[Abstract Title]. - Society for Neuroscience

we are examining channel modulation. Ca 2+ /calmodulin (CaM)-dependent protein kinase II
(CaMKII) is abundant in the dorsal root ganglion (DRG), and is a modulator of Ca 2+ channels
and downstream effectors of Ca 2+ . We therefore examined CaMKII regulation of Ca 2+ after
neuronal injury using patch clamp recordings from acutely dissociated neurons to measure ICa in
the presence of the CaMKII blocker KN-93 (2 µM) or the inactive analog KN-92 (2-5 µM), in
axotomized L5 neurons after spinal nerve ligation (SNL), compared to neurons from nonoperated
controls. Internal solutions included 11 mM EGTA to clamp [Ca 2+ ]c, and external
solutions contained 2 mM Ba 2+ as charge carrier. 100 ms step pulses to maximal ICa were applied
every 10 s from a HP of -100 mV. KN-93 reduced ICa in control neurons by 42.8±3.8%, while ICa
in axotomized neurons was reduced by 13.8±11.8% (p < 0.02 vs control) by KN-93. KN-92 had
minimal effects in either population. These results indicate that CaMKII facilitates Ca 2+ entry at
the plasmalemmal level, and this facilitation is reduced after neuropathic injury.
1.
Sapunar, D., et al., Distinct membrane effects of spinal nerve ligation on injured and adjacent
dorsal root ganglion neurons in rats. Anesthesiology, 2005. 103(2): p. 360-76.
2.
McCallum, J.B., et al., Painful Peripheral Nerve Injury Decreases Calcium Current in
Axotomized Sensory Neurons. Anesthesiology, 2006. 105(1): p. 160-168.
Disclosures: J. McCallum , None; H. Wu, None; Q. Hogan, None.
Poster
268. Neuropathic Pain Mechanisms: Ion Channels
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 268.2/FF33
Topic: D.08.l. Neuropathic pain: Mechanisms
Support: Grants-in-Aid for Scientific Research (H.F. and M.Y.) from Japanese MEXT
Title: In vivo patch-clamp analysis of nociceptive synaptic transmission through calciumpermeable
AMPA receptors in substantia gelatinosa neurons of the rat spinal dorsal horn
following inflammation
Authors: *H. FURUE, M. YOSHIMURA;
Integrative Physiology, Grad Sch. Med. Sci., Kyushu Univ., Fukuoka, Japan
Abstract: Recent studies have suggested that that plastic changes in nociceptive synaptic
transmission in the spinal dorsal horn may contribute to underlying mechanisms for the
development of hyperalgesia or allodynia following tissue injury or nerve damage. In this study,