## Biological Basis of the Code The code provided is a computational model representing both cortical and thalamic neuronal populations and their interconnections, aimed at simulating neuronal dynamics consistent with the studies by Benita et al. (2012) and Soplata et al. (2017). The biological basis of this model revolves around simulating the synaptic and electrical interactions that occur within and between these brain regions, using a detailed mechanistic approach. ### Cortical Model #### Populations 1. **Pyramidal neurons (PYdr and PYso):** - These are excitatory neurons that constitute a significant portion of the cortex. The model separates them into dendritic (PYdr) and somatic (PYso) compartments, highlighting the compartmental nature of their electrical and synaptic activity. - **Mechanisms:** - Ionic currents such as high-voltage activated calcium currents (`iHVA_PYdr_JB12`), persistent sodium currents (`iNaP_PYdr_JB12`), and others are typically involved in action potential generation and dendritic processing. - Applied noise mechanisms likely model the intrinsic synaptic variability and stochastic nature of neuronal activity. 2. **Interneurons (IN):** - These inhibitory neurons modulate cortical excitatory activity through mechanisms like `iGABAA`. Their inhibitory effects are crucial for maintaining the balance of excitatory and inhibitory signals within the cortex. #### Connections - **PY-PY and PY-IN:** - The model includes synaptic connections such as AMPA and NMDA receptors (`iAMPA_PYdr_PYso_JB12`, `iNMDA_IN_PYso_JB12`), which are critical for fast excitatory transmission and synaptic plasticity. - The inhibition is mediated through GABAergic synapses (`iGABAA_PYso_IN_JB12`), crucial for regulating excitability and synchrony in neural circuits. ### Thalamic Model #### Populations 1. **Thalamocortical (TC) neurons:** - These neurons relay sensory information to the cortex. Ionic mechanisms like low-threshold calcium currents (`iT_TC_AS17`) characterize their ability to exhibit bursting activity, important for rhythmic information transfer. 2. **Thalamic Reticular Nucleus (TRN) neurons:** - TRN provides inhibitory feedback to the thalamus, modulating sensory signal flow. The GABAergic mechanisms (`iGABAA_TRN_TRN_AS17`) in the model emphasize their role in gating thalamic sensory information. #### Connections - **TC-TRN:** - Inhibitory mechanisms (`iGABAA_TC_TRN_AS17`) ensure that the TRN can exert control over TC neuron activity, impacting sensory processing through bursts and thalamic oscillations. ### Thalamo-cortical Interactions - **Connections:** - The model includes pathways like `iAMPA_PYdr_TC`, which enable the thalamus to directly influence cortical excitatory neurons, reflecting the sensory signal propagation. - Feedback loops from the cortex to the thalamus through AMPA synapses (`iAMPA_TRN_PYso`) illustrate bidirectional communication essential for sensory processing and cortical rhythm generation. ### Key Biological Aspects - **Synaptic Dynamics:** Incorporation of AMPA and NMDA receptors models fast excitatory transmission and synaptic potentiation/depression processes. - **Ionic Currents:** Detailed ionic currents represent cellular excitability and diverse firing patterns in neurons. - **Stochastic Noise:** The inclusion of noise reflects the inherently variable environment of synaptic transmission and the probabilistic nature of neuronal firing. Overall, the model aims to faithfully replicate the complex dynamics of cortical-thalamic interactions, focusing on excitability, synaptic transmission, and neural feedback mechanisms that are fundamental to understanding brain function and dysfunction.