Sub-second dopaminergic reinforcement orchestrates juvenile social play and is disrupted in Shank3 deficiency. Chen et al.

This dataset accompanies a study testing whether nucleus accumbens dopamine (DA) acts as an action‑contingent reinforcement signal shaping juvenile social play in a sex‑divergent manner, and whether Shank3 deficiency disrupts this signal. We collected multimodal data from wild‑type (WT) and Shank3+/- (PND 35‑85) during same‑sex dyadic interactions. A nine‑camera volumetric system (120 fps) with segmentation‑first instance segmentation (Mask R‑CNN/YOLOv8) and DANNCE tracked 14 body keypoints. The Social‑Seq pipeline derived 32 kinematic/interaction features, segmented interactions into 800‑ms clips, and used Seq2seq RNN with perspective‑invariant active learning to generate 36 behavioral syllables (e.g., sniffing, chasing, pouncing, pinning, rearing). Simultaneously, fiber photometry recorded NAc DA dynamics via GRAB‑DA3m. In Shank3+/- males, a real‑time closed‑loop system (266‑ms latency) delivered 40‑Hz optogenetic stimulation to VTA‑NAc projections specifically upon proactive play initiation over 8 training days, followed by 10 stimulation‑free days. Key findings: In WT males, proactive play (pouncing, pinning) evoked DA surges, while forced submission suppressed DA. In WT females, DA increased during evasion and rearing but not contact‑heavy play. Shank3 mutants showed blunted DA during sniffing/chasing and, critically, a sign‑inverted DA response during pouncing , while solitary rearing produced exaggerated DA only in mutant males . A multi‑agent reinforcement learning model parameterized with empirical DA amplitudes reproduced mutant phenotypes (preserved sniffing, reduced play, disrupted transitions). Closed‑loop DA during play increased targeted play duration persistently and reduced non‑social leaving, establishing causal sufficiency. Data include raw 3D keypoint coordinates, behavioral syllable labels, synchronized DA ΔF/F traces, optogenetic timestamps, and summary metrics (frequencies, durations, transition matrices). Researchers can use these to replicate the ethogram, perform neural‑behavior alignment, parameterize computational models, or evaluate intervention outcomes. Key considerations: sex must be treated as a covariate; behavioral labels have quantitative operational definitions; the Shank3 model (exon 11‑21) is specific to Phelan‑McDermid syndrome; and optogenetic results demonstrate sufficiency, not exclusivity, of DA. This multi‑scale resource supports studies of developmental social reward and autism‑related motivation deficits.