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How Stress Alleviates Pain

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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.

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.”

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.”

Neuron, Vol 56, 880-892, 06 December 2007

Noradrenaline Modulates Transmission at a Central Synapse by a Presynaptic Mechanism

Andrew J. Delaney,1 James W. Crane,1 and Pankaj Sah1,

1 The Queensland Brain Institute, The University of Queensland, QLD 4072 Australia

Corresponding author
Pankaj Sah

The lateral division of the central amygdala (CeAL) is the target of ascending fibers from the pain-responsive and stress-responsive nuclei in the brainstem. We show that single fiber inputs from the nociceptive pontine parabrachial nucleus onto CeAL neurons form suprathreshold glutamatergic synapses with multiple release sites. Noradrenaline, acting at presynaptic α2 receptors, potently inhibits this synapse. This inhibition results from a decrease in the number of active release sites with no change in release probability. Introduction of a presynaptic scavenger of Gβγ subunits blocked the effects of noradrenaline, and botulinum toxin A reduced its effects, showing a direct action of βγ subunits on the release machinery. These data illustrate a mechanism of presynaptic modulation where the output of a large multiple-release-site synapse is potently regulated by endogenously released noradrenaline and suggests that the CeA may be a target for the central nociceptive actions of noradrenaline.


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