadecanoyl-sn-glycero-3-phosphocholine(in) + Na(+)(in) = 1-hexadecanoyl-sn-glycero-3-phosphocholine(out) + Na(+)(out) a 1-acyl-sn-glycero-3-phosphoethanolamine(in) + Na(+)(in) = a 1-acyl-sn-glycero-3-phosphoethanolamine(out) + Na(+)(out) Widely expressed. Exhibits an oscillatory pattern of expression in brown adipose tissue and liver consistent with a circadian rhythm. Enriched in brain micro-vessels, where it is specifically present in endothelium constituting the blood-brain barrier (at protein level) (PubMed:24828044, PubMed:24828040). By fasting in liver and brown adipose tissue as well as by cold exposure in brown adipose tissue. Expression following fasting is dependent on glucagon signaling and Ppara. N-glycosylated. Mice are born at Mendelian ratios, but show increased postnatal mortality early in life (PubMed:24828044). Mice are smaller, leaner and have decreased serum, liver and brown adipose triglycerides (PubMed:23209793). After weaning, mice display motor dysfunction with front-paw clasping during tail suspension. Brain size and weight are also significantly lower. Behavioral tests indicate that mice have deficits in learning, and short- and long-term memory, as well as severe anxiety, a phenotype related to omega-3 fatty-acid deficiency. Lipidomic analysis of knockout mice shows strongly reduced levels of docosahexaenoic acid (DHA) in brain accompanied by neuronal cell loss in hippocampus and cerebellum (PubMed:24828044). Mice also show a leaky blood-brain barrier from embryonic stages through to adulthood, while the normal patterning of vascular networks is maintained. Electron microscopy analysis shows an increase in central nervous system-endothelial-cell vesicular transcytosis not associated with tight-junction defects (PubMed:24828040). Mice have an increase in plasma levels of LPC (PubMed:26005868). Belongs to the major facilitator superfamily.