Motor Cortex Feedback Influences Sensory Processing by Modulating Network State

Zagha, E., Casale, A.E., Sachdev, R.N.S., McGinley, M.J., McCormick, D.A. (2013). Motor Cortex Feedback Influence Sensory Processing by Modulating Network State. Neuron 

Neuromodulators classically recognized as modulating network state, but slow and spatially distributed. Glutamate may play a role in modulation. Analyzing motor and sensory cortical areas of a specific whisker.

Non-whisking: low-frequency rhythms in M1 and S1. Highly coherent
Whisking: increased gamma in M1 and S1 - "activated state". Could see "activated state" even when no whisking or other obvious behavior.

Inactivation of M1 with muscimol reduced whisking, slowed network activity, reversed phase offset of coherence, and generally reduced frequencies in S1. Low freqs increase, high freqs decrease.

ChR2 activation of M1 (not sure which neurons - AAV virus and EMX1 Cre expression) decreases delta power in S1 and increases activity. In anesthitized animals, graded activation of M1 decreases delta and increases gamma. Very rapid - tens of milliseconds. Laminar recordings show that slow oscillations were eliminated in all layers, increased spiking primarily in infraganular neurons.

Now they're doing some layer analysis. Stimulate the whisker and you get current sinks in 2/3, 4, 5, current sources in 1 and 6 in S1. Activate M1 get almost opposite pattern: sinks in 5, 6, 1; sources in 2/3.

Figure 5. Evidence for Involvement of the Corticocortical Feedback Pathway
(A and B) CSD plots of average S1 responses from an example experiment. Brief (5 ms) deflections of the principal whisker (A) evoked onset current sinks in layers IV, II/III, and V and current sources in layers I and VI. Brief (5 ms) vM1 stimuli (B) evoked onset current sinks in layers V, VI, and layer I and current sources in layers II/III. Stimulus durations are depicted by the colored boxes in the bottom left of each plot. Color scales represent ±10 mV/mm stimuli and ±5 mV/mm2 for vM1 stimuli.
(C) Synaptic responses from layer V S1 neurons in vitro, evoked by stimulating axons and terminals of vM1 neurons in S1. The 2 ms light pulses are indicated by blue dots below traces. Responses from a regular spiking (RS) neuron, consisting of a short latency EPSP at rest (top) and an EPSP-IPSP sequence (middle) when depolarized to just below spike threshold. Bottom: EPSP from a fast spiking (FS) neuron at rest.
(D) Population data, quantifying connection probabilities (left), and response amplitudes (right) from vM1 inputs onto regular spiking and fast spiking neurons in S1.
(E) In vivo S1 response to stimulation of vM1 axons in S1. Limiting direct stimulation to the corticocortical vM1 axons was sufficient to evoke S1 activation. Error bars represent SE. See also Figure S3.

They applied CNQX on the surface. Low concentration just blocked the L1 projection of M1, high concentration blocked L1 and L5 projection. L5 neurons still activitated with low concentration.

They next blocked thalamus with mucimol. M1 activation doesnt need thalamus.

Suppressing M1 during stimulation shifts S1 response to biphasic activation. There's an initial stimulus driven burst, followed by silence and LFP rebound, followed by another slower burst. M1 activation during stimulation reduces the variability of responses in S1.


In general it seems that the feedback pathway puts S1 in the "up state", which is also useful because more sensory information can be processed in the up state. There's probably up and down states for different layers. The M1 feedback to the different layers is probably for different purposes -- S1 both needs regulation based on M1 information, and the informatoin itself (S1 needs to know motor state for correct processing).