The code provided models a synaptic mechanism based on the kinetics of neurotransmitter binding to postsynaptic receptors, specifically focusing on NMDA receptor-mediated synaptic transmission. Here are the key biological aspects reflected in the code:
Neurotransmitter Release: The code assumes a pulse of neurotransmitter concentration in the synaptic cleft upon a presynaptic spike. This pulse is characterized by a maximum concentration (Cmax) and duration (Cdur), simulating the release of neurotransmitters such as glutamate in an actual synapse.
Receptor Binding Kinetics: The binding of the neurotransmitter (C) to postsynaptic receptors (Rc) is described by first-order kinetics:
Rc) bind with the neurotransmitter to form open receptors (Ro).Ro) revert to the closed form (Rc).Voltage Dependence: NMDA receptors, unlike other receptors, are known to possess voltage-dependent properties due to the blockade by magnesium (Mg²⁺) ions. The code models this by adjusting the synaptic conductance based on the membrane potential (v) and the external magnesium concentration (mg), reflecting the receptor's voltage dependence.
Magnesium Block: The function mgblock computes the reduction in conductance caused by Mg²⁺ ion blockade, based on a sigmoidal function of the membrane voltage and magnesium concentration. This mimics the biological reality where NMDA receptor activation is both ligand- and voltage-gated.
Isyn) is calculated based on the conductance (g), which depends on the fraction of open NMDA receptors (R), magnesium block, and facilitation factor (F). The equation involves the difference between postsynaptic voltage (V) and the reversal potential (Erev), modeling how current flows through the synapse when NMDA channels are open.F represents synaptic facilitation, a form of short-term plasticity. Upon each presynaptic spike, F increases by a set fraction (f) and decays back to a baseline (Finf) with time constant (Ftau), simulating the phenomenon where consecutive spikes lead to increased synaptic strength.lastrelease and Deadtime are used to ensure that neurotransmitter release doesn't occur back-to-back without a minimum interval. This models the synaptic refractory period between successive neurotransmitter release events, ensuring a realistic timing of synaptic transmission.The code models NMDA receptor-mediated synaptic transmission, capturing key biological phenomena like receptor binding kinetics, voltage-dependent magnesium blockade, synaptic plasticity, and the dynamics of neurotransmitter release. These elements combine to simulate the complex interplay of ionic currents and receptor dynamics that define NMDA-mediated synaptic communication in the brain.