One way to alleviate the pain of banging your shin while on a hike is to encounter a grizzly bear—a well-known phenomenon called stress-induced analgesia. Now, researchers have elucidated a key mechanism by which the stress hormone noradrenaline — which floods the bloodstream during grizzly encounters and other stressful events — affects the brain’s pain-processing pathway to produce such analgesia.
Pankaj Sah and colleagues published their findings in the December 6, 2007, issue of the journal Neuron, published by Cell Press.
In an accompanying perspective article on the research, Harvard Medical School researchers Keith Tully, Yan Li, and Vadim Bolshakov wrote that “The impressive new study… provides important mechanistic clues helping to explain this phenomenon.”
In their experiments, Sah and colleagues studied a region of the amygdala, the brain’s emotion-processing region known to mediate the emotional and stress-related aspects of pain. Researchers had long known that these amygdala-based processes were controlled by neurons that originated in the brainstem and that were regulated by noradrenaline.
Sah and colleagues sought in their studies to understand the mechanism by which noradrenaline influences neuronal transmission of pain inputs from the brainstem region known as the pontine parabrachial (PB).
In their experiments with rats, the researchers analyzed the effects of noradrenaline on electrical stimulation of the pathway between the PB and amygdala. They found that noradrenaline acted as a powerful suppressor of that stimulation. The researchers’ studies also revealed that noradrenaline suppression acted on the “transmission” side of the connections between neurons, called synapses. Their analyses revealed how noradrenaline causes such suppression: by activating specific receptors, called adrenocreceptors, on the PB neurons.
The researchers’ studies showed that noradrenaline’s action appears to reduce the number of sites that launch the chemical signals called neurotransmitters by which one neuron triggers a nerve impulse in another, reported the researchers.
They concluded that “Our results show that an important mediator of stress-induced analgesia could be the potent modulation by noradrenaline of [pain] PB inputs in the central amygdala.”
The researchers include Andrew J. Delaney, James W. Crane, and Pankaj Sah, of the Queensland Brain Institute, The University of Queensland, Australia.