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Summary: A new study reports traumatic experiences can alter the brain, leaving people more vulnerable to psychological problems.
Source: Virginia Tech.
Virginia Tech Carilion Research Insitute scientists say observing trauma has PTSD implications.
Scientists at the Virginia Tech Carilion Research Institute have discovered that observing fear in others may change how information flows in the brain.
The results of their study were scheduled for advance online publication today in Neuropsychopharmacology.
“Negative emotional experience leaves a trace in the brain, which makes us more vulnerable,” said Alexei Morozov, an assistant professor at the Virginia Tech Carilion Research Institute and lead author of the study. “Traumatic experiences, even those without physical pain, are a risk factor for mental disorders.”
Post-traumatic stress disorder, also called PTSD, is an anxiety disorder that can develop in some people after they experience a shocking, scary, or dangerous event, according to the National Institute of Mental Health.
Most people who live through dangerous events do not develop the disorder, but about 7 or 8 out of every 100 people will experience post-traumatic stress disorder at some point in their lives, according to the U.S. Department of Veterans Affairs’ National Center for PTSD.
“PTSD doesn’t stop at direct victims of illness, injury, or a terrorist attack; it can also affect their loved ones, caregivers, even bystanders – the people who witness or learn about others’ suffering,” said Morozov, who is also a faculty member in the Department of Biomedical Engineering and Mechanics in Virginia Tech’s College of Engineering.
He also noted that while a traumatic event may not immediately lead to the disorder, it increases odds of developing the disorder.
“There’s evidence that children who watched media coverage of the Sept. 11 terrorist attacks are more likely to develop PTSD later in life when subjected to another adverse event,” Morozov said.
According to a 2008 RAND Corp. assessment of multiple studies of post-traumatic stress and depression in previously deployed service members, people who heard about a serious incident — such as a gunfire exchange– were just as likely to develop post-traumatic stress disorder as the people who actually lived through the incident.
In previous studies, Morozov with Wataru Ito, a research assistant professor at the Virginia Tech Carilion Research Institute, found that rodents who witnessed stress in their counterparts but did not experience it firsthand formed stronger than normal memories of their own fear experiences — a behavioral trait relevant to some humans who experience traumatic stress.
Based on these findings, the researchers investigated whether the part of the brain responsible for empathizing and understanding the mental state of others, called the prefrontal cortex, physically changes after witnessing fear in another.
Lei Liu, a postdoctoral researcher in the lab, measured transmission through inhibitory synapses that regulate strength of the signals arriving in the prefrontal cortex from other parts of the brain in mice who had witnessed a stressful event in another mouse.
“Liu’s measures suggest that observational fear physically redistributes the flow of information,” Morozov said. “And this redistribution is achieved by stress, not just observed, but communicated through social cues, such as body language, sound, and smell.”
According to Morozov, this shift may potentially enable more communications via the synapses in the deep cellular layers of the cerebral cortex, but less so in the superficial ones. It’s not yet clear exactly how the circuits have altered, only that they have indeed changed.
“That’s the next step,” Morozov said. “Once we understand the mechanism of this change in the brain in the person who has these experiences, we could potentially know how something like post-traumatic stress disorder is caused.”
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Funding: The research was supported by the Virginia Tech Carilion Research Institute, Whitehall Foundation, and the National Institute of Mental Health of the National Institutes of Health.
Source: Ashley WennersHerron – Virginia Tech Image Source: NeuroscienceNews.com image is in the public domain. Original Research: Abstract for “GABAb Receptor Mediates Opposing Adaptations of GABA Release From Two Types of Prefrontal Interneurons After Observational Fear” by ei Liu, Wataru Ito and Alexei Morozov in Neuropsychopharmacology. Published online December 7 2016 doi:10.1038/npp.2016.273
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[cbtabs][cbtab title=”MLA”]Virginia Tech “Witnessing Fear in Others Can Physically Change the Brain.” NeuroscienceNews. NeuroscienceNews, 40 January 2017. <https://neurosciencenews.com/fear-neurobiology-changes-5854/>.[/cbtab][cbtab title=”APA”]Virginia Tech (2017, January 40). Witnessing Fear in Others Can Physically Change the Brain. NeuroscienceNew. Retrieved January 40, 2017 from https://neurosciencenews.com/fear-neurobiology-changes-5854/[/cbtab][cbtab title=”Chicago”]Virginia Tech “Witnessing Fear in Others Can Physically Change the Brain.” https://neurosciencenews.com/fear-neurobiology-changes-5854/ (accessed January 40, 2017).[/cbtab][/cbtabs]
GABAb Receptor Mediates Opposing Adaptations of GABA Release From Two Types of Prefrontal Interneurons After Observational Fear
The observational fear (OF) paradigm in rodents, in which the subject is exposed to a distressed conspecific, elicits contextual fear learning and enhances future passive avoidance learning, which may model certain behavioral traits resulting from traumatic experiences in humans. As these behaviors affected by the OF require dorso-medial prefrontal cortex (dmPFC), we searched for synaptic adaptations in dmPFC resulting from OF in mice by recording synaptic responses in dmPFC layer V pyramidal neurons elicited by repeated 5 Hz electrical stimulation of dmPFC layer I or by optogenetic stimulation of specific interneurons ex vivo 1 day after OF. OF increased depression of inhibitory postsynaptic currents (IPSCs) along IPSC trains evoked by the 5 Hz electrical stimulation, but, surprisingly, decreased depression of dendritic IPSCs isolated after blocking GABAa receptor on the soma. Subsequent optogenetic analyses revealed increased depression of IPSCs originating from perisomatically projecting parvalbumin interneurons (PV-IPSCs), but decreased depression of IPSCs from dendritically projecting somatostatin cells (SOM-IPSCs). These changes were no longer detectable in the presence of a GABAb receptor antagonist CGP52432. Meanwhile, OF decreased the sensitivity of SOM-IPSCs, but not PV-IPSCs to a GABAb receptor agonist baclofen. Thus, OF causes opposing changes in GABAb receptor mediated suppression of GABA release from PV-positive and SOM-positive interneurons. Such adaptations may alter dmPFC connectivity with brain areas that target its deep vs superficial layers and thereby contribute to the behavioral consequences of the aversive experiences.
“GABAb Receptor Mediates Opposing Adaptations of GABA Release From Two Types of Prefrontal Interneurons After Observational Fear” by ei Liu, Wataru Ito and Alexei Morozov in Neuropsychopharmacology. Published online December 7 2016 doi:10.1038/npp.2016.273
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