Chronic pain tagged posts

Andrea Hohmann. Credit: Indiana University

Indiana University neuroscientist Andrea Hohmann has found evidence that the brain’s cannabis receptors may be used to treat chronic pain without the side effects associated with opioid-based pain relievers or medical marijuana. “The most exciting aspect of this research is the potential to produce the same therapeutic benefits as opioid-based pain relievers without side effects like addiction risk or increased tolerance over time,” said Hohmann, a Linda and Jack Gill Chair of Neuroscience and professor in the IU Bloomington College of Arts and Sciences’ Department of Psychological and Brain Sciences.

Chronic pain is estimated to affect nearly 50 million adults in the US...

The yellow and red sections of this brain image shows the unique brain region — the mid frontal gyrus — which Northwestern scientists discovered is responsible for placebo response in pain relief. Credit: Marwan Baliki

Scientists have identified for the first time the region in the brain responsible for the “placebo effect” in pain relief, when a fake treatment actually results in substantial reduction of pain, according to new research from Northwestern Medicine and the Rehabilitation Institute of Chicago (RIC).

Pinpointing the sweet spot of the pain killing placebo effect could result in the design of more personalized medicine for the 100 million Americans with chronic pain...

In the spinal cord, chronic pain can dramatically increase PACAP neurotransmitter levels (top panel, green fluorescent signal with arrows) on the affected side compared to the normal control side. The neurotransmitter signal travels in a neurocircuit that reaches the amygdala in the brain which controls stress-related behaviors (bottom panel, green area in cartoon denotes amygdala region).

New studies show increased expression of PACAP – a peptide neurotransmitter the body releases in response to stress – is also increased in response to neuropathic pain and contributes to these symptoms...

GRK2 interaction with DOR, not kinase activity, desensitizes the receptor at the plasma membrane in
peripheral pain-sensing neurons. Priming by inflammatory mediator BK induces PKC-dependent RKIP sequestration of
GRK2 to the cytosol, enhancing DOR responsiveness. Knock down of GRK2 enhances peripheral DOR-mediated
analgesia in vivo.

Opioid abuse is a growing public health crisis, affecting up to 36 million people worldwide. Many of these individuals first get hooked on prescription painkillers that target mu opioid receptors in the brain. A study in rats published August 25 in Cell Reports suggests that a different approach that targets delta opioid receptors on sensory neurons in peripheral tissues might avoid side effects and high abuse potential of currently available pain relievers.