The code provided is part of a computational model designed to simulate various aspects of synaptic and neuronal behavior, focusing primarily on glutamatergic synaptic transmission. The biological basis of this code involves several key components and mechanisms related to neuronal activity:
Glutamate is the principal excitatory neurotransmitter in the central nervous system (CNS). The code models the effects of varying glutamate-related parameters, indicative of studying excitatory synapses.
Glutamate Amplitude and Location: These variables (glutAmp and glutLoc) likely represent the strength and spatial positioning of glutamate release within a neural circuit. Variations in these parameters can mimic different degrees of synaptic activation, potentially reflecting changes in synaptic weight or post-synaptic sensitivity.
Ratio of AMPA to NMDA Receptors: The parameter ratioAMPANMDA models the relative contributions of AMPA and NMDA receptor-mediated currents to synaptic transmission. AMPA receptors mediate fast excitatory currents, while NMDA receptors are involved in slower synaptic integration and plasticity.
The dynamics of glutamate's action in the synapse are further explored by varying the spread (glutSpread), delay (glutDelay), and decay (glutDecay) of its effects.
Glutamate Spread: Describes how widely neurotransmitter effects spread from the release site, possibly simulating diffusion in the synaptic cleft.
Glutamate Delay: The time taken for the effects of glutamate to manifest, which can correspond to delays in receptor activation or signal propagation.
Glutamate Decay: Represents the reduction of glutamate efficacy over space or time, possibly modeling receptor desensitization or neurotransmitter reuptake.
The parameter allNaScale suggests exploration into sodium channel conductance, specifically the inhibition or facilitation, which could reflect conditions like tetrodotoxin (TTX) application.
The overarching aim of this modeling effort is to explore how different parameters related to glutamatergic transmission and ion channel conductance affect neuronal activity and synaptic integration. Variations in synaptic strength, spatial dynamics, receptor composition, and channel conductance give insight into key mechanisms of neural processing and plasticity, offering potential implications for understanding conditions like synaptic depression, potentiation, and network-level modulations in the CNS.