Abstract
Deletion of NMDA receptors from parvalbumin-positive (PV+) interneurons disrupts gamma oscillations and destabilizes hippocampal spatial representations. How do NMDA receptors contribute to synaptic integration by PV+ interneurons to support robust neuronal assemblies? We show, using two-photon glutamate uncaging, that NMDA receptors underlie supralinear summation of synaptic inputs in mouse hippocampal CA1 PV+ interneurons, but only in dendrites innervated by feedback connections from local pyramidal neurons. Incorporating NMDA receptors at feedback connections in an oscillating excitatory-inhibitory spiking neural network provided for cooperative interactions among clustered inputs, and increased the stability of cell assemblies in the face of distracting inputs. Disrupted cell assembly interactions may underlie cognitive and sensory gating deficits seen with impaired NMDA receptor signaling in PV+ interneurons.
One Sentence Summary Supralinear dendritic integration via NMDA receptors provides a mechanism for input gating in gamma-oscillating circuits.