Nonlinear Dendritic Integration Supports Up-Down States in Single Neurons.

Area of Science:

• Neuroscience
• Computational Neuroscience

Background:

• Cortical neuron activity changes are linked to network dynamics.
• Up-Down states, abrupt neuronal transitions, are typically attributed to afferent neuron activity.
• Cellular physiology and morphology may also influence Up-Down states.

Purpose of the Study:

• To examine the impact of dendritic nonlinearities, specifically voltage-dependent NMDA receptors, on cortical neuron responses.
• To compare neuron models with and without dendritic nonlinearities under balanced synaptic input.
• To investigate the role of cellular properties in the emergence of cortical bistability.

Main Methods:

• Utilized a two-compartment neuron model with segregated dendrites.
• Compared model cells with and without dendritic nonlinearities.
• Simulated balanced excitatory/inhibitory synaptic inputs and cortical-like input.

Main Results:

• NMDA receptors enhanced somatic firing and cross-compartment membrane potential correlation.
• Dendritic nonlinearities induced bimodality in somatic potential distribution.
• Dendritic nonlinearities detected small input fluctuations, generating Up-Down states resembling experimental data.
• Up-Down states occurred in recurrent networks with partially disabled NMDA receptors.

Conclusions:

• Dendritic nonlinearities, mediated by NMDA receptors, are a significant factor in generating cortical Up-Down states.
• Cellular properties can contribute to neuronal bistability independently of network-level features.
• A dissociation exists between cellular and network contributions to Up-Down state emergence.
• Highlights the interplay between dendritic integration and activity-driven dynamics in cortical bistability.