# Biological Basis of the Code The provided code is part of a computational model designed to simulate neuronal behavior at both the cellular and subcellular levels. This model draws inspiration from the biophysical and phenomenological models described in various studies of spike-timing dependent plasticity (STDP). Below, we outline the biological components being modeled: ## Neuronal Structure ### **1. Cell and Compartmentalization:** - **Soma:** The main body of the neuron, modeled with a specific diameter and length. It contains active properties influencing the generation and propagation of action potentials. - **Axon:** Composed of several parts including the initial segment, hillock, nodes of Ranvier, and myelinated sections. These structures facilitate the rapid transmission of electrical signals through saltatory conduction. - **Dendrite and Spine:** Dendrites receive synaptic inputs, and spines are small, protruding structures on dendrites where synaptic communication occurs. Spines have distinct electrical properties modeled here by specific ion channel densities. ### **2. Axonal Geometry:** - **Initial Segment, Hill, and Myelinated Sections:** These compartments enable action potential initiation and propagation. The varying diameters and segment lengths reflect the specialized structure of axons in real neurons. ### **3. Spines:** - **Spine and Neck:** Simulated as small compartments reflecting the postsynaptic structures involved in synaptic plasticity and signal integration. ## Ion Channels and Electrophysiology ### **1. Passive Properties:** - **Membrane Resistance and Capacitance:** These properties define the passive electrical behavior of the neuron, influencing how voltage changes spread across the cell. - **Passive Conductance (g_pas):** Represents background ion leakage crucial for setting the resting membrane potential. ### **2. Active Properties:** - **Sodium (Na+) Channels:** Distributed across the neuron, with varying densities depending on the compartment. They play a vital role in action potential generation and conduction. - **Potassium (K+) Channels:** - **Delayed Rectifier (kv) Channels:** Enable repolarization following an action potential, contributing to its refractory period. - **Slow Potassium (km) Channels:** Provide slow repolarization components that impact neuronal excitability. - **Calcium-activated K+ (kca) Channels:** Link intracellular calcium levels to membrane potential responsiveness. - **Calcium (Ca2+) Channels:** Regulate intracellular calcium dynamics, crucial for synaptic plasticity and signaling pathways in neurons. ### **3. Ion Dynamics:** - **Equilibrium Potentials (Ek, Ena, eca):** Set based on typical physiological gradients, these dictate ion flow under specific electrical conditions. - **Calcium Dynamics:** Managed through distinct compartmentalized accumulations and buffering mechanisms, affecting synaptic efficacy and plasticity. ## Synaptic Mechanisms ### **1. Receptor Insertion:** - **NMDAKIT (NMDA Receptors):** Modeled within spines to facilitate synaptic transmission and plasticity. NMDA receptors are key to synaptic strength modulation as they allow Ca2+ entry, triggering intracellular signaling pathways for STDP. ### **2. PSCs (Post-Synaptic Currents):** - **AMPAKIT Synapse:** Simulates AMPAR-mediated fast excitatory synaptic currents, essential for rapid synaptic response in neurons. ## Summary This model integrates detailed structural and functional neuronal components to mimic realistic electrical signaling and synaptic interactions. The code encapsulates multiple facets of a neuron's behavior, from action potential dynamics to synaptic integration and plasticity, reflecting the biophysical properties of real neurons. By doing so, it provides a basis for investigating complex neuronal phenomena like spike-timing dependent plasticity and signal processing.