Finding on memory could lead to new treatments for post-traumatic stress disorder (PTSD)
FOR IMMEDIATE RELEASE:
August 20, 2007
Belmont, MA - The neurotransmitter norepinephrine is known to play a key role in emotional memory and experiments at the cellular level being reported by researchers at Harvard-affiliated McLean Hospital are helping to explain why. The findings provide an insight into how emotions enhance memory and could lead to new treatments for post-traumatic stress disorder and other psychiatric conditions that involve the fear system of the brain.
The Mechanics of Trauma (Newsweek Health link)
The study, published in the early online issue of the Proceedings of the National Academy of Sciences (PubMed), describes for the first time the cellular mechanisms that may explain why emotionally charged events are not easily forgotten.
Lead author Vadim Bolshakov, PhD, director of the Cellular Neurobiology Laboratory at McLean Hospital, said a surge of norepinephrine-also known as noradrenaline-appears to be the reason.
Bolshakov and his colleagues use the auditory fear conditioning training paradigm to study the mechanisms of fearful behavior. During this form of fear conditioning, animals learn to associate an initially neutral stimulus, sound, with a negative stimulus, a mild foot shock.
"We previously demonstrated that the learning of fear is associated with increased synaptic transmission between neurons in the amygdala and brain regions, which provide information about sound to the amygdala," Bolshakov said. "We found that noradrenaline facilitates this increased transmission."
Norepinephrine or noradrenaline acts as a neurotransmitter for nerve cells and is involved in the fight-or-flight response.
Bolshakov's experiments involved rat brain slices from the amygdala region, a brain structure important for emotional responses and the place where fear memory is formed.
The researchers infused amygdala slices with a solution containing norepinephrine and measured electrical currents flowing between neurons at specialized contacts called synapses. "It was easy to see how enhancements of these currents underlying fear learning were facilitated by norepinephrine (in the infused slices) in neural pathways implicated in fear conditioning," he said
The majority of cells in the amygdala are neurons that receive incoming information about the characteristics of auditory signals during fear learning. Interneurons are a second neuronal cell type in the amygdala. They control the excitability of neurons by releasing on them the inhibitory neurotransmitter GABA. Norepinephrine weakens firing of interneurons leading to suppressed inhibitory drive to principal neurons. Under these conditions, long-lasting changes in neurotransmission in the amygdala, required to form fear memory, are more easily invoked, according to Bolshakov.
Since psychiatric conditions, such as PTSD and generalized anxiety disorder (GAD), are linked to the fear conditioning mechanism, the findings may lead to a better understanding of these illnesses, as well as better treatments for them, Bolshakov said.
"Based on our findings, we can suggest that certain manipulations of the adrenaline system could be used to treat at least some of these disorders," he said.
The idea would be to reduce the fear memory enhancing effects of these neurotransmitters by interfering with receptors for them in the amygdala, he said.
Other McLean researchers who participated in the study are Keith Tully, PhD, Evgeny Tsvetkov, PhD, and Yan Li, PhD.