Abstract
Extracellular signal-regulated kinases (ERK1 and ERK2) are members of the serine/threonine protein kinases implicated in the transduction of neurotrophic and neurochemical signals from the cell surface to the nucleus, which play important roles in synaptic plasticity and memory formation. The locus coeruleus (LC) sends noradrenergic projection to the spinal dorsal horn and contributes to pain modulation. In the present study, the activation of ERK in the LC following the injection of complete Freund's adjuvant (CFA) into the rat hindpaw was examined in order to clarify the mechanisms underlying the dynamic changes in the descending pain modulatory system after peripheral inflammation. Phospho-ERK -immunoreactive (p-ERK-IR) neurons were observed in the LC and the adjacent area. CFA injection induced the activation of ERK in the LC, with a peak at 2 minutes, which was transient. In the LC, the number of p-ERK-IR neurons in rats killed at 2 min after CFA injection (77.4±12.1) was significantly higher than that in the naive rats (4.5±1.3) [p<0.05]. However, there was no significant difference in the number of p-ERK-IR neurons in the LC between CFA and saline groups. The number of p-ERK-IR neurons in the handling group (no injection) was significantly lower than those in both CFA and saline groups. These findings suggest that activation of ERK in the LC may be induced by transient noxious stimulation, such as injection, not by peripheral inflammation. [J Physiol Sci. 2008;58 Suppl:S165]
