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Shoup, A.

Publications and source records attributed to Shoup, A..

3 recordsLinked to original sources

Coordination of spike timing among the neurons of the cerebellum

We tend to think of neurons as either excitatory or inhibitory, but certain neurons chemically inhibit their downstream targets while electrically exciting each other. For example, in the cerebellum, molecular layer interneurons type 1 (MLI1s) inhibit Purkinje cells (P-cells) via release of GABA but promote spiking in each other via gap junctions. P-cells inhibit nucleus neurons while exciting each other via ephaptic coupling. What is gained by excitatory interactions among inhibitory neurons? We recorded from the marmoset cerebellum during saccadic eye movements and found that spike timing in electrically coupled P-cell pairs, as well as MLI1 pairs, exhibited a mathematical regularity: as firing rates increased, the rate of spikes that were within 1ms of each other grew disproportionately while 2-4ms intervals were suppressed. We isolated triplets in which two MLI1s converged onto a single P-cell and found that if the MLI1s spiked within 1ms of each other, they produced superposition of their individual effects on their target; a deep inhibition followed by a post-inhibitory rebound. This enhanced the temporal precision in the downstream P-cells next spike. However, when the MLI1s spiked 2-4ms apart, the two spikes interfered with each other, producing partial cancellation. Thus, electrical coupling of inhibitory neurons promoted production of spike intervals that induced constructive superposition. This reduced the variance of spike timing in the downstream neuron.

neuroscience↗

A vector calculus for neural computation in the cerebellum

Null space theory predicts that a neuron will often generate spikes not to produce behavior, but to prevent another neurons impact on behavior. Here, we present a direct test of this theory in the brain. In the marmoset cerebellum, spike-triggered averaging identified a vector for each Purkinje cell (P-cell) along which its spikes displaced the eyes. Two spikes in two different P-cells produced superposition of their vectors. In the resulting population activity, the spikes were canceled if their contributions were perpendicular to the intended movement. Mossy fibers provided a copy of the motor commands and the sensory goal of the movement. Molecular layer interneurons transformed these inputs so that the P-cell population predicted when the movement had reached the goal and should be stopped.

neuroscience↗

Rejuvenating silicon probes for acute electrophysiology

Electrophysiological recording with a new probe often yields better signal quality than with a used probe. Why does the signal quality degrade after only a few experiments? Here, we considered silicon probes in which the contacts are densely packed, and each is coated with a conductive polymer that increases its surface area. We tested 12 Cambridge Neurotech silicon probes during 61 recording sessions from the brain of 3 marmosets. Out of the box, each probe arrived with an electrodeposited polymer coating on 64 gold contacts, and an impedance of around 50k Ohms. With repeated use, the impedance increased and there was a corresponding decrease in the number of well-isolated neurons. Imaging of the probes suggested that the reduction in signal quality was due to a gradual loss of the polymer coating. To rejuvenate the probes, we first stripped the contacts, completely removing their polymer coating, and then recoated them in a solution of 10 mM EDOT monomer with 32 uM PSS using a current density of about 3mA/cm2 for 30 seconds. This recoating process not only returned probe impedance to around 50k Ohms, it also yielded significantly improved signal quality during neurophysiological recordings. Thus, insertion into the brain promoted loss of the polymer that coated the contacts of the silicon probes. This led to degradation of signal quality, but recoating rejuvenated the probes.

neuroscience↗