Zinc enriched (ZEN) neurons and terminals are abundant in the rodent spinal cord.
Zinc ions have been suggested to modulate the excitability of primary afferent fibers believed to be important in nociceptive transmission. To test the hypothesis that vesicular
zinc concentration is related to
neuropathic pain we applied Chung's rodent
pain model on BALB/c mice, and traced
zinc transporter 3 (ZnT3)
proteins and
zinc ions with immunohistochemistry and autometallography (AMG), respectively. Under
anesthesia the left fifth lumbar spinal nerve was ligated in male mice in order to produced
neuropathic pain. The animals were then sacrificed 5 days later. The ZnT3 immunoreactivity was found to have decreased significantly in dorsal horn of fourth, fifth, and sixth lumbar segments. In parallel with the depressed ZnT3 immunoreactivity the amount of vesicular
zinc decreased perceptibly in superficial gray matters of especially layer I-IV of the same segments. The transection-induced reduction of vesicular
zinc in ZEN terminals of the dorsal horn was synchronic to reduced pain threshold, as measured by von Frey method. In a separate study, we observed intensive
zinc selenite precipitation in somata of the smaller spinal ganglion cell, but 5 days after spinal nerve transection
zinc precipitation was also found in the lager
ganglion cells. The present results indicate that
zinc may be involved in
pain mechanism in the spinal ganglion level. These results support the hypothesis that vesicular
zinc might have a modulatory role for
neuropathic pain. Thus, increased
pain sensitivity might be related to reduce vesicular
zinc level in the dorsal spinal gray matter.