The provided code simulates a GABA_B receptor-mediated synaptic conductance incorporating pre-synaptic short-term plasticity. Here's a breakdown of the biological concepts underpinning this model: ### GABA_B Receptors GABA_B receptors are a type of metabotropic receptor, which, unlike ionotropic receptors, do not form ion channels themselves but instead mediate slower, longer-lasting inhibitory effects through G-protein coupled mechanisms. These receptors are typically activated by the neurotransmitter gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. In this code, the GABA_B receptor activity is modeled using a dual-exponential profile with parameters `tau_rise` and `tau_decay`, which represent the rise and decay times of the synaptic conductance. This dual-exponential model reflects the delayed and extended signaling that is characteristic of metabotropic receptor activation. ### Synaptic Conductance The synaptic conductance (g) changes as neurotransmitters bind to the receptors, influencing the neuronal membrane potential. This is captured through variables `A` and `B`, which interact to generate the dual-exponential conductance profile. The effect of this conductance on the neuronal membrane potential is governed by the reversal potential (`e`), which for GABAergic systems is typically hyperpolarizing, as reflected in the value set to -95 mV. ### Short-Term Plasticity Short-term synaptic plasticity is a mechanism through which synaptic strength is transiently modified by the history of activity. This model incorporates this phenomenon using parameters `U1`, `tau_rec`, and `tau_fac`, following the mechanisms described in Fuhrmann et al., 2002. - **Facilitation** (`tau_fac`): Involves a temporary increase in synaptic strength following an action potential, which decreases over time. The parameter `Use` represents a dynamic usage-dependent increase in probability for vesicle release. - **Depression** (`tau_rec`): This occurs when synaptic resources diminish with activity and recover over time.`P` symbolizes the probability of neurotransmitter release and recovery dynamics. - **Utilization of Release** (`U1`): Reflects the fraction of available neurotransmitter release sites that become active after an action potential. Together, `stp` is a boolean control that switches the synaptic plasticity mechanism on or off, allowing the modeler to focus either on the pure receptor dynamics or the influence of plasticity. ### Overall Model The model integrates these aspects to provide a realistic simulation of slow inhibitory synaptic transmission at GABA_B receptors, considering both the timescales of receptor binding and the transient changes in synaptic strength due to recent activity. This is significant for studying how inhibitory synapses modulate neuronal circuit dynamics and contribute to computational properties like neuronal network synchrony and stability.