Melanocortin-4 receptor expression in the cuneiform nucleus is involved in modulation of opioidergic signaling.
10.1007/s11596-015-1486-2
- Author:
Yong-tang SONG
1
;
Tao-tao LIU
2
;
Li FENG
2
;
Tao ZHANG
3
;
Hong-bing XIANG
2
Author Information
1. Medical Association of Hubei Province, Wuhan, 430060, China. songyongtang@sina.com.
2. Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
3. Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. zhangtao19611@163.com.
- Publication Type:Journal Article
- Keywords:
cuneiform nucleus;
melanocortin-4 receptor;
mu opioid receptor;
opioidergic signaling
- MeSH:
Animals;
Gene Expression Regulation;
Gene Knock-In Techniques;
Genes, Reporter;
Green Fluorescent Proteins;
genetics;
metabolism;
Mice;
Mice, Transgenic;
Microtomy;
Midbrain Reticular Formation;
cytology;
metabolism;
Neurons;
cytology;
metabolism;
Receptor, Melanocortin, Type 4;
genetics;
metabolism;
Receptors, Opioid, mu;
genetics;
metabolism;
Recombinant Fusion Proteins;
genetics;
metabolism;
Signal Transduction
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2015;35(5):662-665
- CountryChina
- Language:English
-
Abstract:
Substantial evidence has suggested that deep brain stimulation of the cuneiform nucleus has become a remarkable treatment option for intractable pain, but the possible mechanism is poorly understood. Using a melanocortin-4 receptor (MC4R)-green fluorescent protein (GFP) reporter knockin mouse, we showed that a large number of MC4R-GFP-positive neurons were expressed in the cuneiform nucleus. Immunofluorescence revealed that approximately 40%-50% of MC4R-GFP-positive neurons expressed mu opioid receptors, indicating that they were opioidergic signaling. Our findings support the hypothesis that MC4R expression in the cuneiform nucleus is involved in the modulation of opioidergic signaling.
