Voluntary movements are driven by coordinated activity across a large population of motor cortical neurons. Formation of this activity is controlled by local interactions and long-range inputs. How remote areas of the brain communicate with motor cortical neurons to effectively drive movement remains unclear. We address this question by studying the cerebellar-thalamocortical system. We find that thalamic input to the motor cortex triggers feedforward inhibition by contacting inhibitory cells via highly effective GluR2-lacking AMPA receptors and that, during task performance, the activity of parvalbumin (PV) and pyramidal cells exhibits relations comparable with movement parameters. We also find that the movement-related activity of PV interneurons precedes firing of pyramidal cells. This counterintuitive sequence of events, where inhibitory cells are recruited more strongly and before excitatory cells, may amplify the cortical effect of cerebellar signals in a way that exceeds their sheer synaptic efficacy by suppressing other inputs.
Bibliographical noteFunding Information:
We thank Prof. A. Thiele, Dr. Christian Brandt, and Dr. Jochem van Kempen for teaching us the method of ionophoresis developed in Thiele’s lab. This work was funded by the Israel Science Foundation ( ISF-1801/18 ), the Deutsche Forschungsgemeinschaft (431549029 -SFB 1451 ), the NIH ( R01 NS012542 to S.I.P.), the Edmund and Lily Safra fellowship for postdoctorate research (to A.N.), and generous support from the Baruch Foundation (to Y.P.).
© 2022 The Author(s)
- CP: Neuroscience
- PV-positive interneurons
- feedforward inhibition
- motor control
- non-human primates