RT Journal Article
SR Electronic
T1 A Network Model of the Modulation of γ Oscillations by NMDA Receptors in Cerebral Cortex
JF eneuro
JO eNeuro
FD Society for Neuroscience
SP ENEURO.0157-23.2023
DO 10.1523/ENEURO.0157-23.2023
VO 10
IS 11
A1 Susin, Eduarda
A1 Destexhe, Alain
YR 2023
UL http://www.eneuro.org/content/10/11/ENEURO.0157-23.2023.abstract
AB Psychotic drugs such as ketamine induce symptoms close to schizophrenia and stimulate the production of γ oscillations, as also seen in patients, but the underlying mechanisms are still unclear. Here, we have used computational models of cortical networks generating γ oscillations, and have integrated the action of drugs such as ketamine to partially block NMDA receptors (NMDARs). The model can reproduce the paradoxical increase of γ oscillations by NMDA receptor antagonists, assuming that antagonists affect NMDA receptors with higher affinity on inhibitory interneurons. We next used the model to compare the responsiveness of the network to external stimuli, and found that when NMDA channels are blocked, an increase of γ power is observed altogether with an increase of network responsiveness. However, this responsiveness increase applies not only to γ states, but also to asynchronous states with no apparent γ. We conclude that NMDA antagonists induce an increased excitability state, which may or may not produce γ oscillations, but the response to external inputs is exacerbated, which may explain phenomena such as altered perception or hallucinations.