Independent contributions of alcohol and stress axis hormones to painful peripheral neuropathy

Autor: Emma Levine, Jon D. Levine, Luiz F. Ferrari
Rok vydání: 2013
Předmět:
Male
Alcoholic Neuropathy
Alcohol abuse
Neurodegenerative
Rats
Sprague-Dawley
Substance Misuse
Alcohol Use and Health
Catecholamines
stress hormones
nociceptor
2.1 Biological and endogenous factors
Psychology
Aetiology
General Neuroscience
Pain Research
Peripheral Nervous System Diseases
painful peripheral neuropathy
Alcoholism
Mental Health
Nociception
Hyperalgesia
Neuropathic pain
Nociceptor
Cognitive Sciences
Chronic Pain
medicine.symptom
Pain Threshold
medicine.medical_specialty
alcohol neurotoxicity
Stress
Basic Behavioral and Social Science
Article
Internal medicine
Behavioral and Social Science
Threshold of pain
medicine
Animals
Glucocorticoids
Peripheral Neuropathy
hyperalgesia
Neurology & Neurosurgery
Ethanol
business.industry
Prevention
Neurosciences
medicine.disease
Rats
Good Health and Well Being
Peripheral neuropathy
Endocrinology
Acoustic Stimulation
Adrenal Medulla
Neuralgia
Psychological
Sprague-Dawley
business
Stress
Psychological
Zdroj: Neuroscience. 228:409-417
ISSN: 0306-4522
DOI: 10.1016/j.neuroscience.2012.10.052
Popis: Painful small-fiber peripheral neuropathy is a debilitating complication of chronic alcohol abuse. Evidence from previous studies suggests that neuroendocrine mechanisms, in combination with other, as yet unidentified actions of alcohol, are required to produce this neuropathic pain syndrome. In addition to neurotoxic effects of alcohol, in the setting of alcohol abuse neuroendocrine stress axes release glucocorticoids and catecholamines. Since receptors for these stress hormones are located on nociceptors, at which they can act to cause neuronal dysfunction, we tested the hypothesis that alcohol and stress hormones act on the nociceptor, independently, to produce neuropathic pain. We used a rat model, which allows the distinction of the effects of alcohol from those produced by neuroendocrine stress axis mediators. We now demonstrate that topical application of alcohol and exposure to unpredictable sound stress, each alone, has no effect on the nociceptive threshold. However, when animals that had previous exposure to alcohol were subsequently exposed to stress, they rapidly developed mechanical hyperalgesia. Conversely, sound stress followed by topical alcohol exposure also produced mechanical hyperalgesia. The contribution of stress hormones was prevented by spinal intrathecal administration of oligodeoxynucleotides antisense to β 2 -adrenergic or glucocorticoid receptor mRNA, which attenuates receptor level in nociceptors, as well as by adrenal medullectomy. These experiments establish an independent role of alcohol and stress hormones on the primary afferent nociceptor in the induction of painful peripheral neuropathy.
Databáze: OpenAIRE
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