Expression of c-Fos in arcuate nucleus induced by electroacupuncture: Relations to neurons containing opioids and glutamate

• Published in: Brain research 2007-08, Vol.1166, p.65-76
• Main Authors: Guo, Zhi-Ling, Longhurst, John C
• Format: Article
• Language: English
• Subjects: Acupuncture; Acupuncture Points; Animals; Arcuate nucleus; Arcuate Nucleus of Hypothalamus - cytology; Arcuate Nucleus of Hypothalamus - metabolism; Arousal - physiology; Biological and medical sciences; c-Fos; Cats; Electroacupuncture; Enkephalin; Female; Glutamate; Glutamic Acid - metabolism; Immunohistochemistry; Male; Median Nerve - metabolism; Medical sciences; Miscellaneous; Neural Pathways - metabolism; Neurology; Neurons - metabolism; Opioid Peptides - metabolism; Proto-Oncogene Proteins c-fos - metabolism; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects); β-Endorphin
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2007.06.042

Abstract Electroacupuncture (EA) at the Neiguan–Jianshi acupoints (P5–P6, overlying the median nerve) attenuates sympathoexcitatory reflexes probably through the opioid system. The arcuate nucleus (ARC) within hypothalamus is an important brain area that produces opioid peptides. Physiological studies have demonstrated that the predominant response to EA is excitation in the ARC and that excitatory projections from the ARC to the ventrolateral periaqueductal gray during EA at P5–P6 contribute to inhibition of sympathoexcitatory cardiovascular reflexes. These data imply that ARC neurons activated by EA also may contain excitatory neurotransmitters. Thus, the present study evaluated activation of the ARC induced by EA at P5–P6, in relation to the opioid system and glutamate, by detecting c- Fos , an immediate early gene, opioid peptides and vesicular glutamate transporter 3 (VGLUT3). To enhance detection of perikarya containing the opioid peptides, colchicine (90–100 μg/kg) was administered in cats 28–30 h before EA or the sham-operated control. EA was performed at P5–P6 for 30 min. Compared to controls ( n = 5), c-Fos-positive cells and neurons double-labeled with c-Fos and β-endorphin, enkephalin or VGLUT3 in the ARC were significantly increased in EA-treated cats ( n = 6; all P < 0.05). Moreover, neurons triple-labeled with c-Fos, β-endorphin and VGLUT3 were noted in this region following EA stimulation, but not in controls. Thus, EA at P5–P6 activates neurons in the ARC, some of which contain opioids as well as glutamate or both. The results imply that EA at P5–P6 has the potential to influence ARC neurons containing multiple neuronal substances that subsequently modulate cardiovascular function.