RT Journal Article
SR Electronic
T1 Astroglia in Medullary Dorsal Horn (Trigeminal Spinal Subnucleus Caudalis) Are Involved in Trigeminal Neuropathic Pain Mechanisms
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 11161
OP 11171
DO 10.1523/JNEUROSCI.3365-09.2009
VO 29
IS 36
A1 Akiko Okada-Ogawa
A1 Ikuko Suzuki
A1 Barry J. Sessle
A1 Chen-Yu Chiang
A1 Michael W. Salter
A1 Jonathan O. Dostrovsky
A1 Yoshiyuki Tsuboi
A1 Masahiro Kondo
A1 Junichi Kitagawa
A1 Azusa Kobayashi
A1 Noboru Noma
A1 Yoshiki Imamura
A1 Koichi Iwata
YR 2009
UL http://www.jneurosci.org/content/29/36/11161.abstract
AB The aim of this study was to investigate whether astroglia in the medullary dorsal horn (trigeminal spinal subnucleus caudalis; Vc) may be involved in orofacial neuropathic pain following trigeminal nerve injury. The effects of intrathecal administration of the astroglial aconitase inhibitor sodium fluoroacetate (FA) were tested on Vc astroglial hyperactivity [as revealed by glial fibrillary acid protein (GFAP) labeling], nocifensive behavior, Vc extracellular signal-regulated kinase phosphorylation (pERK), and Vc neuronal activity in inferior alveolar nerve-transected (IANX) rats. Compared with sham-control rats, a significant increase occurred in GFAP-positive cells in ipsilateral Vc at postoperative day 7 in IANX rats, which was prevented following FA administration. FA significantly increased the reduced head withdrawal latency to high-intensity heat stimulation of the maxillary whisker pad skin in IANX rats, although it did not significantly affect the reduced escape threshold to low-intensity mechanical stimulation of the whisker skin in IANX rats. FA also significantly reduced the increased number of pERK-like immunoreactive cells in Vc and the enhanced Vc nociceptive neuronal responses following high-intensity skin stimulation that were documented in IANX rats, and glutamine administration restored the enhanced responses. These various findings provide the first documentation that astroglia is involved in the enhanced nociceptive responses of functionally identified Vc nociceptive neurons and in the associated orofacial hyperalgesia following trigeminal nerve injury.