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Parvalbumin Interneurons Shape Neuronal Vulnerability in Blunt TBI
Akila Chandrasekar1, Florian Olde Heuvel1, Lilla Tar1
1Department of Neurology, Ulm University, Ulm-DE, Germany.
Cerebral Cortex (New York, N.Y. : 1991)
|July 9, 2018
Summary
In traumatic brain injury (TBI), inhibiting Parvalbumin (PV) interneurons protects neurons and reduces damage. Conversely, activating PV interneurons worsens neuronal survival after TBI.
Area of Science:
- Neuroscience
- Traumatic Brain Injury Research
- Cellular Neurophysiology
Background:
- Traumatic brain injury (TBI) can cause excessive neuronal excitation, leading to acute damage.
- Parvalbumin (PV) interneurons are critical for regulating cortical excitability and inhibition, but their specific role in TBI pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of PV interneurons in neuronal vulnerability following acute TBI.
- To explore how modulating the activity of PV interneurons impacts neuronal survival and brain injury cascades.
Main Methods:
- Utilized chemogenetics (Pharmacologically Selective Activation Module/Pharmacologically Selective Effector Module) to control PV-Cre+ neurons.
- Employed Designer Receptors Exclusively Activated by Designer Drug (DREADD) technology to manipulate principal neuron excitability in a TBI model.
- Assessed neuronal survival and gliosis at 7 days post-injury (dpi).
Main Results:
- Inactivation of PV interneurons shortly after TBI enhanced principal neuron survival and reduced gliosis.
- Activation of PV interneurons led to decreased neuronal survival.
- The neuroprotective effect of PV interneuron inactivation was dependent on activity-dependent signaling in principal neurons, as indicated by suppression with a nuclear calcium buffer.
- Directly increasing principal neuron excitability using DREADDs also conferred protection.
Conclusions:
- Sustaining neuronal excitation in the early stages of TBI may promote activity-dependent survival and reduce vulnerability.
- Overactivation of perisomatic inhibition by PV interneurons is detrimental to neuronal integrity after TBI.
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