The code provided models synaptic transmission and plasticity mechanisms in a neural network, specifically focusing on the interaction between pyramidal cells and interneurons via AMPA and NMDA receptors, with an emphasis on calcium dynamics. ### Biological Basis 1. **Neuron Types and Synaptic Connectivity:** - **Pyramidal Cells to Interneurons:** The model describes synaptic interactions where excitatory pyramidal neurons affect interneurons. This is a common arrangement in cortical circuits, where excitatory and inhibitory neurons interact to regulate neural network activity. 2. **Synaptic Receptors:** - **AMPA and NMDA Receptors:** The synapse incorporates both AMPA and NMDA receptors, which are crucial for fast excitatory synaptic transmission and synaptic plasticity, respectively. AMPA receptors mediate rapid synaptic responses, while NMDA receptors, which require membrane depolarization and glutamate binding, allow calcium influx that is vital for synaptic plasticity. 3. **Calcium Dynamics:** - **Local Ca²⁺ Pool and Calcium-Dependent Processes:** The model simulates a localized calcium pool influenced by NMDA receptor activity, representing the intracellular calcium concentration ([Ca²⁺]i). Calcium influx is critical for triggering various cellular processes, including synaptic plasticity, by activating intracellular signaling pathways. - **Calcium Concentration-Dependent Plasticity:** The model uses functions to calculate calcium-dependent changes in synaptic strength, mimicking long-term potentiation (LTP) and long-term depression (LTD), known as flow of reference from calcium dynamics to synaptic weight change. 4. **Plasticity Mechanisms:** - **Long-Term Plasticity:** The model implements a form of synaptic plasticity based on calcium concentration, representing changes in synaptic strength over longer timescales. The parameters and equations are inspired by rules for spike-timing-dependent plasticity (STDP) and calcium-based models that track changes in synaptic efficacy in response to specific patterns of neural activity. - **Short-Term Plasticity:** Mechanisms for short-term facilitation and depression are also present, which affect synaptic transmission dynamically in response to recent activity, capturing transient increases or decreases in synaptic strength due to presynaptic factors. 5. **Mathematical Functions:** - **sfunc:** This function approximates the magnesium block removal from NMDA receptors, which is voltage-dependent and a unique property of NMDA channels that contributes to their role as coincidence detectors in synaptic plasticity. - **eta and omega Functions:** These functions establish plasticity rules in response to calcium levels, translating calcium signals into changes in synaptic weight, supporting the idea that intracellular calcium is a key mediator of synaptic plasticity. 6. **Weight Dynamics:** - The code includes mechanisms to control synaptic weights, ensuring they are bounded and appropriately regulated by calcium-dependent plasticity, preventing runaway excitation or complete synaptic silencing. ### Conclusion This model integrates key components of synaptic transmission and plasticity, particularly focusing on the pivotal role of calcium signaling. The simulation provides insight into how pyramidal neurons modulate interneuron activity through both rapid synaptic transmission and more enduring synaptic plasticity, reflecting core concepts in computational neuroscience regarding brain plasticity and neural network regulation.