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Neonatal brain injury causes cerebellar learning deficits and Purkinje cell dysfunction
Aaron Sathyanesan1, Srikanya Kundu1, Joseph Abbah1
1Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC, USA.
Nature Communications
|August 15, 2018
Summary
Neonatal brain injury from hypoxia causes lasting motor problems in mice. A GABA reuptake inhibitor treatment improved motor function and Purkinje cell activity, suggesting a therapeutic target for prematurity-related movement disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Motor Control
Background:
- Premature infants face higher risks of locomotor disorders compared to full-term infants.
- Neonatal brain injury, induced by chronic sub-lethal hypoxia (Hx), affects cerebellar white matter and delays Purkinje cell (PC) development.
- The behavioral impact of these cellular changes in Hx mice remains largely uncharacterized.
Purpose of the Study:
- To investigate the long-term behavioral consequences of Hx-induced neonatal brain injury on motor function and cerebellar learning.
- To explore the role of Purkinje cell activity in Hx-related locomotor deficits.
- To assess the therapeutic potential of targeting the GABAergic system for prematurity-related motor impairments.
Main Methods:
- Utilized a chronic sub-lethal hypoxia (Hx) mouse model to simulate neonatal brain injury.
- Employed the Erasmus Ladder for assessing cerebellar-dependent motor behavior and learning.
- Conducted optogenetics experiments to measure Purkinje cell (PC) firing patterns.
- Administered a gamma-aminobutyric acid (GABA) reuptake inhibitor to evaluate treatment effects.
Main Results:
- Hx mice exhibited significant locomotor malperformance and long-term cerebellar learning deficits.
- Optogenetic stimulation revealed a marked decrease in spontaneous and photoevoked PC firing frequency in Hx mice.
- Treatment with a GABA reuptake inhibitor partially restored locomotor performance and enhanced PC firing.
Conclusions:
- Neonatal brain injury in Hx mice leads to a persistent phenotype of motor incoordination and impaired cerebellar learning.
- The developing GABAergic network is implicated as a critical factor in prematurity-related locomotor deficits.
- Targeting GABA reuptake presents a potential therapeutic strategy for addressing motor impairments in premature infants.
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