If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
) demonstrate associations between plasma oxytocin (OT) levels and genetic variability
in the OT pathway, implying that OT is responsible for parent/infant interactions
and confirming its role in bond formation in humans. Further evidence of early social
influences on the system is that parental care received during infancy is paralleled
by higher levels of plasma OT in adulthood. Neurogenetics suggests that these events
are associated with polymorphisms in the oxytocin receptor (OXTR) and CD38 genes (
). Figure 1 shows a schematic representation of the sequence leading from the secretion of OT
by hypothalamic neurons to its uptake by OXTR, highlighting the key role played by
CD38. Some points are still unexplored. Here we focus on the points grounded in basic
science, but conducted in human models.
Figure 1Proposed schematic view of the CD38/OT/OXTR axis. Several steps are still hypothetical.
CD38 and OXTR are molecules with polymorphic genes. OT, oxytocin; OXTR, oxytocin receptor;
NAD+, nicotinamide adenine dinucleotide; cADPR, cyclic adenosine diphosphate-ribose; NAADP,
nicotinic acid adenine dinucleotide phosphate.
Research in mammals has demonstrated the involvement of oxytocin (OT) in social bond formation; yet, its role in human bonding remains unclear. Plasma OT has been used as a proxy for central activity and studies indicate its association with human affiliative behaviors. Molecular genetic studies also reveal a role for OT neuropathways in shaping the social brain. However, the links between peripheral OT, genetic markers, and their combined contribution to human parenting are unknown.
