Classification of neurons in the primate reticular formation and changes after recovery from pyramidal tract lesion

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Abstract

The reticular formation is important in primate motor control, both in health and during recovery after brain damage. Little is known about the different neurons present in the reticular nuclei. Here we recorded extracellular spikes from the reticular formation in five healthy female awake behaving monkeys (193 cells), and in two female monkeys 1 year after recovery from a unilateral pyramidal tract lesion (125 cells). Analysis of spike shape and four measures derived from the interspike interval distribution identified four clusters of neurons in control animals. Cluster 1 cellshadaslowfiringrate. Cluster 2 cell shad narrow spikes and irregular firing, which of ten included high-frequencybursts. Cluster3cellswere highly rhythmic and fast firing. Cluster 4 cells showed negative spikes. A separate population of 42 cells was antidromically identified as reticulospinal neurons in five anesthetized female monkeys. The distribution of spike width in these cells closely overlaid the distribution for cluster 2, leading us tentatively to suggest that cluster 2 included neurons with reticulospinal projections. In animals after corticospinal lesion, cells could be identified in all four clusters. The firing rate of cells in clusters 1 and 2 was increased in lesioned animals relative to control animals (by 52% and 60%, respectively); cells in cluster 2 were also more regular and more bursting in the lesioned animals. We suggest that changes in both membrane properties and local circuits within the reticular formation occur following lesioning, potentially increasing reticulospinal output to help compensate for lost corticospinal descending drive.

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Zaaimi, B., Soteropoulos, D. S., Fisher, K. M., Riddle, C. N., & Baker, S. N. (2018). Classification of neurons in the primate reticular formation and changes after recovery from pyramidal tract lesion. Journal of Neuroscience, 38(27), 6190–6206. https://doi.org/10.1523/JNEUROSCI.3371-17.2018

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