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Capsaicin increases GFAP and glutamine synthetase immunoreactivity in rat arcuate nucleus and median eminence
Journal article   Peer reviewed

Capsaicin increases GFAP and glutamine synthetase immunoreactivity in rat arcuate nucleus and median eminence

Chuma O Okere and Barry D Waterhouse
Neuroreport, v 15(2)
09 Feb 2004
PMID: 15076747

Abstract

Animals Arcuate Nucleus of Hypothalamus - cytology Arcuate Nucleus of Hypothalamus - drug effects Arcuate Nucleus of Hypothalamus - metabolism Astrocytes - drug effects Astrocytes - enzymology Capsaicin - pharmacology Glial Fibrillary Acidic Protein - drug effects Glial Fibrillary Acidic Protein - metabolism Glutamate-Ammonia Ligase - drug effects Glutamate-Ammonia Ligase - metabolism Glutamic Acid - metabolism Glutamine - biosynthesis Hypothalamo-Hypophyseal System - cytology Hypothalamo-Hypophyseal System - drug effects Hypothalamo-Hypophyseal System - enzymology Immunohistochemistry Male Median Eminence - cytology Median Eminence - drug effects Median Eminence - metabolism Neuronal Plasticity - drug effects Neuronal Plasticity - physiology Neurons - drug effects Neurons - enzymology Nitric Oxide - metabolism Rats Rats, Long-Evans Stress, Physiological - enzymology Stress, Physiological - physiopathology Up-Regulation - drug effects Up-Regulation - physiology
Antibodies to glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) were used to determine the effect of s.c. capsaicin (after 75 min) on astroglial cells in the rat arcuate nucleus-median eminence (ARC-ME). Compared to vehicle, capsaicin significantly increased GFAP and GS immunoreactivity in the ARC-ME. Co-localization of GFAP and GS was observed in the ARC-ME complex. Since GS is primarily responsible for glutamate-glutamine metabolism, the increase in total immunostaining for GFAP-and GS- staining suggests a functional adjustment to cope with some of the capsaicin-induced effects. Together with the involvement of nitric oxide synthase in the ARC-ME response to capsaicin, these observations indicate activity-dependent plasticity of the neuron-glia network in response to this stressful/noxious stimulus.

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