Delevich, K. Tucciarone, J. Huang, Z. J. Li, B.
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, and MSTP/Neuroscience Graduate Program, Stony Brook University, Stony Brook, New York 11790.
Although the medial prefrontal cortex (mPFC) is classically defined by its reciprocal connections with the mediodorsal thalamic nucleus (MD), the nature of information transfer between MD and mPFC is poorly understood. In sensory thalamocortical pathways, thalamic recruitment of feedforward inhibition mediated by fast-spiking, putative parvalbumin-expressing (PV) interneurons is a key feature that enables cortical neurons to represent sensory stimuli with high temporal fidelity. Whether a similar circuit mechanism is in place for the projection from theMD(a higher-order thalamic nucleus that does not receive direct input from the periphery) to themPFCis unknown. Here we show in mice that inputs from the MD drive disynaptic feed forward inhibition in the dorsal anterior cingulate cortex (dACC) sub region of them PFC. In particular, we demonstrate that axons arising from MD neurons directly synapse onto and excite PV interneurons that in turn mediate feedforward inhibition of pyramidal neurons in layer 3 of the dACC. This feedforward inhibition in the dACC limits the time window during which pyramidal neurons integrate excitatory synaptic inputs and fire action potentials, but in a manner that allows for greater flexibility than in sensory cortex. These findings provide a foundation for understanding the role of MDPFC circuit function in cognition.
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The Journal of Neurosceicne
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