This is the 2D top-down counterpart of the 3D gap-junction simulator: the underlying model was already a graph — 61 cells arranged on a hexagonal axial lattice (q,r), wired to their up-to-6 neighbours by gap-junction "edges" — the 3D version only added a perspective camera and cosmetic height jitter on top of that same flat graph. Here the identical diffusion-on-a-network ODE is solved and rendered directly from above, with a live coupling strip-chart alongside it.
dCᵢ/dt = Σⱼ g·ρ·P(M)·(1-G)·(Cⱼ-Cᵢ) − k·Cᵢ
g = base single-channel conductance
ρ = connexon channel density (Density slider)
P(M) = pore permeability for tracer of size M (Tracer select)
G = gating closure fraction, Ca²⁺/H⁺-driven (Gating slider)
k = degradation / uptake rate
- Tracer molecule — the connexin pore has a functional size cutoff near 1 kDa. Small ions and second messengers (Ca²⁺, cAMP, IP₃) pass almost freely; a >1 kDa dextran is essentially excluded, exactly as in real dye-coupling assays used to map tissue connectivity.
- Connexon channel density — the number of open connexons packed into a junction plaque; this is what's lost when connexin expression drops (e.g. Cx43 loss in ischemic heart tissue, causing conduction block).
- Gating closure — a rise in intracellular Ca²⁺ or a fall in pH closes gap junction channels within seconds, uncoupling the tissue — a real protective reflex that isolates a dying or injured cell from its healthy neighbours.
- Coupling index — the fraction of first-ring neighbour concentration relative to the source, the same metric used in scrape-loading / dye-transfer experiments to quantify how well-coupled a tissue is.
Real-world relevance: this exact electrical/chemical coupling mechanism synchronises cardiac and smooth-muscle contraction, propagates astrocyte Ca²⁺ waves in the brain, and — when connexin genes (GJB2/GJB6) are mutated — causes the most common form of inherited deafness by breaking potassium recycling in the cochlea.