The Changes in Serum and Cerebrospinal Fluid Ca2+, Mg2+, and Ca2+/Mg2+ Ratio in Neuropathic Rats

Jeong, Sung Moon; Park, Chul Ho; Shin, Jin Woo; Lim, Jeong Gil; Lee, Chung; Han, Sung Min

Abstract

BACKGROUND: Central sensitization of neuropathic pain is associated with an influx of extracellular calcium via the opening of N-methyl-D-aspartate (NMDA) receptor-gated ion channels, which is usually blocked by a magnesium plug. Many studies have found that intrathecal or intraperitoneal magnesium suppress neuropathic pain. Therefore, it is possible that serum and cerebrospinal fluid Ca2+, Mg2+, and Ca2+/Mg2+ ratio are changed in neuropathic pain. The purpose of this study was evaluated changes in serum and cerebrospinal fluid Ca2+, Mg2+, and Ca2+/Mg2+ ratio in neuropathic rats.
METHODS
Male Sprague-Dawley rats were prepared with tight ligation of the left lumbar 5th and 6th spinal nerves to produce neuropathic pain. The threshold of mechanical allodynia was evaluated by the up-down method using withdrawal response to a von Frey filaments stimulus on the 3rd, 7th, and 14th day. Rats with a threshold of less than 4 gram were selected as the experimental group. On the 16th day, serum and cerebrospinal fluid Ca2+, Mg2+, and Ca2+/Mg2+ ratio were measured. Experimental group data were then compared with those of an unoperated control group and an unligated sham group; each group contained 10 animals.
RESULTS
No statistic differences were found between groups.
CONCLUSIONS
Our results suggest that serum and cerebrospinal fluid Ca2+, Mg2+, and Ca2+/Mg2+ ratio in neuropathic rats do not differ from those of normal rats because of physiologic homeostasis is maintained by active transport through the blood-brain-barrier despite of activation of NMDA receptor-gated ion channels. However, we believe that the Mg2+ ion-dependent voltage-gating in rats with neuropathic pain may be deficient in a chronic condition due to a decreased Mg2+ binding affinity of the NMDA receptor-gated channel, as has been found in hippocampal granule cells in epileptic rats.