Evidence map›Paper›PMID 36711682›Full record

ArticlebioRxiv : the preprint server for biology2023

Post-Ischemic Reorganization of Sensory Responses in Cerebral Cortex.

P Hayley, C Tuchek, S Dalla, J Borrell, M D Murphy, R J Nudo, D J Guggenmos

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

P HayleyDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas.
C TuchekDepartment of Neurosurgery, University of Kansas Medical Center, Kansas City, Kansas.
S DallaUniversity of Kansas School of Medicine Wichita, Wichita, Kansas.
J BorrellDepartment of Biomechanics, University of Nebraska Omaha, Omaha, Nebraska.
M D MurphyNeuroscience Institute, Carnegie Mellon University, Pittsburgh, Pennsylvania.
R J NudoDepartment of Rehabilitation Medicine and the Landon Center on Aging, University of Kansas Medical Center, Kansas City, Kansas.
D J GuggenmosDepartment of Rehabilitation Medicine and the Landon Center on Aging, University of Kansas Medical Center, Kansas City, Kansas.
University of Kansas Medical Center · USCarnegie Mellon University · USUniversity of Kansas · USUniversity of Nebraska at Omaha · US

Funding

REORGANIZATION OF MOTOR CORTEX FOLLOWING BRAIN INJURYR01NS030853 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI NUDO, RANDOLPH J. · 1993 to 2020
$6.5M
Kansas University Training Program in Neurological and Rehabilitation SciencesT32HD057850 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jacob J. Sosnoff · 2009 to 2026
$3.4M
NICHD NIH HHS T32 HD057850NINDS NIH HHS R01 NS030853
6 · The paper itself

Abstract

Sensorimotor integration is critical for generating skilled, volitional movements. While stroke tends to impact motor function, there are also often associated sensory deficits that contribute to overall behavioral deficits. Because many of the cortico-cortical projections participating in the generation of volitional movement either target or pass-through primary motor cortex (in rats, caudal forelimb area; CFA), any damage to CFA can lead to a subsequent disruption in information flow. As a result, the loss of sensory feedback is thought to contribute to motor dysfunction even when sensory areas are spared from injury. Previous research has suggested that the restoration of sensorimotor integration through reorganization or de novo neuronal connections is important for restoring function. Our goal was to determine if there was crosstalk between sensorimotor cortical areas with recovery from a primary motor cortex injury. First, we investigated if peripheral sensory stimulation would evoke responses in the rostral forelimb area (RFA), a rodent homologue to premotor cortex. We then sought to identify whether intracortical microstimulation-evoked activity in RFA would reciprocally modify the sensory response. We used seven rats with an ischemic lesion of CFA. Four weeks after injury, the rats' forepaw was mechanically stimulated under anesthesia and neural activity was recorded in the cortex. In a subset of trials, a small intracortical stimulation pulse was delivered in RFA either individually or paired with peripheral sensory stimulation. Our results point to post-ischemic connectivity between premotor and sensory cortex that may be related to functional recovery. Premotor recruitment during the sensory response was seen with a peak in spiking within RFA after the peripheral solenoid stimulation despite the damage to CFA. Furthermore, stimulation evoked activity in RFA modulated and disrupted the sensory response in sensory cortex, providing additional evidence for the transmission of premotor activity to sensory cortex and the sensitivity of sensory cortex to premotor cortex's influence. The strength of the modulatory effect may be related to the extent of the injury and the subsequent reshaping of cortical connections in response to network disruption.

Identifiers

PMID36711682
PMCPMC9882270
OpenAlexW4317603922

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.