CD38 and its role in oxytocin secretion and social behavior
Open accessAbstract
Here, we review the functional roles of cyclic ADP-ribose and CD38, a transmembrane protein with ADP-ribosyl cyclase activity, in mouse social behavior via the regulation of oxytocin (OXT) release, an essential component of social cognition. Herein we describe data detailing the molecular mechanism of CD38-dependent OXT secretion in CD38 knockout mice. We also review studies that used OXT, OXT receptor (OXTR), or CD38 knockout mice. Additionally, we compare the behavioral impairments that occur in these knockout mice in relation to the OXT system and CD38. This review also examines autism spectrum disorder (ASD), which is characterized by social and communication impairments, in relation to defects in the OXT system. Two single nucleotide polymorphisms (SNPs) in the human CD38 gene are possible risk factors for ASD via inhibition of OXT function. Further analysis of CD38 in relation to the OXT system may provide a better understanding of the neuroendocrinological roles of OXT and CD38 in the hypothalamus and of the pathophysiology of ASD. This article is part of a Special Issue entitled Oxytocin, Vasopressin, and Social Behavior.
AI snapshot
Written from the paper’s full text.
TL;DR
This review argues that CD38, via cyclic ADP-ribose and calcium signaling, is required for oxytocin secretion and normal social behavior in mice, and that human CD38 variants may contribute to autism spectrum disorder (ASD) risk. It summarizes CD38, OXT, and OXTR knockout mouse phenotypes plus human CD38 SNP and plasma OXT findings.
Key findings
- CD38 knockout mice show social and maternal behavioral deficits: CD38−/− pups emitted fewer ultrasonic vocalizations per 2-min session (average reduction 38%) than wild-type controls, and CD38−/− dams had longer pup-retrieval latency (76 ± 8 s) than wild-type dams (43 ± 3 s; p < 0.01).
- CD38−/− mice have reduced plasma and cerebrospinal fluid OXT levels but elevated hypothalamic/pituitary OXT, and the phenotype was normalized by subcutaneous OXT injection or viral re-expression of human CD38.
- In humans, the CD38 intronic SNP rs3796863 was significantly associated with high-functioning autism in American subjects (p < 0.005, n = 104), while the exonic R140W SNP was found in 3 of 29 ASD subjects (10.3%) versus 3 of 315 controls (allelic frequency 0.0048; ASD frequency 0.052; p < 0.029).
- Plasma OXT was lower in R140W carriers (161.3 ± 26.5 pg/ml, n = 12) than in non-carrier relatives (345.8 ± 61.3 pg/ml, n = 10; p < 0.01); among ASD subjects, five R140W carriers had lower OXT (79.2 ± 16.6 pg/ml) than ASD subjects lacking the mutation (147.7 ± 15.0 pg/ml; p < 0.01, n = 26) and than 101 control adults (198.2 ± 24.7 pg/ml; p < 0.01).
Methods
- Narrative review of mouse and human studies on CD38, cADPR, OXT, OXTR, and social behavior, including CD38−/−, Oxt−/−, and Oxtr−/− mouse models.
- Human data included CD38 mRNA/protein expression in brain, CD38 SNP screening in 29 unrelated ASD subjects and 201 non-clinical controls from Kanazawa, additional ASD/control cohorts, 252 trios and 104 HFA trios, 315 healthy controls, and three R140W proband families.
- Analyses summarized include genetic association, haplotype transmission disequilibrium testing, clinical/AQ evaluation, and plasma OXT/AVP measurements in carriers versus non-carriers.
Limitations
- The paper states that many fundamental questions remain: whether CD38 activity is sensitive to environmental and social contexts, whether CD38–ASD association implies immunological irregularity, and which additional molecules interact with CD38 to regulate OXT secretion.
- The paper notes that the intronic SNP’s functional importance remains to be determined, that the fetal/infant exogenous-OXT hypothesis needs empirical testing, and that larger-scale studies with increased statistical power are warranted.
- Evident from the text: this is a review rather than a systematic primary study, some human analyses rely on small samples (e.g., 3 ASD families, 5 R140W ASD carriers), and mouse findings may not fully translate to human ASD pathophysiology.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 25 cited sources checked · 0 supported · 0 flagged
- Findingcitation
CD38 mRNA is highest in the human hypothalamus.
“The highest level of CD38 was found in the hypothalamus (Munesue et al., 2010).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Munesue et al., 2010 source
Not checked in the free run.
- Findingown data
The rs3796863 (C > A) SNP in CD38 intron 7 shows a significant association with high-functioning autism in individuals of American descent (p < 0.005, n=104).
“By examining CD38 SNPs from another subclass of ASD, the rs379863 (C > A) SNP in CD38 intron 7 showed a significant association with high-functioning autism (HFA) in individuals of American (p < 0.005, n=104) or non-Japanese (p = 0.23, n=188) descent.”
Quote in the paperSubstantial claim - Findingnone given
Human CD38 protein is detected post-mortem in the hypothalamus of Japanese and American human brains.
“The human CD38 protein was detected (post-mortem) in the hypothalamus of Japanese and American human brains by immunoreactivity to the anti-human CD38 antibody.”
Quote in the paperSubstantial claim - Findingown data
There is no difference in AVP levels between CD38 mutation carriers and non-carriers within the same pedigrees.
“Furthermore, as expected, there was no difference in the AVP levels of CD38 mutation carriers and non-carriers within the same pedigrees (Fig. 4 b, d, f).”
Quote in the paperSubstantial claim - Findingown data
OXT levels of carrier ASD individuals are significantly lower than those in 101 control adults (198.2 ± 24.7 pg/ml; p < 0.01).
“Furthermore, the OXT levels of carrier ASD individuals were significantly lower than those in 101 control adults (198.2 ± 24.7 pg/ml; p < 0.01, n = 101).”
Quote in the paperSubstantial claim
- Findingown data
Control carriers of the R140W allele did not have lower OXT levels.
“In addition, control carriers of the R140W allele did not have lower OXT levels (Fig. 3).”
- Also stated in: § 10. Conclusion · plain
“Note that the plasma OXT level in the R140W carriers of the non-idiopathic control group is not low.”
Quote in the paperSubstantial claim - Also stated in: § 10. Conclusion · plain
- Findingcitation
OXT plasma concentrations of five R140W carriers (79.2 ± 16.6 pg/ml) are lower than those of ASD subjects lacking the mutation (147.7 ± 15.0 pg/ml; p < 0.01; n=26).
“The OXT plasma concentrations of the five R140W carriers (79.2 ± 16.6 pg/ml; n = 5; Munesue et al., 2010) were lower than those of ASD subjects lacking the mutation (147.7 ± 15.0 pg/ml; p < 0.01; n = 26).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Munesue et al., 2010 source
Not checked in the free run.
- Findingown data
Plasma OXT levels in carriers of the R140W mutation (161.3 ± 26.5 pg/ml; n=12) are lower than in non-carrier relatives (345.8 ± 61.3 pg/ml; n=10; p < 0.01).
“Plasma OXT levels in the carriers of the R140W mutation (161.3 ± 26.5 pg/ml; n = 12) were lower than those in the relatives of non-carriers (345.8 ± 61.3 pg/ml; n = 10; p < 0.01) (Fig. 4a, c, e).”
Quote in the paperSubstantial claim - Premisecitation
CD38 is required for some social behaviors in mice via the regulation of OXT secretion from the hypothalamus and pituitary.
“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).”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
CD38 possesses ADP-ribosyl cyclase activity that produces cyclic ADP-ribose (cADPR) from β-NAD+.
“CD38 possesses ADP-ribosyl cyclase activity (Lee, 2001;Higashida et al., 2001a and2007;Boittin et al., 2003;Guse, 2005) that produces cyclic ADP-ribose (cADPR) from β-NAD + , also known as Vitamin B3, an abundant substrate in the brain (Denu, 2005).”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
CD38 is required for normal social behavior in mice.
“It is also required for normal social behavior in mice (Jin et al., 2007).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jin et al., 2007 source
Not checked in the free run.
- Interpretationcitation
The R140W mutation causes significant modifications and damage to the predicted protein structure of human CD38.
“Therefore, the R140W mutation causes significant modifications and damage to the predicted protein structure in comparison with the human wild-type (R140) CD38 (see Fig. 7 of Munesue et al., 2010).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Munesue et al., 2010 source
Not checked in the free run.
- Premisecitation
CD38 -/- male pups on postnatal day 7 have significantly higher locomotor activity than wild-type during the first 3 min after separation from the dam.
“CD38 -/-male pups on postnatal day 7 had significantly higher levels of locomotor activity, compared to wild-type individuals, during the first 3 min after separation from the dam when they were examined individually in a grid-crossing test performed in an observation chamber (Liu et al., 2008).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Liu et al., 2008 source
Not checked in the free run.
- Premisereasoning
CD38 -/- dams often drop pups during retrieval.
“In addition, CD38 -/-dams often dropped the pups during retrieval, suggesting that they did not remember the way to the nest and resulting in the pups becoming scattered to multiple locations.”
Quote in the paperSubstantial claim - Premisecitation
CD38 -/- males show sustained high levels of investigation at every encounter with the same female.
“In contrast, CD38 -/-males showed sustained high levels of investigation at every encounter with the same female (Jin et al., 2007).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jin et al., 2007 source
Not checked in the free run.
- Interpretationcitation
The mechanisms underlying social behavior require CD38-dependent OXT secretion.
“This indicates that the mechanisms underlying social behavior require CD38-dependent OXT secretion (Fig. 1).”
Quote in the paperSubstantial claim - Premisecitation
Social amnesia is not rescued by local expression of human R140W-CD38 in the hypothalamus of CD38 knockout mice.
“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).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jin et al., 2007 source
Not checked in the free run.
- Premisecitation
Mutant R140W-CD38 shows one-third of the ADP-ribosyl cyclase activity of R140 CD38 when expressed in CHO cells.
“As expected, the mutant R140W-CD38 showed one-third of the ADP-ribosyl cyclase activity of R140 CD38 when expressed in CHO cells (Yagui et al., 1998).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Yagui et al., 1998 source
Not checked in the free run.
- Premisecitation
CD38 -/- pups emit fewer ultrasonic vocalization calls (average reduction of 38%) than wild-type controls.
“The USV calls per 2-min session were less frequent (an average reduction of 38%) in CD38 -/-pups than in wild-type controls (Liu et al., 2008).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Liu et al., 2008 source
Not checked in the free run.
- Premisecitation
ADP-ribosyl cyclase activity in the hypothalamus is significantly higher in CD38 +/+ than in CD38 -/- mice from the second week of life onward.
“CD38 +/+ mice showed significantly higher levels of ADP-ribosyl cyclase activity in the hypothalamus from the second week of life onward, and the difference in comparison with CD38 -/-mice increased markedly (Higashida et al., 2010).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Higashida et al., 2010 source
Not checked in the free run.
- Premisecitation
The behavioral phenotype of CD38 -/- mice can be normalized by a single subcutaneous OXT injection.
“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).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jin et al., 2007 source
Not checked in the free run.
- Interpretationreasoning
The abnormality in social memory in CD38 -/- mice is due to amnesia with respect to conspecifics.
“This abnormality in social memory found in CD38 -/-mice is due to the males' amnesia with respect to conspecifics.”
Quote in the paperSubstantial claim - Premisenone given
Arginine vasopressin (AVP) release is relatively insensitive to the CD38 null mutation.
“Interestingly, argine vasopressin (AVP) release is relatively insensitive to the CD38 null mutation.”
Quote in the paperSubstantial claim - Interpretationnone given
There is increasing evidence for the critical role of CD38 in social behavior in mice and humans.
“There is increasing evidence for the critical role of CD38 in social behavior in mice and humans.”
Quote in the paperNot a substantial claim - Premiseown data
The rs3796863 SNP in CD38 positively correlates with American high-functioning autism and low-functioning ASD in Israel.
“The association study using Tag SNPs showed one SNP (rs3796863) in CD38 that positively correlated with American HFA and low functioning ASD in Israel.”
Quote in the paperSubstantial claim - Interpretationnone given
rs3796863 and rs1800561 (R140W) SNPs may cause low levels of oxytocin (OXT) in the brain or plasma by lowering the expression or enzymatic activity of CD38.
“rs3796863 and rs1800561 (R140W) SNPs may cause low levels of oxytocin (OXT) in the brain or plasma by lowering the expression or enzymatic activity of CD38.”
Quote in the paperNot a substantial claim - Interpretationreasoning
CD38 SNPs may provide a genetic basis for some autism spectrum disorders.
“Therefore, it is possible that CD38 SNPs may provide a genetic basis for some ASDs, and therefore warrants further investigation.”
Quote in the paperSubstantial claim - Interpretationreasoning
These data support the existence of mechanisms of ASD pathogenesis other than CD38 SNPs.
“Altogether, these data support the existence of mechanisms of ASD pathogenesis other than CD38 SNPs.”
Quote in the paperSubstantial claim - Interpretationreasoning
CD38 defects in the OXT signal system may be involved in the pathophysiology of ASD.
“Therefore, CD38 defects in the OXT signal system may be involved in the pathophysiology of ASD.”
Quote in the paperSubstantial claim - Interpretationown data
The R140W mutation is a risk factor for Asian ASD.
“These results suggest that the mutation is a risk factor of Asian ASD.”
Quote in the paperSubstantial claim - Interpretationcitation
A subgroup of ASD subjects with the R140W SNP and intelligence impairments may be effectively treated with OXT.
“Our preliminary studies suggest that a subgroup of ASD subjects with the R140W SNP and intelligence impairments may be effectively treated with OXT (Munesue et al., 2010)”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Munesue et al., 2010 source
Not checked in the free run.
- Interpretationown data
The R140W mutation appears to be an autosomal dominant trait.
“The mutation appears to be an autosomal dominant trait.”
Quote in the paperNot a substantial claim
- May combine two claims. 10
- The quote only partly states this claim. 1
- Classified as probably not a substantial claim. 2
May combine two claims.
FindingcitationR140W heterozygosity was found in 3 of 29 ASD subjects (prevalence 10.3%) and in 3 of 315 healthy controls (allelic frequency 0.0048).
“140R/W (C4693T) heterozygosity was found in 3 male subjects (2 autistic and 1 Asperger) of the 29 ASD subjects examined (23 males and 6 females; mean age, 22.8 ± 7.6 years; prevalence, 10.3%).We examined 315 healthy unscreened control subjects from the Kanazawa area.Two females and 1 male were positive for the heterozygous mutation, representing an allelic frequency of 0.0048 (Munesue et al., 2010”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Munesue et al., 2010
Not checked in the free run.
May combine two claims.
FindingcitationThe R140W allele frequency in ASD patients (0.052) is 10.8-fold higher than in controls (0.0048; p < 0.029).
“This frequency is 10.8-fold lower than that (0.052) in the ASD patient group from the same residential area (p < 0.029).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationCD38 -/- mice have reduced OXT levels in the plasma and cerebrospinal fluid but elevated levels in the hypothalamus and pituitary tissues.
“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.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jin et al., 2007 source
Not checked in the free run.
May combine two claims.
PremisecitationRe-expression of CD38 in CD38 knockout mice normalizes plasma and CSF OXT levels and social memory.
“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).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jin et al., 2007 source
Not checked in the free run.
May combine two claims.
Premisecitationrs3796863 is significantly associated with low-functioning autism, but not necessarily high-functioning autism.
“Work by Lerer et al., (2010), showed that rs3796863 is significantly associated with low-functioning autism, but not necessarily HFA.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Lerer et al., (2010)
Not checked in the free run.
May combine two claims.
InterpretationcitationThe C allele of rs3796863 may be a protective allele and the A allele may be a risk allele in American high-functioning autism cases.
“Based on the results of our SNP analysis and haplotype transmission disequilibrium test, the C allele of rs3796863 in CD38 may be a protective allele, and the A allele may be a risk allele in American HFA cases (Fig. 4 in Munesue et al., 2010; Fig. 5).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Munesue et al., 2010
Not checked in the free run.
May combine two claims.
PremisecitationPlasma OXT concentration in CD38 -/- pups at 1-3 weeks of age is similar to wild-type, but at 2 months of age is significantly lower than in CD38 +/+ mice.
“Surprisingly, the plasma OXT concentration in CD38 -/-pups at 1 -3 weeks of age does not decrease but is similar to that in CD38 +/+ mice of the same age (Liu et al., 2008).However, as expected, at 2 months of age (young adult) following weaning, there is a significantly lower plasma concentration of OXT in CD38 -/-mice than in CD38 +/+ mice.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Liu et al., 2008
Not checked in the free run.
The quote only partly states this claim.
PremisecitationCD38 -/- dams take significantly longer to begin pup retrieval (average latency 76 ± 8 s vs 43 ± 3 s; p < 0.01).
“while CD38 -/-dams took a significantly longer time to begin retrieval (average latency, 76 ± 8 s; p < 0.01; Lopatina et al., 2011)”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Lopatina et al., 2011
Not checked in the free run.
Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenASD may be triggered by additional strong risk factors and/or other weak protective factors.
“ASD may be triggered by additional strong risk factors and/or other weak protective factors.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenProtection from ASD may also be induced by other weak risk factors and/or strong protective factors, including female hormones such as OXT.
“Additionally, protection from ASD may also be induced by other weak risk factors and/or strong protective factors, including female hormones such as OXT.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationnone givenLow OXT levels are not only caused by CD38 SNPs but are also caused by other unknown reasons.
“However, low OXT levels are not only caused by CD38 SNPs but are also caused by other unknown reasons (Fig. 5).”
- Also stated in: § 10. Conclusion · hedged
“The low plasma OXT level may also be produced by other unknown causes.”
Quote in the paperSubstantial claim- Also stated in: § 10. Conclusion · hedged
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Exogenous oxytocin has behavioural effects in humans, particularly in social deficit-related psychiatric disorders such as autism and schizophrenia.
“Exogenous oxytocin in humans also appears to have behavioural effects, particularly in such social deficit-related psychiatric disorders as autism and schizophrenia9–13.”
From Vascular RAGE transports oxytocin into the brain to elicit its maternal bonding behaviour in mice (2019) · cites this paper as [9]
Peripheral oxytocin replacement restores normal maternal behaviour in Oxt−/− and Cd38−/− mice but not Oxtr−/− mice, implying that circulating oxytocin crosses the blood-brain barrier.
“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.”
From Vascular RAGE transports oxytocin into the brain to elicit its maternal bonding behaviour in mice (2019) · cites this paper as [9]
Another study of adolescent males with ASD observed no significant benefits of oxytocin after an eight-week administration period compared to placebo, but exploratory analyses revealed that parents who believed their child had received oxytocin reported significant improvements irrespective of actual treatment assignment.
“Another study of adolescent males with ASD observed no significant benefits of oxytocin after an eight week administration period, compared to placebo.54 No changes were observed on primary outcomes of social behaviours and ratings of clinical improvement, or secondary outcomes examining social cognition, repetitive and other ASD-related behaviours.However, exploratory analyses revealed that”
From Beyond the hype and hope: critical considerations for intranasal oxytocin research in autism spectrum disorder (2017) · cites this paper as [54]
Expectation biases of randomization to oxytocin were found to significantly moderate parental reports of ASD symptom improvement.
“For example, expectation biases of randomization to oxytocin were found to significantly moderate parental reports of ASD symptom improvement.54”
From Beyond the hype and hope: critical considerations for intranasal oxytocin research in autism spectrum disorder (2017) · cites this paper as [54]
Four randomized placebo-controlled trials of children and adolescents have employed oxytocin dosages stratified by weight or age.
“Guided by other pharmaceutical trials, four randomized placebo-controlled trials of children and adolescents have employed dosages stratified by weight or age.38,49,51,54”
From Beyond the hype and hope: critical considerations for intranasal oxytocin research in autism spectrum disorder (2017) · cites this paper as [54]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
The same intronic SNP is given two identifiers
MinorThe paragraph introduces the intron 7 SNP as rs379863, then refers to the C and A alleles of rs3796863 as the SNP under discussion. The identifiers differ.
“the rs379863 (C > A) SNP in CD38 intron 7”
“the C allele of rs3796863 in CD38 may be a protective allele, and the A allele may be a risk allele”
The citation lists haven’t been fetched yet
References 82 · Cited by 98
- Authors
- Higashida, H., Yokoyama, S., Kikuchi, M., & Munesue, T.
- Affiliations
- Kanazawa University (JP)
- Corresponding author
- Higashida, Haruhiro
- Venue
- Hormones and Behavior
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 61
- Issue
- 3
- Pages
- 351-358
- ISSN
- 0018-506X (ISSN-L)
- OpenAlex
- W2024093484
- Semantic Scholar
- dd6066efe3148da672962efe253a9531c29d6cbc
- Cited by
- 98
- References
- 82
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 7 · 2023: 1 · 2022: 1 · 2021: 6 · 2020: 12 · 2019: 5 · 2018: 3 · 2017: 13 · 2016: 7 · 2015: 12 · 2014: 8 · 2013: 13 · 2012: 6
- FWCI
- 1.13
- Type
- journal article
- Language
- en
- Open access
- Locations
- Hormones and Behavior (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Kanazawa University Repository for Academic Resources (DSpace) (Kanazawa University) (submittedVersion, cc-by-nc-nd)
- Funders
- Core Research for Evolutional Science and Technology
- Ministry of Education, Culture, Sports, Science and Technology
- Japan Science and Technology Agency
- Topics
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- CD38, cyclic ADP-ribose, oxytocin secretion, oxytocin receptor, social behavior, autism spectrum disorder, CD38 knockout mice, hypothalamus, single nucleotide polymorphisms, social cognition, neuroendocrinology
- MeSH terms
- Animals, Autistic Disorder, Exons, Humans, Introns, Oxytocin, Social Behavior, Mice, Knockout, Polymorphism, Single Nucleotide, ADP-ribosyl Cyclase, Cyclic ADP-Ribose, Mice, ADP-ribosyl Cyclase 1
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