Research targets long-term brain deficits in cardiac arrest survivors
LSU Health Sciences Center New Orleans News Jul 27, 2017
Research conducted by Jason Middleton, PhD, Assistant Professor of Cell Biology and Anatomy, and Neuroscience at LSU Health New Orleans School of Medicine, and colleagues may lead to a treatment to prevent long–term sensory problems by restoring normal brain function in survivors of cardiac arrest.
The study, done in a rodent model and using modeling data, was published online in the journal eNeuro.
The research team studied the long–term impact of cardiac arrest on the cortex in a rat model. They measured sensory response and found that after oxygen deprivation, the sensory circuits in the cortex are less responsive with behavioral deficits. Their data suggest that cardiac arrest and resuscitation permanently affect cortical circuit function in survivors.
ÂOur work characterizes the changes that occur in the sensory cortex after a form of global hypoxic injury in juvenile rats, notes Dr. Middleton. ÂThe injury did not result in widespread cell death as occurs in other forms of acute, focal ischemic injury; the deficits uncovered were subtler and reflected decreased ability of the cortex to discriminate sensory stimuli. We used computer modeling of the neural network to implicate changes in the balance of excitatory and inhibitory synaptic transmission in the cortex.Â
ÂThese findings lay the groundwork for further studies to pinpoint therapeutic targets to restore excitatory/inhibitory balance in the injured brain and mitigate sensory deficits later in life, concludes Middleton.
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The study, done in a rodent model and using modeling data, was published online in the journal eNeuro.
The research team studied the long–term impact of cardiac arrest on the cortex in a rat model. They measured sensory response and found that after oxygen deprivation, the sensory circuits in the cortex are less responsive with behavioral deficits. Their data suggest that cardiac arrest and resuscitation permanently affect cortical circuit function in survivors.
ÂOur work characterizes the changes that occur in the sensory cortex after a form of global hypoxic injury in juvenile rats, notes Dr. Middleton. ÂThe injury did not result in widespread cell death as occurs in other forms of acute, focal ischemic injury; the deficits uncovered were subtler and reflected decreased ability of the cortex to discriminate sensory stimuli. We used computer modeling of the neural network to implicate changes in the balance of excitatory and inhibitory synaptic transmission in the cortex.Â
ÂThese findings lay the groundwork for further studies to pinpoint therapeutic targets to restore excitatory/inhibitory balance in the injured brain and mitigate sensory deficits later in life, concludes Middleton.
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