Calcium Signaling Oscillator

Ca²⁺ Signal Oscillator

Oscillating

IP3 level (ligand → GPCR → IP3) 40%

IP3-receptor sensitivity 0.90

SERCA pump strength 65

Cytosolic Ca²⁺

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ER store Ca²⁺

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Spike period

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Frequency

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How it works

A hormone or neurotransmitter binding a GPCR activates phospholipase C, which produces IP3. IP3 opens Ca²⁺ channels on the endoplasmic reticulum (ER), releasing stored Ca²⁺ into the cytosol; the released Ca²⁺ itself further opens nearby channels (calcium-induced calcium release, CICR), while SERCA pumps continuously reload the ER. This push-pull between release and re-uptake is a classic activator-inhibitor oscillator:

dCa_cyto/dt = v0 + v1·IP3 − v_pump + v_release + leak − k·Ca_cyto
dCa_ER/dt   = v_pump − v_release − leak

IP3 level — the strength of the incoming hormonal signal. Cells don't encode signal strength as a bigger single spike; they encode it as spike frequency — watch the trace speed up as you raise IP3, exactly as in real hepatocytes and oocytes.
IP3-receptor sensitivity — how easily cytosolic Ca²⁺ triggers further release; higher sensitivity narrows the IP3 window where stable oscillations occur.
SERCA pump strength — how fast Ca²⁺ is pumped back into the ER between spikes; a weak pump broadens spikes and slows the rhythm.
Block SERCA pump — stops ER refilling entirely: the store empties, CICR runs dry, and oscillations collapse into a flat low plateau — this is exactly how SERCA-inhibiting drugs like thapsigargin behave in real cells.

Real-world relevance: frequency-encoded Ca²⁺ signaling controls muscle contraction timing, insulin secretion pulses, fertilization waves in eggs, and gene-expression programs that read pulse frequency through calcium/calmodulin-dependent kinases.

Cytosolic Ca²⁺ ER store Open IP3 receptor

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