For those with Post Traumatic Stress Disorder (PTSD), norepinephrine and serotonin levels remain high during the rapid eye movement (REM) sleep stage. This condition reduces the brain’s ability to inhibit fear-expression neurons through neural rhythms sent between the prefrontal cortex and amygdala. This stage tends to be fraught with emotionally charged dreams. A new study by Virginia Tech researchers offers insights into how therapeutic strategies that unlock the higher frequencies could improve sleep quality for PTSD patients.
The sleep stage is critical for processing emotional memories. Previous experiments have shown that rhythmic interactions between the amygdala and the prefrontal cortex during REM sleep reduce the expression of fear-associated memories. Usually, the sleeping brain can evoke emotional memories, process them, and lessen their emotional charge. Study author and assistant professor of neuroscience Dr. Vijayan said that it is a process that may be explained by an evolutionary drive to evaluate important memories, specifically those associated with fear. PTSD patients experience recurring nightmares or traumatic memories that seem resistant to losing their emotional charge.
Creating biophysically based models of REM sleep enabled the team to study what allows brain rhythms to help with emotional memory processing. In particular, this approach illuminated how PTSD disrupts this processing and causes patients to relive memories. The models allowed the scientists to manipulate the REM sleep conditions to focus on neurotransmitter levels. They began with models of sleep conditions considered reflective of a healthy individual’s brain and reduced norepinephrine and serotonin levels to simulate REM sleep (the neurotransmitter levels of norepinephrine and serotonin usually drop during REM sleep).
The researchers linked lowered neurotransmitter levels to the brain’s ability to inhibit fear expression cells by analyzing the rhythms sent between the prefrontal cortex and the amygdala of these models. The team then examined how the atypical neurotransmitter levels seen in the sleeping PTSD patient’s brain could disrupt the fear-reducing capability of those brain rhythms.
They found that rhythmic neural interactions between the prefrontal cortex and the amygdala strengthened connections between those two areas. Brain rhythms emitting from the prefrontal cortex effectively inhibited the activity of fear memory cells in the amygdala.
The team also found that a specific frequency of brain rhythms was especially effective at inhibiting fear expression cells. Inputting frequencies in the theta range of rhythms typical for humans (four to eight hertz) revealed that lower-frequency theta rhythms (around four hertz) most effectively strengthened connections between frontal areas and the amygdala.
The researchers then modeled REM sleep in PTSD patients. The researchers mimicked those conditions and observed that brain rhythms at four to eight hertz could no longer suppress fear expression cells.
Sources: Journal of Neuroscience, Neuroscience News