thesis

Cell type specific connections from primary motor to primary somatosensory cortex.

Abstract

Anatomical studies have shown that primary somatosensory (S1) and primary motor (M1) cortices are reciprocally connected. The pathway from primary motor cortex (M1) to primary somatosensory cortex (S1) is thought to influence activity in S1 by conveying a general modulatory signal and/or a copy of the motor command. In these studies, we investigated M1 synaptic inputs to S1 by injecting an AAV virus containing channelrhodopsin-2 and a fluorescent tag into M1. Consistent with previous results, we found labeling of M1 axons within S1 that was most robust in the deep layers and in L1. We recorded in vitro from excitatory neurons and two classes of inhibitory interneurons, fast-spiking and somatostatin-expressing inhibitory interneurons. All three cell types had a high probability of receiving direct excitatory M1 input, with both excitatory and inhibitory cells in L4 being the least likely to receive input from M1. Disynaptic inhibition was observed frequently, indicating that M1 recruits substantial inhibition within S1. A subpopulation of pyramidal neurons in layers 5 and 6 received especially strong input from M1, suggesting M1 differentially contacts classes of pyramidal neurons, such as those projecting to different sensorimotor centers at cortical and subcortical levels. We tested this hypothesis by combining optogenetic techniques to specifically label M1 synaptic inputs to S1 and retrograde tracing to identify specific populations of projection neurons in infragranular layers of S1. We determined that both the intrinsic properties and the magnitude of M1 input to an S1 pyramidal neuron is highly dependent on its projection target. Overall, our results suggest that activation of M1 evokes within S1 a general increase in excitatory and inhibitory synaptic activity that could contribute in a layer-specific manner to state-dependent changes in S1. Our results further indicate that M1 may specifically engage subcircuits within S1 in order to differentially regulate particular downstream cortical and subcortical processing centers

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