# CORTICOSPINAL MECHANISMS FOR HIGH FAT DIET IMPEDING STROKE RECOVERY

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2020 · $333,568

## Abstract

SUMMARY / ABSTRACT
Comorbid metabolic conditions of stroke, including obesity and diabetes, worsen stroke injury and reduce the
capacity for stroke recovery. Given that stroke and these comorbid metabolic conditions are highly prevalent,
the goal of this project is to understand how their interactions mechanistically affect the corticospinal motor
system using high fat diet (HFD) as a model of metabolic disruption. In preliminary testing, HFD profoundly
worsens behavioral motor recovery after experimental stroke. HFD and experimental stroke also cause an
abnormal and profound emergence of lower extremity motor commands in areas of motor cortex that show little
of these commands in otherwise healthy conditions or with experimental stroke injury and control diet. These
abnormal lower extremity motor commands appear to be mechanistically due to increased synaptic signaling
within the corticospinal system at connections that have not been well identified in this pathway. Volitional skilled
motor control of the extremities is primarily achieved by the corticospinal tract and this pathway is often damaged
by stroke resulting in severe disability. The canonical view of the corticospinal tract is that it is a synaptic circuit,
from layer 5 pyramidal cells (L5PCs) in motor cortex, to spinal motor neurons that themselves signal skeletal
muscle (CST= L5PCs→ spinal motor neurons→ skeletal muscle). L5PCs that project to cervical spinal cord
(cervical-projecting) are thought to control upper extremity function whereas L5PCs that project to lumbar spinal
cord (lumbar-projecting) are thought to control lower extremity function. What is less known is whether single
L5PCs can innervate cervical and lumbar levels of spinal cord and thus contribute motor control to upper and
lower extremities. Similarly, it is recognized that L5PCs synapse on one-another (L5PCs→L5PCs) however it is
not known whether this is true between cervical-projecting L5PCs and lumbar-projecting L5PCs during stroke
recovery. Experiments here will test these seldom studied connections of the corticospinal system because they
may underpin the abnormal emergence of lower extremity motor commands that arise when HFD is combined
with experimental stroke. To investigate these hypotheses, we propose 3 aims: Aim 1. Determine whether
distribution and in vivo signaling of cervical- and lumbar-projecting L5PCs can support abnormal emergence of
hindlimb motor commands in anterior motor cortex when HFD is combined with experimental stroke. Aim 2. Test
whether physiology of cervical- and lumbar-projecting L5PCs can support abnormal emergence of hindlimb
motor commands in anterior motor cortex when HFD is combined with experimental stroke. Aim 3. Test timing,
duration and persistence of HFD to exacerbate upper and lower extremity deficits after experimental stroke
injury. This proposal aims to determine the corticospinal circuits responsible for this abnormal plasticity of lower
extremity motor control in ord...

## Key facts

- **NIH application ID:** 9866627
- **Project number:** 1R01NS114651-01
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **Principal Investigator:** JEFFERY ALLEN BOYCHUK
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $333,568
- **Award type:** 1
- **Project period:** 2019-12-15 → 2024-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9866627

## Citation

> US National Institutes of Health, RePORTER application 9866627, CORTICOSPINAL MECHANISMS FOR HIGH FAT DIET IMPEDING STROKE RECOVERY (1R01NS114651-01). Retrieved via AI Analytics 2026-06-14 from https://api.ai-analytics.org/grant/nih/9866627. Licensed CC0.

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