A Miniature Brain Transformer: Thalamic Gating, Hippocampal Lateralization, Amygdaloid Salience, and Prefrontal Working Memory in Attention-Coupled Latent Memory

TL;DR

This paper introduces a miniature brain transformer architecture with multiple brain-region analogues, demonstrating how prefrontal working memory and inhibition synergistically induce lateralization, advancing neurobiologically inspired sequence modeling.

Contribution

It presents a novel brain-inspired transformer model incorporating thalamic, amygdaloid, prefrontal, and cerebellar modules, revealing the critical role of working memory in lateralization.

Findings

Inhibitory callosal coupling alone does not lateralize hippocampal banks.

Adding prefrontal working memory causes a sharp phase transition in lateralization.

Cerebellar fast-path accelerates the transition without affecting asymptotic behavior.

Abstract

We present a miniature brain transformer architecture that extends the attention-coupled latent memory framework with four additional brain-region analogues: a thalamic relay, an amygdaloid salience module, a prefrontal working-memory (PFC) buffer, and a cerebellar fast-path, all coupled by inhibitory callosal cross-talk between lateralized hippocampal banks. We evaluate on a two-domain benchmark -- MQAR (Multi-Query Associative Recall; episodic domain) and modular arithmetic (+1 mod 10; rule-based domain) -- using a seven-variant additive ablation. The central empirical finding is a surprise: inhibitory callosal coupling alone never lateralizes the banks (variants 1-5 maintain D_sep ~ 0.25 and P_ct ~ 0.25 for all 30 epochs). Functional lateralization requires the synergy of PFC and inhibition: only when the PFC buffer is added (variant 6) does a sharp, discontinuous phase transition fire -- at epoch 11 for the PFC-only variant and epoch 10 for the full model -- collapsing P_ct from 0.25 to ~0.002 and more than doubling D_sep from 0.251 to 0.501 in a single gradient step. The PFC buffer acts as a symmetry-breaker: its slowly drifting domain context creates the initial asymmetry that the inhibitory feedback loop then amplifies irreversibly. The cerebellar fast-path accelerates the transition by one epoch (epoch 10 vs. epoch 11) with no asymptotic change, confirming its convergence-acceleration role. The result constitutes a novel, falsifiable prediction -- no lateralization without working memory context -- and a principled, neurobiologically motivated blueprint for hierarchical persistent memory in sequence models.