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Journal article

Functional disruption of oxytocin projections participates atypical social and anxiety-like behaviours in BTBR mouse model of autism

Open Biology, 2025

DOI 10.1098/rsob.240387 · PubMed 40858267 · PMC12380489

Licence: CC-BY-4.0

5 claims from this source

clm-1dafftwph9presentretrograde tracerproposed

PVH (Paraventricular hypothalamic nucleus) MBA:38 projects to BST (Bed nuclei of the stria terminalis) MBA:351 · Mouse

A retrograde AAV carrying mCherry under an oxytocin promoter injected into the BnST labelled oxytocin-immunoreactive cells throughout the rostral-to-caudal PVN of B6 mice, identifying PVN oxytocin neurons that innervate the BnST; such double-labelled cells were only sparsely found in BTBR mice (strain effect F(1,52) = 18.15, p = 0.0001).

Fig. 5E,F

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.

clm-c9a5xy220ypresentoptogenetic circuit mappingproposed

PVH (Paraventricular hypothalamic nucleus) MBA:38 functionally connects to BST (Bed nuclei of the stria terminalis) MBA:351 · Mouse

Chemogenetic excitation of PVN oxytocin neurons lowered AVPR1a mRNA in the BnST of both strains and raised BnST oxytocin receptor mRNA in B6 mice but not in BTBR mice, while c-fos mRNA in the BnST was unchanged, indicating a strain-dependent modulatory action of PVN oxytocin neurons on the BnST.

Fig. 4; Results, 'mRNA profiles following chemogenetic oxytocin activation'

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) disagrees. “The manipulation was chemogenetic (hM3Dq/C21), not optogenetic circuit mapping as the evidence type states.”

clm-m2fn55wgtfpresentoptogenetic circuit mappingproposed

PVH (Paraventricular hypothalamic nucleus) MBA:38 functionally connects to MEA (Medial amygdalar nucleus) MBA:403 · Mouse

Chemogenetic excitation of PVN oxytocin neurons (oxytocin-promoter hM3Dq plus C21) raised oxytocin receptor mRNA in the MeA of both B6 and BTBR mice, although c-fos mRNA in the MeA was not increased by this manipulation, indicating a neuromodulatory influence of the PVN oxytocin population on the MeA.

Fig. 4; Results, 'mRNA profiles following chemogenetic oxytocin activation'

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) disagrees. “Evidence type is mislabelled as optogenetic; the paper used DREADD chemogenetic activation with qPCR.”

clm-vd8xgvg01epresentanterograde tracerproposed

PVH (Paraventricular hypothalamic nucleus) MBA:38 projects to BST (Bed nuclei of the stria terminalis) MBA:351 · Mouse

Fluoro-Ruby placed in the PVN produced labelled axons in the BnST of B6 mice; the same injection in BTBR mice yielded much weaker terminal labelling there, which the authors interpret as degraded PVN-to-BnST projections in the autism model strain (n = 4 per strain).

Fig. 5D; Results, 'Oxytocin neural projection patterns reveal strain difference'

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.

clm-xpd6x4jst0presentretrograde tracerproposed

PVH (Paraventricular hypothalamic nucleus) MBA:38 projects to MEA (Medial amygdalar nucleus) MBA:403 · Mouse

Retrograde oxytocin-promoter AAV injected into the MeA labelled oxytocin-positive PVN neurons, mostly in the caudal PVN, with comparable densities in B6 and BTBR mice (no strain difference, F(1,39) = 1.13, p = 0.294).

Fig. 5G,H

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.