Correction of vasopressin deficit in the lateral septum ameliorates social deficits of mouse autism model
Open accessAbstract
Intellectual and social disabilities are common comorbidities in adolescents and adults with MAGE family member L2 (MAGEL2) gene deficiency characterizing the Prader-Willi and Schaaf-Yang neurodevelopmental syndromes. The cellular and molecular mechanisms underlying the risk for autism in these syndromes are not understood. We asked whether vasopressin functions are altered by MAGEL2 deficiency and whether a treatment with vasopressin could alleviate the disabilities of social behavior. We used Magel2-knockout mice (adult males) combined with optogenetic or pharmacological tools to characterize disease modifications in the vasopressinergic brain system and monitor its impact on neurophysiological and behavioral functions. We found that the activation of vasopressin neurons and projections in the lateral septum were inappropriate for performing a social habituation/discrimination task. Mechanistically, the lack of vasopressin impeded the deactivation of somatostatin neurons in the lateral septum, which predicted social discrimination deficits. Correction of vasopressin septal content by administration or optogenetic stimulation of projecting axons suppressed the activity of somatostatin neurons and ameliorated social behavior. This preclinical study identified vasopressin in the lateral septum as a key factor in the pathophysiology of Magel2-related neurodevelopmental syndromes.
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Suppressed activity of Sst-expressing neurons in the dorsal LS is associated with improved social discrimination behavior in mice.
“while suppressed activity of Sst-expressing neurons in the dorsal LS is associated with improved social discrimination behavior (Borie et al., 2021) in mice.”
From Vasopressin regulates social play behavior in sex-specific ways through glutamate modulation in the lateral septum (2025) · cites this paper as Borie et al., 2021
Bed nucleus of the stria terminalis vasopressin cell ablation impairs social recognition in males, likely through its projection to the lateral septum, and restoration of BNST-LS vasopressin signaling in Magel2-KO mice ameliorated social discrimination deficits.
“For example, BNST AVP cell ablation impairs social recognition in males, likely through its projection to the LS (94, 108, 109), and restoration of BNST-LS AVP signaling in Magel2-KO mice ameliorated social discrimination deficits (110).”
From Oxytocin, Vasopressin, and Social Behavior: From Neural Circuits to Clinical Opportunities (2022) · cites this paper as [110]
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- J Clin Invest. 2021;131(2):e144450 https://doi.org/10.1172/JCI144450 NaCl, 1.2 KCl, 26 NaHCO 3 , 15 glucose, 1.2 KH 2 PO 4 , 1 CaCl 2 , 2 MgCl 2 , 195 sucrose; osmolality adjusted to 300 mOsmol/L; pH = 7.4, 95% O 2 and 5% CO 2 ). Slices were allowed to recover for 1 hour at 37°C in arti- ficial cerebrospinal fluid (in mM: 110 NaCl, 3.6 KCl, 26 NaHCO 3 , 10 Slice electrophysiology. Animals (4-8-week-old males) were anes- thetized using isoflurane and quickly decapitated. Coronal slices (300 μm) containing the LS were prepared using a vibratome (Campden Instruments) and collected in an ice-cold slicing solution (in mM: 10
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ResultBrain circuits that regulate social behavior
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“As an example, using mice as an autism animal model, it was shown that Magel2 KO adult male mice exhibit social deficits that were correlated with inappropriate AVP activation in projection neurons to LS and optogenetic stimulation of AVP neurons or administration of AVP rescued social deficits observed in Magel2+/−p…”
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“This also confirmed the mechanism of oxytocin involved in the autism phenotype.([6,12,13]) MAGEL2 is a member of the MAGE family of ubiquitin ligase regulators.”
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“However, centrally administered AVP has been shown to “rescue” social deficits in Magel2-deficient mice (73).”
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“5 ), suggesting that PVN AVP neurons modulate mood disorders specifically, rather than social behaviors [ 79 ].”
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“Those include oxytocin and vasopressin (Borie et al., 2021; Oliveira et al., 2021) as well as type1 and type2 corticotropin-releasing factor receptor, Crfr1 and Crfr2 (Radulovic et al., 1999; Anthony et al., 2014; de León Reyes et al., 2023).”
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“In humans and animals, disruptions of AVP circuits are widely associated with neurological (8, 9) and neurodevelopmental (10–12) disorders.”
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“Apart from well-documented developmental de fi cits, PWS and SYS patients also show high comorbidity with autism symptoms [3, 4] including decreased social responsiveness in nonthreatening contexts [5], increased temper outbursts [6 – 8], and social fear [9].”
Crespi, B. J., Procyshyn, T. L., & Mökkönen, M. (2022) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2022.814230 · Cited by 3 · see citing works
Neuropeptides and the Autonomic Nervous System in Prader–Willi Syndrome
Höybye, C., & Petersson, M. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms27010352 · Cited by 2 · see citing works
“Restoration of vasopressin signaling in this region has been shown to improve social deficits in these animals [45].”
Mini review of molecules involved in altered postnatal neurogenesis in autism
Bukatová, S., Bačová, Z., Osacká, J., & Bakoš, J. (2023) · International Journal of Neuroscience · doi:10.1080/00207454.2023.2269304 · Cited by 2 · see citing works
“…therefore, a link between the gut microbiota-brain axis and changes in neurogenesis and synaptogenesis should be carefully considered in autism conditions. in recent years, increasing interest in nonapeptides OXt and AvP is mainly due to the association with neurodevelopmental diseases [101,102].”
Bao, X., Zhou, B., & Wen, M. (2024) · Frontiers in Bioscience-Landmark · doi:10.31083/j.fbl2911394 · Cited by 2 · see citing works
“Numerous animal and human studies have demonstrated that intranasal inhalation of AVP significantly improves social behavior, but the exact central mechanism is still unclear [16,19,44].”
Wang, S., Wu, X., Dong, S., Zheng, L., Pan, L., Zhan, L., Xiao, H., Yang, L., Wang, X., Ma, H., et al. (2026) · EBioMedicine · doi:10.1016/j.ebiom.2026.106478 · Cited by 1 · see citing works
“22 Previous studies have demonstrated that pharmacological manipulation of these neuropeptide systems can modulate social discrimination, social habituation, and social novelty in both wild-type mice and ASD models.”
A vasopressin circuit that modulates sex-specific social interest and anxiety-like behavior in micePreprint
Rigney, N., Campos‐Lira, E., Kirchner, M. K., Wei, W., Belkasim, S., Beaumont, R., Singh, S. P., Vries, G. J. D., & Petrulis, A. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.11.06.564847 · Cited by 1 · see citing works
Borie, A. M., Muscatelli, F., Desarménien, M. G., & Jeanneteau, F. D. (2021) · médecine/sciences · doi:10.1051/medsci/2021134
Hypothalamic vasopressin sex differentiation is established during embryonic neurogenesisPreprint
Zheng, J., Moazen, P., Baimoukhametova, D. V., Lebel, C. A., Bains, J. S., & Kurrasch, D. M. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.11.17.516788
Arakawa, H., & Higuchi, Y. (2023) · Springer eBooks · doi:10.1007/978-3-031-42383-3_6
New regulators in oxytocin and vasopressin release : role of the endolysosomal two-pore channels
Martucci, L. L. (2021) · theses.fr (ABES) · doi:10.70675/027d1ae2zd2ebz4677za019ze6ccd94cafe9
Circuit logic of oxytocin and vasopressin complementary actions
Jeanneteau, F. D., Chakraborty, P., Petitjean, H., & Charlet, A. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1875731
Maturation of social adaptation circuits from ontogeny to pathology
Gleske, M., Jeanneteau, F. D., Opendak, M. M., & Coutellier, L. D. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106874
Fu, H., Liu, Z., Zhou, J., Zhang, L., Liu, C., Tang, D., Zhang, S., Li, A., & Wang, D. (2026) · PLoS Biology · doi:10.1371/journal.pbio.3004044
“The LS acts as a pivotal neural hub in the regulation of feeding behavior [34].”
- Authors
- Borie, A. M., Dromard, Y., Guillon, G., Olma, A., Manning, M., Muscatelli, F., Desarménien, M. G., & Jeanneteau, F.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- University of Toledo (US)
- Inserm (FR)
- Venue
- Journal of Clinical Investigation
- Published
- 2021-01-19
- Volume
- 131
- Issue
- 2
- Pages
- e144450
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC7810497
- OpenAlex
- W3107618247
- Cited by
- 41
- References
- 51
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 9 · 2023: 11 · 2022: 7 · 2021: 5
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- Locations
- Journal of Clinical Investigation (publishedVersion, other-oa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (PRADOX)
- University of Montpellier (PhD fellowship)
- Fondation pour la recherche medicale (Fin de these,Equipe FRM)
- Fondation Jérôme Lejeune (Research grant)
- Topics
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- vasopressin, lateral septum, Prader-Willi syndrome, Schaaf-Yang syndrome, autism spectrum disorder, social behavior deficits, somatostatin neurons, optogenetic stimulation, social discrimination, neurodevelopmental syndrome
- MeSH terms
- Animals, Antigens, Neoplasm, Autistic Disorder, Behavior, Animal, Disease Models, Animal, Humans, Male, Neurons, Proteins, Septal Nuclei, Social Behavior, Vasopressins, Mice, Knockout, Intracellular Signaling Peptides and Proteins, Mice, Intrinsically Disordered Proteins
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