Activated glia play a major role in mediating behavioral hypersensitive state following peripheral inflammation. Electroacupuncture is well known to relieve persistent inflammatory pain. The present study was undertaken to examine whether fluorocitrate, a glial metabolic inhibitor, could synergize electroacupuncture antagonizing thermal hyperalgesia and mechanical allodynia evoked by ankle joint inflammation. Monoarthritis of rat ankle joint was induced by an intra-articular injection of Complete Freund's Adjuvant (CFA). The paw withdrawal latency (PWL) from a thermal stimulus and paw withdrawal threshold (PWT) from von Frey hairs were measured in awake rats. Intrathecal (i.t.) injection of 1 nmol fluorocitrate markedly suppressed monoarthritis-induced thermal hyperalgesia and mechanical allodynia. Unilateral electroacupuncture stimulation of "Huantiao" (GB30) and "Yanglingquan" (GB34) acupuncture points (100/2 Hz alternation, 1-2-3 mA) significantly elevated the PWLs and PWTs for 45 min after cessation of electroacupuncture in monoarthritic rats. Co-application of 0.1 or 1 nmol fluorocitrate with electroacupuncture significantly potentiated electroacupuncture analgesia, although 0.1 nmol fluorocitrate alone had no effect on PWLs and PWTs in monoarthritic rats. These results suggested that electroacupuncture and disrupting glial function could synergistically antagonize inflammatory pain, which might provide a potential strategy for the treatment of arthritic pain.
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http://dx.doi.org/10.1016/j.expneurol.2005.11.011 | DOI Listing |
Behav Brain Res
June 2024
Instituto de Farmacología Experimental de Córdoba (IFEC-CONICET) - Departamento de Farmacología Otto Orsingher (FCQ-UNC), Córdoba, Argentina. Electronic address:
Growing evidence indicates a critical role of astrocytes in learning and memory. However, little is known about the role of basolateral amygdala complex (BLA-C) astrocytes in contextual fear conditioning (CFC), a paradigm relevant to understand and generate treatments for fear- and anxiety-related disorders. To get insights on the involvement of BLA-C astrocytes in fear memory, fluorocitrate (FLC), a reversible astroglial metabolic inhibitor, was applied at critical moments of the memory processing in order to target the acquisition, consolidation, retrieval and reconsolidation process of the fear memory.
View Article and Find Full Text PDFInt J Neurosci
March 2022
Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
Aims: Evidence suggests that glial cells are influenced by Traumatic brain injury (TBI). Both protective and damaging roles have been attributed to reactive glial cells, but their role after TBI has not been well understood. In this study, the role of glial cells in TBI-induced cognitive impairment was investigated.
View Article and Find Full Text PDFFront Mol Neurosci
June 2019
Department of Veterinary Physiology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, South Korea.
We have recently demonstrated that sciatic nerve injury increases the expression of spinal cytochrome P450c17, a key neurosteroidogenic enzyme, which plays a critical role in the development of peripheral neuropathic pain. However, the modulatory mechanisms responsible for the expression of spinal P450c17 have yet to be examined. Here we investigated the possible involvement of interleukin-1β (IL-1β) in altering P450c17 expression during the induction phase of neuropathic pain.
View Article and Find Full Text PDFCell Mol Neurobiol
November 2019
Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, Jiangsu Key Laboratory of Neuropsychiatric Diseases, The Second Affiliated Hospital of Soochow University, Institute of Neuroscience, Soochow University, Suzhou, China.
Ischemic stroke often causes motor and cognitive deficits. Deregulated glia gap junction communication, which is reflected by increased protein levels of glial fibrillary acidic protein (GFAP) and connexin 43 (Cx43), has been observed in ischemic hippocampus and has been associated with cognitive impairment in animal stroke models. Here, we tested the hypothesis that reactive astrocytes-mediated loss of synaptophysin (SYP) and CREB-regulated transcription coactivator 1 (CRTC1) contribute to dysfunction in glia gap junction communication and memory impairment after ischemic stroke.
View Article and Find Full Text PDFAm J Physiol Regul Integr Comp Physiol
June 2016
Autonomic Neurosciences Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana; and
The hindbrain contains critical neurocircuitry responsible for generating defensive physiological responses to hypoglycemia. This counter-regulatory response (CRR) is evoked by local hindbrain cytoglucopenia that causes an autonomically mediated increase in blood glucose, feeding behavior, and accelerated digestion; that is, actions that restore glucose homeostasis. Recent reports suggest that CRR may be initially triggered by astrocytes in the hindbrain.
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