# Motor Cortex Microcircuitry Underlying Movement Control and Learning

> **NIH NIH R01** · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · 2020 · $342,344

## Abstract

Project Abstract
 Plasticity in primary motor cortex (M1) circuitry is essential for motor learning and skilled
performance. Maladaptive plasticity contributes to movement disorders such as dystonia. This
proposal focuses on the role of inhibition in adaptive plasticity. How specific types of inhibitory
neurons in M1 are recruited by sensorimotor inputs is unknown.
 Aim 1 explores monosynaptic excitation to three different interneuron types: parvalbumin
(PV), somatostatin (SOM) and vasoactive intestinal peptide (VIP) expressing neurons. We will
quantify the strength of corticocortical and thalamocortical inputs to each of these three cell
types. We will use whole-cell recording of transgenically labeled neurons in acute brainslices.
We will use optogenetic approaches to specifically stimulate corticocortical and thalamocortical
inputs and quantify synaptic strength. Our preliminary data show that thalamus and cortex
excite PV+ interneurons in complementary subsets of interneurons in different cortical layers.
Since synaptic plasticity follows different rules between these two pathways, and inhibition
regulates cortical plasticity, this different may help explain why plasticity in these circuits is
different. Aim 2 studies the disynaptic inhibition provided by cortical and thalamic inputs. We will
determine if inhibition is recruited in pathway-specific circuits, or as a general blanket for
silencing all of cortex. We hypothesize that different M1 inputs recruit different sources of
inhibition, allowing cortical circuits to specifically tune the gain of inhibition to the incoming input,
instead of a generically downregulating all local circuitry. Aim 3 will identify sites of plasticity at
interneuron connections by developing an M1-dependent skilled reaching task. We will then
record inhibition to neurons active and inactive during the task to compare amplitude of
inhibition from PV+ or SOM+ interneurons.
 Collectively, these Aims will determine the connections by which inhibition is recruited by
distinct inputs to motor cortex, identifying the specific cell types targeted and how these circuits
contribute to plasticity during motor learning. Because disruption of M1 circuitry is implicated in
movement disorders, knowledge about the circuitry of M1 may contribute to targeted
approaches to treat M1 dysfunction.

## Key facts

- **NIH application ID:** 9829588
- **Project number:** 5R01NS103993-03
- **Recipient organization:** UNIVERSITY OF PITTSBURGH AT PITTSBURGH
- **Principal Investigator:** Bryan McIver Hooks
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $342,344
- **Award type:** 5
- **Project period:** 2017-12-01 → 2022-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9829588

## Citation

> US National Institutes of Health, RePORTER application 9829588, Motor Cortex Microcircuitry Underlying Movement Control and Learning (5R01NS103993-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9829588. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*