CD38 is critical for social behaviour by regulating oxytocin secretion

In the citing paper

“A seminal study showed that OTR and D2 receptor activation must occur concurrently for partner preference to develop in female prairie voles [66].”

In the citing paper

“In addition, research has pointed to the central role of transmembrane glycoprotein CD38 in OT neuropathways and in the release of OT from axon terminalis (Jin et al., 2007), and recent findings showed associations between plasma OT, genetic variability in the CD38 rs3796863 SNP, and the degree of reciprocity and touch between parents and their infants (Feldman et al., in press), pointing to the”

In the citing paper

“Blockade of D2 receptors in the NAcc shell prevented OT-mediated partner preferences, while blockade of OTR in the NAcc shell prevented D2 receptor mediated partner preferences in female prairie voles.”

In the citing paper

“Blockade of D2 receptors in the NAcc shell prevented OT-mediated partner preferences,”

In the citing paper

“Blockade of D2 receptors in the NAcc shell prevented OT-mediated partner preferences, while blockade of OTR in the NAcc shell prevented D2 receptor mediated partner preferences in female prairie voles.”

In the citing paper

“CD38 catalyzes the synthesis of the Ca2+-responsive messenger cyclic ADP-ribose (cADPR) by use of NAD+ and plays a key role in multiple physiological processes such as immunity, metabolism, inflammation, and even social behaviors (Jin et al., 2007).”

In the citing paper

“CD38 was also reported to affect social behaviour, as was its homologue CD157 (REFS166,167)”

In the citing paper

“Mice with impaired OT release or signalling display impairments in maternal responsiveness (3,4).”

In the citing paper

“The role of the OXT system has been investigated in rodent models, but uniquely using OXT-related mutant mice and giving OXT through intracerebroventricular (ICV), intraperitoneal (IP) and subcutaneous (SC) injections (Bielsky and Young, 2004;Jin et al, 2007;Popik et al, 1996;Sala et al, 2012;Sala et al, 2011;Takayanagi et al, 2005;Winslow and Insel, 2002).”

In the citing paper

“Specifically, CD38 is involved in oxytocin secretion via Ca2+ release15”

In the citing paper

“Normal maternal behaviour is restored by peripheral oxcytocin replacement in Oxt−/− and Cd38−/−, but not Oxtr−/− mice, implying that circulating oxcytocin crosses the blood-brain barrier.”

In the citing paper

“Loss of maternal nurturing and social interactive behaviours in Cd38−/− mice have been restored following peripheral administration of oxytocin, consistent with transport of peripherally administered exogenous oxytocin into brain5.”

In the citing paper

“Compared to placebo, oxytocin administered to eight adolescent and adult males with FXS significantly increased overall eye gaze during a brief social interaction.59 Interestingly, lower doses of oxytocin in this sample appeared to show a greater effect than the higher administered dose, consistent with a recent study in healthy adults.60”

In the citing paper

“recent investigations into dose-dependent effects of oxytocin on social cognition have demonstrated superior effects at lower (8 IU) doses.60”

In the citing paper

“Initial evidence suggests that lower dose (8IU) oxytocin delivered via this device is effective in modulating aspects of emotional behaviour.60”

In the citing paper

“In comparison with wild-type mice, CD38 -/-mice have reduced OXT levels in the plasma and cerebrospinal fluid (CSF) (Jin et al., 2007) but elevated levels in the hypothalamus and pituitary tissues.”

In the citing paper

“It is also required for normal social behavior in mice (Jin et al., 2007).”

In the citing paper

“We have recently shown that CD38 is required, as shown by the decreased formation of cADPR and by CICR, for some social behaviors in mice via the regulation of OXT secretion from the hypothalamus and pituitary (Jin et al., 2007;Higashida et al., 2010;Salmina et al., 2010).”

In the citing paper

“We used a genetic approach to re-express CD38 by infusing a virus carrying the human CD38 gene into the third ventricle of knockout mice.This procedure resulted in the normalization of the plasma and CSF OXT levels, thereby normalizing social memory (see Fig. 2 of Jin et al., 2007).”

In the citing paper

“In addition, social amnesia was not rescued by the local expression of human R140W-CD38, via a lentiviral infection, in the hypothalamus of CD38 knockout mice (Fig. 2 of Jin et al., 2007).”

In the citing paper

“The behavioral phenotype of CD38 -/-mice could be normalized by a single subcutaneous OXT injection because OXT is able to enter into the brain, probably through the blood-brain barrier (see Supplementary Fig. S7 of Jin et al., 2007).”

In the citing paper

“In contrast, CD38 -/-males showed sustained high levels of investigation at every encounter with the same female (Jin et al., 2007).”

In the citing paper

“These results suggested that CD38 may have an important role in OT release in the human hypothalamus, as in the mice (Jin et al., 2007;Liu et al., 2008).”

In the citing paper

“They showed that CD38 regulates OT secretion in the mouse hypothalamus and posterior pituitary, which is critical for mouse social behavior (Jin et al., 2007;Liu et al., 2008).”

In the citing paper

“Moreover, social amnesia was not rescued by local re-expression of human W140-CD38 in the hypothalamus in the Cd38 null mice (Jin et al., 2007).”