Glial cells influence brain activity by releasing molecules that activate NMDA receptors (NMDARs) found on the surface of neurons, thereby triggering slow inward currents in neurons. However, the bulk of research on NMDAR-dependent slow inward currents has focused on the cell body rather than neuronal projections called dendrites, which help integrate signals from multiple cells and process information in the brain.
Researchers used electrophysiological and pharmacological techniques to examine slow excitatory potentials, the voltage responses to slow inward currents in the cell bodies and dendrites of neurons in brain slices from the rat hippocampus. The authors found that the majority of NMDAR-dependent slow excitatory potentials originated in dendrites rather than the cell body.
The magnitude and time course of slow excitatory potentials in dendrites were regulated by voltage-gated ion channels, which compartmentalized the spread of slow excitatory potentials within specific segments of the dendritic arbor.
According to the authors, the findings reveal mechanisms by which slow excitatory potentials could generate localized neuronal responses that distinguish between the activation of different glial cells, thereby enhancing the neuron’s information processing capacity.
Further, the study demonstrates that dendrites and their voltage-gated ion channels play an active role in regulating neuron–glia communication and network plasticity.