Glia: novel counter-regulators of opioid analgesia
Humans; Analgesics; Animals; Opioid/administration & dosage; Drug Tolerance; Brain/drug effects/metabolism; Neuroglia/drug effects/metabolism; Neurotransmitter Agents/metabolism; Nociceptors/drug effects/metabolism; Pain/metabolism/prevention & control; Spinal Cord/drug effects/metabolism
Development of analgesic tolerance and withdrawal-induced pain enhancement present serious difficulties for the use of opioids for pain control. Although neuronal mechanisms to account for these phenomena have been sought for many decades, their bases remain unresolved. Within the past four years, a novel non-neuronal candidate has been uncovered that opposes acute opioid analgesia and contributes to development of opioid tolerance and tolerance-associated pain enhancement. This novel candidate is spinal cord glia. Glia are important contributors to the creation of enhanced pain states via the release of neuroexcitatory substances. New data suggest that glia also release neuroexcitatory substances in response to morphine, thereby opposing its effects. Controlling glial activation could therefore increase the clinical utility of analgesic drugs.
2005
Watkins LR; Hutchinson MR; Johnston IN; Maier SF
Trends In Neurosciences
2005
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/j.tins.2005.10.001" target="_blank" rel="noreferrer">10.1016/j.tins.2005.10.001</a>
Neurohormonal factors in the development of catabolic/anabolic imbalance and cachexia
Humans; Animals; Heart Failure; Cachexia/etiology/metabolism; Neurotransmitter Agents/metabolism; Biological Markers/blood; Congestive/complications/metabolism; Cytokines/metabolism; Glucocorticoids/metabolism; Insulin-Like Growth Factor I/metabolism; Renin-Angiotensin System/physiology
Mechanisms that lead to cachexia are still poorly understood. The neurohormonal changes that occur in severe disease states may cause an imbalance between protein synthesis and degradation at the cellular level, followed by muscle wasting. Here, we review actions of angiotensin II, TNF-alpha, corticosteroids, insulin-like growth factor-I (IGF-I), and the IGF binding proteins, factors that may each contribute to the metabolic imbalance. The complex endocrine, autocrine and intracellular interactions between these factors will be described with examples from patient, rat and cell culture studies. Moreover, some of the data supporting that each of these hormones may directly affect cellular protein degradation mechanisms will be reviewed. Knowledge on these regulatory mechanisms will facilitate the development of new pharmaceutical strategies to treat cachexia.
2002
Brink M; Anwar A; Delafontaine P
International Journal Of Cardiology
2002
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/s0167-5273(02)00239-5" target="_blank" rel="noreferrer">10.1016/s0167-5273(02)00239-5</a>