Support for the Low-Dimensional Movement Control Hypothesis
Julien Rossato, Simon Avrillon, Kylie Jane Tucker, Dario Farina, and Francois Hug
(see article e0702242024)
To generate a movement, spinal motor neurons must receive the correct inputs from the brain. This sounds simple enough, but it remains unclear how neurons in the brain can accurately target such a large quantity of motor neurons with high precision. Rossato et al. explored this in their study in this issue. In a group of male participants, they assessed how well motor units (defined as a motor neuron and all the skeletal fibers innervated by that neuron) could be controlled independently. To do this, they used an online program that presents firing rates as visual feedback while participants perform different muscle contractions. They found that individual motor units could not be controlled independently and that they were segregated into synergistic groups. These findings suggest that there are common synaptic inputs from the cortex onto groups of motor neurons and not individual motor neurons, which supports the “low-dimensional movement control” hypothesis in the field.
Molecular, Cellular, and Circuit-Based Insights into Recovery from Anesthesia
Yi Zhao, Mengchan Ou, Jin Liu, Jingyao Jiang, Donghang Zhang et al.
(see article e1808232024)
Our understanding of how anesthesia works is centered on neuronal activity. While there is evidence for astrocytes promoting recovery from anesthesia, mechanisms through which this occurs are unknown. To this end, Zhao et al. used in vivo and in vitro electrophysiological recordings in mice to explore mechanisms of astrocyte-mediated recovery from anesthesia, specifically sevoflurane. They found that activating astrocytes in the paraventricular thalamus (PVT) promoted consciousness following sevoflurane. Pointing to a mechanism, they found that knocking down inward rectifying potassium channel 4.1 (Kir4.1) also promoted consciousness recovery. Following these discoveries, Zhao et al. used single-cell RNA sequencing to uncover two glutamatergic neuron subtypes in the PVT. Recording from these cells using patch-clamp electrophysiology revealed that astrocytic Kir4.1-mediated modulation of sevoflurane worked primarily on a PVT neuron subpopulation projecting to the medial prefrontal cortex (mPFC). Altogether, these findings suggest that increased activity of PVT neurons projecting to the mPFC enhances recovery from sevoflurane and that this may be attributed to inhibition of Kir4.1 on PVT astrocytes. These findings uncover how astrocytes support recovery from anesthesia on a molecular, cellular, and circuit level and are highly informative for future preclinical and clinical work.
Representative images of the immunofluorescence staining that was done to show expression of choline acetyltransferase (ChAT) or metabotropic glutamate receptor 1 (Grm1) in the PVT. See Zhao et al. for more information.
Footnotes
This Week in The Journal was written by Paige McKeon
