The study measures five components of rapid spatial cognition in one reconfigurable 11Γ11 two-layer "Manhattan Maze" (2^(11Γ11) β 10^36 configurations). Naive wildtype mice (n=25) dropped reward intervals to ~0.15 and traverse duration to ~0.2 of initial values within ~20 rewards; error rates started below chance (corridor error 0.26 vs. 0.44 for a memoryless walker), indicating latent learning of a "forward rule" before any reward .
In cyclic Mask D (two bicliques joined by bottlenecks, n=6), mice preferentially chose the bottleneck corridor remote from reward within ~3 outbound rewards, and the first homebound journey already showed above-chance bottleneck choice β inconsistent with TD(0) Q-learning, whose value propagates one step per rewarded episode. Simulated Endotaxis (model-based, map-before-goal) reproduced the behavior; simulated Q-learning did not .
Acortical mice (Pals1^loxp/loxp; Emx1-Cre+, n=18, verified by MRI/dissection) were ~3x slower to obtain the first four rewards due to repetitive scanning, but successful learners (4 of 6 on Mask A) reached wildtype-level late performance and learning rates, retained solutions across gaps up to ~60 days (median relative traverse duration ~0.4), and generalized to new masks (D0 ~0.3 of first-maze values) .
Acortical D0 bar is inverted relative to others (impairment >1); all others show improvement <1.
Selection bias in acortical analyses. Only successful learners (β₯20 rewards/session) were analyzed: 47% (7/15) learned Mask A; 5 of 11 learned Mask D. Claims of "preserved" cognition apply to a survivorship-selected subset; the authors acknowledge this but the headline framing risks overgeneralization . The small control cohort (n=3 for Mask A) precludes meaningful genotype comparison CIs β the authors honestly plot controls as individual points.
Brain-rewiring confound. The acortical brain is not a normal brain minus cortex: retinal input to dLGN is largely absent, thalamocortical targets are rewired, and compensatory developmental reorganization occurred without any maze-relevant selection pressure. The conclusion "subcortical circuits suffice" is therefore about the rewired mutant brain, and the claim that normal mice use the same circuits is explicitly conjectural.
Modeling limitations. Endotaxis parameters (Ξ³=0.21, ΞΈ=0.2, Ξ±=0.2) were chosen for illustration, not fitted; "similar qualitative behavior over a broad range" is asserted with "data not shown" β a weak evidentiary basis for excluding model-free RL, though the analytic TD(0) staircase prediction (errors at chance for first d traverses, then 0) is clean and clearly contradicted by the data.
What would change the conclusion: targeted, reversible silencing of hippocampus/cortex in normal mice during specific learning stages (the authors flag this as future work), neural recordings in an open-top maze variant, or demonstration that naive acortical mice that fail to learn simply had motor/sensory deficits rather than cognitive ones. Prior work shows neodecorticated animals retain Pavlovian learning but impair instrumental learning, making this result consistent with, but still surprising against, the classical lesion literature .
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