The provided code models synaptic channels in neuronal simulations, focusing on glutamatergic (excitatory) and GABAergic (inhibitory) synaptic transmissions. Here’s a detailed look at the biological basis: ### Biological Context 1. **Synaptic Transmission**: - Synaptic transmission is the process by which neurons communicate with each other. This communication can be excitatory or inhibitory, primarily mediated by glutamate and GABA neurotransmitters, respectively. 2. **Excitatory Synapses**: - **Glutamate** is the primary neurotransmitter for excitatory synapses in the brain. When glutamate binds to its receptors on the postsynaptic neuron, it typically results in depolarization, making the neuron more likely to fire an action potential. - In the code, excitatory postsynaptic currents (EPSCs) are mediated by AMPA receptors, which are ionotropic glutamate receptors. These are modeled using the `Ex_chSPIKEAMPA` synchan, specifically setting the reversal potential (`Ek`) to 0 mV, a typical approximation for excitatory synapses. 3. **Inhibitory Synapses**: - **GABA (γ-Aminobutyric Acid)** functions as the main inhibitory neurotransmitter in the central nervous system. When GABA binds to its receptors, it generally causes hyperpolarization, making the neuron less likely to fire. - Although the code snippet does not define a specific function for GABAergic synapses, it mentions variables related to these channels, suggesting similar modeling constructs would apply. 4. **Synaptic Conductance Changes**: - The code models synaptic conductance changes using an alpha-function approach, which simulates the time course of synaptic conductance following neurotransmitter release. Specifically, the parameters `tau1` and `tau2` define the decay times of the synaptic conductance changes, reflecting how quickly the synaptic current diminishes after an excitatory event. 5. **NMDA Receptor Influences**: - Parameters related to NMDA, such as `CMg`, `eta`, and `gamma`, suggest an intention to model calcium and voltage-dependent NMDA receptor channels, though they are not instantiated in the provided snippet. NMDA receptors require simultaneous glutamate binding and postsynaptic depolarization to remove the magnesium block and allow calcium influx, crucial for synaptic plasticity processes such as long-term potentiation (LTP). ### Modeling Goals This code aims to simulate the basic biophysical properties of synaptic transmission in neurons by modeling the dynamics of excitatory and inhibitory post-synaptic potentials. By capturing these fundamental processes using parameters like conductance, decay times, and reversal potentials, this model provides a controlled environment to study neuronal network behavior, synaptic integration, and potentially the effects of neuromodulation and synaptic plasticity. In summary, the code outlines a simplified but biologically relevant approach to understanding neuronal communication through synaptic events, emphasizing the role of AMPA-mediated glutamatergic transmission within the modeled neural circuitry.