ABSTRACT
Title
Autophagy in experimental models of pain
Authors
L. Berliocchi1, R. Russo2, M. Maiarù2 and M.T. Corasaniti1
1Department of Pharmacobiological Sciences, University Magna Graecia of Catanzaro (Italy) and 2Department of Pharmacobiology and UCHAD Section of Neuropharmacology of Normal and Pathological Neuronal Plasticity, University of Calabria, Rende (CS), Italy
1Department of Pharmacobiological Sciences, University Magna Graecia of Catanzaro (Italy) and 2Department of Pharmacobiology and UCHAD Section of Neuropharmacology of Normal and Pathological Neuronal Plasticity, University of Calabria, Rende (CS), Italy
Abstract
Chronic pain is a debilitating condition affecting life quality and has dramatic economic impact on national health systems. However, our ability to treat this condition is currently limited and there is an urgent need for more effective treatments. This goal can be achieved through a better understanding of the neurobiology of pain and its mechanisms.
The contribution of spinal neuronal cell death to neuropathic pain has been investigated in several animal models, but it remains still controversial. However, research so far has focussed on only one mode of cell death, namely apoptosis, without considering other neurodegenerative mechanisms which are clearly playing an important role in other pathological conditions.
We investigated novel cell mechanisms linked to neuronal dysfunctions, such as the autophagic process, in the dorsal horn of the adult mouse spinal cord following spinal nerve injury.
Autophagy is a cytoprotective mechanism serving homeostatic functions such as cytoplasmic, protein and organelle turnover and providing metabolic substrates when cell energetic demands are increased. Basal autophagy is a highly regulated processes and an imbalance in its fine tuning, both towards an increase or an inhibition, may be detrimental for cell survival.
Our data showed that autophagy is impaired in the spinal nerve ligation model of neuropathic pain and suggest a potential role for this degradative pathway in pain processing.
(We thank Mr Guido Fico for technical assistance. This work was supported by the Italian Ministry of Health, ex art 56/2005–PS 05.15)
The contribution of spinal neuronal cell death to neuropathic pain has been investigated in several animal models, but it remains still controversial. However, research so far has focussed on only one mode of cell death, namely apoptosis, without considering other neurodegenerative mechanisms which are clearly playing an important role in other pathological conditions.
We investigated novel cell mechanisms linked to neuronal dysfunctions, such as the autophagic process, in the dorsal horn of the adult mouse spinal cord following spinal nerve injury.
Autophagy is a cytoprotective mechanism serving homeostatic functions such as cytoplasmic, protein and organelle turnover and providing metabolic substrates when cell energetic demands are increased. Basal autophagy is a highly regulated processes and an imbalance in its fine tuning, both towards an increase or an inhibition, may be detrimental for cell survival.
Our data showed that autophagy is impaired in the spinal nerve ligation model of neuropathic pain and suggest a potential role for this degradative pathway in pain processing.
(We thank Mr Guido Fico for technical assistance. This work was supported by the Italian Ministry of Health, ex art 56/2005–PS 05.15)