🧠 Tier: Standard Undergraduate · Type I & II · Phase Plane · Ca²⁺ Channels
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§ 01
Interactive Simulation
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T sim (ms)500
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§ 02
The Idea, Step by Step
▸ From a Self-Resetting Switch to Two Coupled Equations
START — The everyday picture
A neuron is like a light switch that flips itself back off. Tap it gently and nothing happens. Tap it hard enough and it snaps fully ON — a sharp pulse called a spike — and then, all by itself, it resets to OFF, ready for the next tap. Almost everything a neuron computes comes from this one trick: an all-or-nothing snap followed by an automatic reset.
BUILD — Two ions, two jobs
Two kinds of charged particle do the work. Calcium ($\text{Ca}^{2+}$) rushes in quickly and pushes the membrane voltage up — that is the "snap ON." Potassium ($\text{K}^{+}$) leaks out slowly and pulls the voltage back down — that is the "reset." We track two numbers: the membrane voltage $V$ and the fraction of K⁺ gates that are open, $w$. The rule in words: voltage climbs whenever the inward Ca²⁺ current beats the outward K⁺ and leak currents. A worked number: at rest $V \approx -60$ mV. Inject enough current $I$ to drag $V$ up past about $-20$ mV and the Ca²⁺ channels fling open together; $V$ jumps to roughly $+30$ mV in a couple of milliseconds — one spike — before the slow K⁺ current hauls it back below rest.
DEEPEN — The precise two-variable system
Written exactly, the model is two coupled equations: $C_m \frac{dV}{dt} = I - g_{Ca}\,m_\infty(V)(V-E_{Ca}) - g_K\,w\,(V-E_K) - g_L(V-E_L)$ and $\frac{dw}{dt} = \phi\,\frac{w_\infty(V)-w}{\tau_w(V)}$. The Ca²⁺ gate $m_\infty(V)$ is so fast it tracks the voltage instantly, so it never gets its own equation; the K⁺ gate $w$ lags behind, and that lag is the recovery that ends each spike. The sliders map straight onto these symbols: Input I is the injected current that drives the cell toward threshold; the parameter sliders shift the channel activation curves (their $V$-midpoints and the rate factor $\phi$), which is exactly what decides whether firing begins smoothly from 0 Hz (Type I) or jumps to a minimum rate (Type II).
TRY THIS — In the sim above
(1) Start with Input $I$ low and watch the cell sit silently at rest, then raise $I$ until the very first spike appears — you have just found the firing threshold. (2) Push $I$ higher and the single spike becomes a steady train; watch the firing-rate readout climb. (3) Lower the recovery rate $\phi$ and notice each spike grows wider and the cell takes longer to reset between firings.
§ 03
Equation Derivation
▸ Morris-Lecar Equations (1981)
Proposed by Catherine Morris and Harold Lecar (1981) to model barnacle giant muscle fibre with Ca²⁺ and K⁺ channels. The ML model is the simplest biophysical model that can exhibit both Type I and Type II excitability depending on parameters.
Unlike HH Na⁺ channels, Ca²⁺ channels in the ML model activate very rapidly (τ_m ≪ τ_w) — so fast that m can be treated as instantaneously at its steady state m∞(V). This reduces the 3D system (V, m, w) to 2D (V, w), making full phase-plane analysis tractable. Ca²⁺ provides the fast inward current (like Na⁺ in HH); K⁺ provides the slow outward current (like n in HH).
STEP 2 — Type I vs Type II via V_3 and φ
The ML model can be tuned between Type I (SNIC bifurcation, f starts from 0 Hz) and Type II (Hopf bifurcation, f jumps to minimum) by changing V_3 and φ. Type I params: V_3=2 mV, φ=0.04. Type II params: V_3=12 mV, φ=0.23. This makes ML the canonical model for studying excitability classes. The bifurcation type is determined by the position and slope of the w-nullcline relative to the V-nullcline cubic.
STEP 3 — Nullcline Analysis
V-nullcline: I = g_Ca m∞(V)(V−E_Ca) + g_K w(V−E_K) + g_L(V−E_L), solved for w(V). This is an N-shaped curve. w-nullcline: w = w∞(V) (sigmoidal). Fixed points at intersections. If the intersection is on the middle (negative-slope) branch of the V-nullcline → unstable → oscillation. Stability depends on whether Tr(J) > 0 at the fixed point.
STEP 4 — RK4 Integration
Both equations are integrated with RK4 at dt = 0.1 ms. The ML model is not stiff (no fast singularities), but V can change rapidly during a spike (Ca²⁺ upstroke). The φ parameter controls the timescale separation: small φ → w very slow → large excursions; large φ → faster recovery → smaller APs. At physiological φ values, one AP upstroke takes ~3–5 ms.
▸ Worked Example — Fixed Point Stability (Type I)
Type I params, I=0. Find fixed point and assess stability. At rest: V* ≈ −60 mV, w* ≈ w∞(−60) ≈ 0.01. Jacobian at (V*, w*):
For Type I at rest: Tr(J) < 0, Det(J) > 0 → stable fixed point. As I increases toward I_SNIC, a saddle-node pair approaches the rest fixed point on the V-nullcline → Type I onset. For Type II parameters: Tr(J) = 0 at I_Hopf → Hopf bifurcation.
▸ References
[ML81]
Morris & Lecar — Voltage oscillations in the barnacle giant muscle fibre, Biophys. J. 35:193–213, 1981
[RE89]
Rinzel & Ermentrout — Analysis of neural excitability, in Methods in Neuronal Modeling, MIT Press, 1989
[IZH07]
Izhikevich — Dynamical Systems in Neuroscience, Ch. 4–5. Free: dynamicalsystems.org
🔬 SimulationWhat tabs are shown and how do they differ from FitzHugh-Nagumo?▼
The ML model uses millivolt units and real ionic currents (Ca²⁺, K⁺, leak) — all axis labels are in mV, ms, mA/cm². The Phase Plane tab shows the V-nullcline (N-shaped, from the Boltzmann Ca²⁺ activation) and w-nullcline (sigmoidal K⁺ activation), which are more complex than FHN's simple cubic+line. The Type I/II toggle changes V_3 and φ, switching the bifurcation type — observe how the fixed point position on the V-nullcline shifts and the trajectory shape changes. The Conductance tab shows g_Ca(t) and g_K(t) as functions of V in real time.
Key takeaway: ML is biophysically grounded (real ions, real units) — the nullclines have Boltzmann shapes that directly map to voltage-clamp measurements. FHN is a dimensionless cartoon; ML is a minimal biophysical model.
🧠 ConceptualWhy is Ca²⁺ treated as instantaneous but K⁺ is not?▼
Ca²⁺ channels in the Morris-Lecar model (barnacle muscle Ca²⁺ channels, and similar to HVA Ca²⁺ channels in neurons) activate very rapidly — time constant τ_m < 1 ms at physiological voltages. K⁺ channels activate on a timescale of 5–50 ms (τ_w). The timescale separation is τ_w/τ_Ca ≫ 1, justifying the quasi-static approximation m ≈ m∞(V). This is identical to HH's observation that τ_m ≪ τ_n — Hodgkin and Huxley also treated m as quasi-static in some analyses. The quasi-static approximation reduces a 3D system (V,m,w) to 2D (V,w), enabling full phase-plane analysis.
Key takeaway: Ca²⁺ instantaneous ≈ m∞(V) because τ_Ca ≪ τ_K. This timescale separation is what makes the 2D reduction valid and the phase plane tractable — the same approximation used in HH analysis.
🌍 AppliedWhere is the Morris-Lecar model used in research and medicine?▼
ML is the standard model for: (1) Cortical excitability classification — theorists use ML (rather than HH) to derive the Rinzel-Ermentrout Type I/II classification because of its analytical tractability; (2) Cardiac myocyte modelling — early models of cardiac Ca²⁺ channels used ML-type equations (later extended to Luo-Rudy); (3) Smooth muscle — Ca²⁺-dependent contractions in arterial smooth muscle use ML-type models; (4) Endocrine cells — pancreatic beta cell bursting (Chay-Keizer model) is a direct extension of ML; (5) Bursting pacemakers — thalamic and hippocampal cells use ML with additional currents. ML is preferred over FHN for these because it uses biophysically interpretable parameters.
Key takeaway: ML is used wherever Ca²⁺ channels provide the regenerative current and K⁺ provides recovery — cardiac, smooth muscle, endocrine, and some neuronal applications. Its Boltzmann functions connect directly to voltage-clamp measurements.
💡 Non-ObviousWhy does changing V_3 by only 10 mV switch between Type I and Type II excitability?▼
V_3 sets the midpoint of the K⁺ activation curve w∞(V). Shifting V_3 moves the w-nullcline horizontally in the V-w phase plane. When V_3 is small (e.g., +2 mV for Type I): the w-nullcline intersects the left (stable) branch of the V-nullcline — fixed point is on the stable branch, SNIC bifurcation possible. When V_3 is larger (+12 mV for Type II): the w-nullcline shifts right, its intersection moves to the middle (unstable) branch — the fixed point destabilises via Hopf. A 10 mV shift in the midpoint of one Boltzmann function is enough to change the mathematical class of the entire neuron's excitability. Biologically, this small shift corresponds to different K⁺ channel subtypes or different neuromodulatory states.
Key takeaway: A 10 mV shift in V_3 (K⁺ activation midpoint) can switch a neuron between SNIC (Type I) and Hopf (Type II) bifurcation. Small changes in a single channel parameter qualitatively alter firing dynamics.
📐 ComputationalWhat is the φ parameter and how does it affect the simulation?▼
φ (phi) is a temperature scaling factor for the K⁺ activation kinetics: dw/dt = φ × (w∞−w)/τ_w. Larger φ → faster K⁺ recovery → shorter APs, higher maximum firing rate, faster spike-frequency adaptation. The original Morris-Lecar model used φ = 0.04 (barnacle muscle at 5°C). For Type II parameters: φ = 0.23 (faster, mammalian-like). φ affects the Hopf bifurcation onset: increasing φ increases the minimum frequency at onset (ω_Hopf = φ × Im(eigenvalue)/τ_w). In the simulation, dragging φ from 0.04 to 0.23 with Type II parameters shows the transition from near-Type I (slow recovery, very low onset frequency) to clear Type II (fast recovery, 20+ Hz minimum firing rate).
Key takeaway: φ scales K⁺ channel kinetics — it controls the timescale separation between V (fast) and w (slow). Large φ = fast recovery = Type II-like high onset frequency. Small φ = slow recovery = Type I-like low onset frequency.
🎓 DeepHow does the Morris-Lecar model relate to the theta model (canonical Type I)?▼
The theta model (Ermentrout & Kopell, 1986) is the exact normal form of the SNIC bifurcation: dθ/dt = 1 − cos θ + I(1 + cos θ). Near the SNIC bifurcation in the Morris-Lecar Type I model, the dynamics on the invariant circle (just above I_SNIC) are exactly described by the theta model. The relationship: V ≈ tan(θ/2), so the ML action potential corresponds to a single rotation of θ from −π to +π. The ML model is thus the 2D biophysical embedding of the 1D theta model: away from the bifurcation, ML adds the w variable providing recovery; near the bifurcation, the w dynamics are enslaved and ML reduces to theta. This connection enables exact analytical results for ML synchronisation properties using theta model analysis.
Key takeaway: ML Type I near I_SNIC reduces exactly to the theta model dθ/dt = 1 − cos θ + I(1 + cos θ). This connection enables analytical synchronisation and phase-response curve calculations.
🧠 ConceptualWhat makes the ML model the preferred teaching model over HH for phase plane analysis?▼
Three key reasons: (1) Only 2 variables — V and w can be drawn as a 2D phase portrait; HH needs 4D. (2) Clearly separated timescales — Ca²⁺ is instantaneous (m≈m∞), K⁺ is slow (w), making the fast-slow decomposition transparent. (3) Tunable excitability type — by changing V_3 and φ, you can demonstrate Type I vs Type II within the same model framework, which is impossible in HH without changing the channel type. For HH, all phase plane analysis requires projecting the 4D system onto 2D subspaces, losing intuition. ML provides all the qualitative richness of HH in a form where every feature of the trajectory can be understood geometrically.
Key takeaway: ML is the preferred pedagogical model because: 2D phase plane fully visible, timescale separation explicit (Ca²⁺ instantaneous), and Type I/II both accessible within the same parameter family.
§ 04 Best Resources
Izhikevich — Dynamical Systems in Neuroscience, MIT Press, 2007. Free: dynamicalsystems.org
Gerstner et al. — Neuronal Dynamics, Cambridge, 2014. neuronaldynamics.epfl.ch
Strogatz — Nonlinear Dynamics and Chaos, Westview, 2015
Ermentrout & Terman — Mathematical Foundations of Neuroscience, Springer, 2010
§ 05
Misconceptions & Common Errors
Sub-block A — Conceptual Misconceptions
❌"The Morris-Lecar model uses calcium spikes, not sodium action potentials — it cannot model cortical neurons."
✅The ML model uses Ca²⁺ as the regenerative inward current, but the mathematical structure (inward current with fast activation + outward K⁺ with slow activation) is identical to the Na⁺/K⁺ structure of HH. The model is a generic template: you can substitute g_Ca/E_Ca with g_Na/E_Na and get an equivalent model for sodium-based neurons. In fact, many cortical neuron models replace the ML Ca²⁺ current with a Na⁺ persistent current (I_NaP) to model subthreshold oscillations. The key insight is that ML captures the universal topological features of excitable systems — the specific ion species is secondary to the fast-inward/slow-outward structure.
❌"Setting w₀ = 0 is always correct because K⁺ channels are closed at rest."
✅At rest (V = V_rest), K⁺ channels are not fully closed — w_rest = w∞(V_rest) > 0. For ML Type I with V_3 = 2 mV: w_rest = w∞(−60) = 0.5×(1 + tanh((-60-2)/30)) = 0.5×(1+tanh(-2.07)) ≈ 0.5×(1-0.97) ≈ 0.015. Setting w₀ = 0 instead of w₀ = w∞(V₀) gives a transient where w rapidly adjusts toward its equilibrium — producing an artefactual current transient at t=0 that looks like a large IPSP or EPSP. Always initialise w₀ = w∞(V₀) for a proper resting-state start.
❌The Ca²⁺ conductance term is written as g_Ca × (V − E_Ca) treating g_Ca as constant — forgetting that g_Ca = g_Ca_max × m∞(V) is voltage-dependent.
✅Ca²⁺ current must include the voltage-dependent activation: I_Ca = g_Ca_max × m∞(V) × (V − E_Ca). The term g_Ca alone is the maximal conductance — a constant. The actual conductance at voltage V is g_Ca_max × m∞(V), which varies from 0 (at hyperpolarised V) to g_Ca_max (at depolarised V). Using g_Ca × (V − E_Ca) without m∞(V) gives a linear (ohmic) Ca²⁺ current that cannot produce the regenerative threshold crossing — the neuron will not fire regardless of I.
🔍 Why: Forgetting that g_Ca in the code is the maximal conductance constant, not the instantaneous conductance — the m∞(V) factor is the 'missing' voltage-dependence.
§ 05 References
Izhikevich — Dynamical Systems in Neuroscience, MIT Press, 2007
Gerstner et al. — Neuronal Dynamics, Cambridge, 2014. neuronaldynamics.epfl.ch
Ermentrout & Terman — Mathematical Foundations of Neuroscience, Springer, 2010
Strogatz — Nonlinear Dynamics and Chaos, Westview, 2015