Neuroscience letters
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Neuroscience letters · Jun 2012
ReviewImaging central neurochemical alterations in chronic pain with proton magnetic resonance spectroscopy.
Proton magnetic resonance spectroscopy has been used extensively in the study of various neurobiological disorders: depression, schizophrenia, autism, etc. But its application to chronic pain is relatively new. Not many studies in chronic pain have used (1)H-MRS. ⋯ The combination of (1)H-MRS imaging with pharmacologic interventions holds significant promise as a direct one-to-one matching of disease pathology with drug mechanism of action can be made. As such (1)H-MRS may be useful in discovery of novel compounds for chronic pain. Research in these areas may lead to improved diagnosis and treatment of these complex patients.
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Pain is highly modifiable by psychological factors, including expectations. However, pain is a complex phenomenon, and expectations may work by influencing any number of processes that underlie the construction of pain. Neuroimaging has begun to provide a window into these brain processes, and how expectations influence them. ⋯ Expectancy effects on subjective experience are driven by responses in these regions as well as regions less reliably activated by changes in noxious input, including the dorsolateral prefrontal cortex and the orbitofrontal cortex. Thus, multiple systems are likely to interact and mediate the pain-modulatory effects of expectancies. Finally, we address open questions regarding the psychological processes likely to play an intervening role in expectancy effects on pain.
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We briefly summarize recent advances regarding brain functional representation of chronic pain, reorganization of resting state brain activity, and of brain anatomy with chronic pain. Based on these observations and recent theoretical advances regarding network architecture properties, we develop a general concept of the dynamic interplay between anatomy and function as the brain progresses into persistent pain, and outline the role of mesolimbic learning mechanisms that are likely involved in maintenance of chronic pain.
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Human brain imaging has provided much information about pain processing and pain modulation, but brain imaging in rodents can provide information not attainable in human studies. First, the short lifespan of rats and mice, as well as the ability to have homogenous genetics and environments, allows for longitudinal studies of the effects of chronic pain on the brain. Second, brain imaging in animals allows for the testing of central actions of novel pharmacological and nonpharmacological analgesics before they can be tested in humans. ⋯ Pharmacological imaging in rodents shows overlapping activation patterns with pain and opiate analgesics, similar to what is found in humans. Despite the many structural imaging studies in human chronic pain patients, only one study has been performed in rodents, but that study confirmed human findings of decreased cortical thickness associated with chronic pain. Future directions in rodent pain imaging include miniaturized PET for the freely moving animal, as well as new MRI techniques that enable ongoing chronic pain imaging.
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Neuroscience letters · Jun 2012
Brainstem facilitations and descending serotonergic controls contribute to visceral nociception but not pregabalin analgesia in rats.
Pro-nociceptive ON-cells in the rostral ventromedial medulla (RVM) facilitate nociceptive processing and contribute to descending serotonergic controls. We use RVM injections of neurotoxic dermorphin-saporin (Derm-SAP) in rats to evaluate the role of putative ON-cells, or μ-opioid receptor-expressing (MOR) neurones, in visceral pain processing. Our immunohistochemistry shows that intra-RVM Derm-SAP locally ablates a substantial proportion of MOR and serotonergic cells. ⋯ We measure visceromotor responses in the colorectal distension (CRD) model in control and Derm-SAP rats, and using the 5-HT(3) receptor antagonist ondansetron, we demonstrate pro-nociceptive serotonergic modulation of visceral nociception and a facilitatory drive from RVM MOR cells. The α(2)δ calcium channel ligand pregabalin produces state-dependent analgesia in neuropathy and osteoarthritis models relating to injury-specific interactions with serotonergic facilitations from RVM MOR cells. Although RVM MOR cells mediate noxious mechanical visceral input, we show that their presence is not a permissive factor for pregabalin analgesia in acute visceral pain.