Chronic pain-induced astrocyte activation in the cingulate cortex with no change in neural or glial differentiation from neural stem cells in mice

Kuzumaki, Naoko; Narita, Minoru; Narita, Michiko; Hareyama, Nana; Niikura, Keiichi; Nagumo, Yoko; Nozaki, Hiroyuki; Amano, Taku; Suzuki, Tsutomu

doi:10.1016/j.neulet.2006.12.057

Cited by 51 publications

(35 citation statements)

References 17 publications

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“…A potential local antinociceptive action of PPF on phase II formalin-induced nociception was reported following PPF administration in the hind paw either before or after formalin injury (Dorazil-Dudzik et al 2004). A supraspinal site of action of PPF is suggested with the report of a prolonged antihyperalgesic/allodynic effect of a single administration of PPF in the cingulate cortex 24 h prior to nerve injury (Kuzumaki et al 2007). It remains to be seen whether post-treatment is similarly effective in this paradigm.…”

Section: Ppf As An Antiallodynic Agentmentioning

confidence: 99%

Propentofylline: Glial Modulation, Neuroprotection, and Alleviation of Chronic Pain

Sweitzer

Leo

2010

Handbook of Experimental Pharmacology

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Propentofylline is a unique methylxanthine with clear cyclic AMP, phosphodiesterase, and adenosine actions, including enhanced synaptic adenosine signaling. Both in vitro and in vivo studies have demonstrated profound neuroprotective, antiproliferative, and anti-inflammatory effects of propentofylline. Propentofylline has shown efficacy in preclinical models of stroke, opioid tolerance, and acute and chronic pain. Clinically, propentofylline has shown efficacy in degenerative and vascular dementia, and as a potential adjuvant treatment for schizophrenia and multiple sclerosis. Possible mechanisms of action include a direct glial modulation to decrease a reactive phenotype, decrease glial production and release of damaging proinflammatory factors, and enhancement of astrocyte-mediated glutamate clearance. This chapter reviews the literature that supports a myriad of protective actions of this small molecule and implicates propentofylline as a potential therapeutic for the treatment of chronic pain. From these studies, we propose a CNS multipartite synaptic action of propentofylline that includes modulation of pre- and postsynaptic neurons, astrocytes, and microglia in the treatment of chronic pain syndromes, including, but not limited to, neuropathic pain.

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Section: Ppf As An Antiallodynic Agentmentioning

confidence: 99%

Propentofylline: Glial Modulation, Neuroprotection, and Alleviation of Chronic Pain

Sweitzer

Leo

2010

Handbook of Experimental Pharmacology

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“…It was found that chronic painful stimuli induced astrocyte activation in mouse ACC [42] and that mice with chronic pain exhibit anxiety-like behavior and an increase of astrocytes in ACC due to the dysfunction of cortical delta-opioid receptor systems [43] .…”

Section: Neurotransmitter and Receptor Mechanisms Underlying Acc Invomentioning

confidence: 99%

“…Recent studies indicate that glial cells are closely associated with pain modulation at subcortical levels [106,107] and are activated in the cortex in some pain conditions [42,43,[108][109][110] as well as decreased in number and density in mood-disordered subjects [111] . Contrarily, a study by Zhang [112] indicates that the microglia in cerebral cortex are not activated by peroneal nerve (CPN) ligation in heterozygous Cx3cr1GFP/+mice.…”

Section: Perspectivementioning

confidence: 99%

Cerebral cortex modulation of pain

2008

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Pain is a complex experience encompassing sensory-discriminative, affective-motivational and cognitiv e-emotional components mediated by different mechanisms. Contrary to the traditional view that the cerebral cortex is not involved in pain perception, an extensive cortical network associated with pain processing has been revealed using multiple methods over the past decades. This network consistently includes, at least, the anterior cingulate cortex, the agranular insular cortex, the primary (SΙ) and secondary somatosensory (SΠ) cortices, the ventrolateral orbital cortex and the motor cortex. These cortical structures constitute the medial and lateral pain systems, the nucleus submedius-ventrolateral orbital cortex-periaqueductal gray system and motor cortex system, respectively. Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine, are involved in the modulation of pain by these cortical structures. In addition, glial cells may also be involved in cortical modulation of pain and serve as one target for pain management research. This review discusses recent studies of pain modulation by these cerebral cortical structures in animals and human.

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“…Animal studies have demonstrated that prolonged nociceptive input from peripheral nerve injury (eg, sciatic nerve ligation) leads to spinal microglial activation, accounting for some aspects of pain behavior (ie, tactile allodynia) [34,39] and even to remote astrocyte activation in the cingulate gyrus (without any detectable effect on proliferation or differentiation of neuronal cells) [40]. Astrocytes, as one subtype of neuroglia, are critically involved in potassium homeostasis and glutamate reuptake, thereby having direct infl uence on neuronal activity and metabolism [41].…”

Section: Neuronal and Neuroglial Changesmentioning

confidence: 99%

Variations in brain volume and regional morphology associated with chronic pain

Schmidt‐Wilcke

2008

Curr Rheumatol Rep

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Various peripheral and spinal mechanisms have been hypothesized to contribute to pain amplification and chronicity. However, the role of the brain in chronic pain states remains to be fully elucidated. Functional brain imaging techniques, such as positron emission tomography and functional magnetic resonance imaging, have frequently been used to investigate brain activity during acute/experimental pain perception, which has helped to establish the notion of the human pain network. In the context of chronic pain, the assessment of brain chemistry (by way of spectroscopy) and brain morphology is of growing interest, and there is a quickly expanding body of evidence that persons with chronic pain conditions, including chronic low back pain, chronic tension-type headache, and fibromyalgia, display changes in global and regional brain morphology. It has been suggested that prolonged nociceptive input to the brain might induce functional and morphologic maladaptive processes that in turn further exacerbate the experience of chronic pain. Alternatively, morphologic changes might predispose toward vulnerability to develop a chronic pain state. The purpose of this review is to examine current literature regarding altered brain morphology in patients with various chronic pain states, summarize these findings, and evaluate their implications for our understanding of the pathophysiology of chronic pain.

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Chronic pain-induced astrocyte activation in the cingulate cortex with no change in neural or glial differentiation from neural stem cells in mice

Cited by 51 publications

References 17 publications

Propentofylline: Glial Modulation, Neuroprotection, and Alleviation of Chronic Pain

Propentofylline: Glial Modulation, Neuroprotection, and Alleviation of Chronic Pain

Cerebral cortex modulation of pain

Variations in brain volume and regional morphology associated with chronic pain

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