Slc22a23 Proficiency Influences Rat Behavioral Responses After Lysophosphatidylcholine C20:4n6 Administration.

Background: The solute carrier family 22 member 23 (Slc22a23), a gene encoding a membrane-orphan transporter, is irreversibly upregulated in the brains of rats following fetal undernutrition. Materials and Method: To identify potential substrates of the SLC22A23 transporter, we analyzed the plasma of both Slc22a23-proficient and deficient rats. Results: We found that the level of lysophosphatidylcholine a C20:4 (LPC(20:4)) in plasma was more than twofold lower in the Slc22a23-/- rats than in the Slc22a23+/+ rats. We then conducted a series of animal behavioral tests on Slc22a23-proficient (Slc22a23+/+) and deficient (Slc22a23-/-) rats to investigate the effects of LPC(20:4) administration. We observed considerable effects in both Slc22a23+/+ and Slc22a23-/- rats, with more pronounced effects in the Slc22a23+/+ rats. These effects included reductions in total distance travelled in an open field test, reductions in access to the novel objects in a novel object recognition test, reductions in sociability to a familiar rat in a social interaction test, and shorter latencies to the target in the Morris water maze test. Discussion: These findings suggest that LPC(20:4) administration enhances memory acquisition in both Slc22a23+/+ and Slc22a23-/- rats, though it appears to be more effective in the Slc22a23+/+ rats. While the SLC22A23 transporter is likely involved in facilitating the transport of LPC(20:4), other transporters may also play a role in its transport in vivo.