The code provided is a computational model in NEURON simulating synaptic transmission and plasticity between a tone stimulus and pyramidal cells in the brain, with a focus on the dual-receptor involvement of AMPA and NMDA receptors and the dynamics of calcium ion (Ca2+) pools. Here are the key biological elements encapsulated by the code: ### Synaptic Transmission #### AMPA and NMDA Receptors - **Receptor Types**: The model represents synapses using two primary excitatory neurotransmitter receptors: AMPA and NMDA receptors. - **AMPA Receptors**: These receptors mediate fast synaptic transmission. Parameters like `Cdur_ampa`, `AlphaTmax_ampa`, and `Beta_ampa` define their kinetics. The reversal potential is set at `Erev_ampa = 0 mV`, typical for excitatory synapses. - **NMDA Receptors**: NMDA receptors are characterized by slower kinetics (`Cdur_nmda`, `AlphaTmax_nmda`, `Beta_nmda`). They also require a depolarization of the postsynaptic membrane to relieve magnesium block, and their conductance is described by the `sfunc(v)` function, which models this voltage-dependent block. #### Calcium Dynamics - **Calcium Influx**: Critical to the NMDA receptor's function is its permeability to Ca2+, used as a secondary messenger in synaptic plasticity. The influx of Ca2+ through NMDA receptors is represented by `ICa` and tied to ongoing synaptic activity via `g_nmda` and the membrane potential difference `(v - eca)`. - **Local Calcium Pool**: The code models a local calcium pool (`capoolcon`) whose dynamics are influenced by calcium influx and a decay to a baseline concentration (`Cainf`). These changes are determined by factors like `fCa`, `tauCa`, and `Afactor`, which integrate into calcium-dependent signaling processes central to synaptic plasticity. ### Synaptic Plasticity #### Plasticity Mechanisms - **Weight Adjustment**: The code models synaptic strength (`W`, `W_nmda`) adjusted based on calcium concentration signals. The variables `lambda1`, `lambda2`, `threshold1`, and `threshold2` help regulate long-term potentiation (LTP) and long-term depression (LTD), critical processes in synaptic plasticity. - **Dynamics of Plasticity**: The weight changes are conditioned on `normW` and bounded by `Wmax` and `Wmin`. Function `omega()`, influenced by calcium concentration, serves as a gating factor for synaptic modifications, where crossing calcium thresholds can induce synaptic modification. - **Learning Rules**: The code incorporates rules such as `eta()` and `omega()`, which represent learning and plasticity constraints modulated by calcium levels, reflecting the role of calcium as a key intracellular signal for neuroplasticity. Overall, this NEURON model encapsulates the biological mechanisms of excitatory synaptic transmission and synaptic plasticity in pyramidal neurons, highlighting the interplay between AMPA and NMDA receptors and their downstream calcium-mediated effects on synaptic weights. These models are vital for understanding learning and memory processes in computational neuroscience.