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[Abstract Title]. - Society for Neuroscience

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understood. The cytokine GRO/KC (growth-related oncogene; CXCL1) shows strong, rapid<br />

upregulation in dorsal root ganglion (DRG) in both nerve injury and inflammatory pain models.<br />

We examined the direct effects of GRO/KC on small diameter DRG neurons, which are<br />

predominantly nociceptive. Whole cell voltage clamp technique was used to measure voltageactivated<br />

K currents in acutely cultured adult rat small diameter sensory neurons. Fluorescently<br />

labeled isolectin B4 (IB4) was used to classify cells as IB4-positive or IB4-negative. In IB4negative<br />

neurons, voltage-activated K current densities of both transient and sustained<br />

components were increased 1.6 fold after overnight incubation with GRO/KC (1.5 nM), without<br />

changes in voltage dependence or kinetics. The average values <strong>for</strong> the slow and fast decay time<br />

constants at 20 mV were unchanged by GRO/KC. The amplitudes of the fast inactivating<br />

component and the steady-state component were increased significantly with no shift in the<br />

voltage dependence of inactivation. These effects on K currents were completely blocked by coincubation<br />

with protein synthesis inhibitor cycloheximide (CHX) or NF-kB inhibitor pyrrolidine<br />

dithiocarbamate (PDTC). In contrast, the voltage-activated K current of IB4-positive neurons<br />

was unchanged by GRO/KC. Results suggest that GRO/KC has important effects in<br />

inflammatory process via its direct actions on sensory neurons, and activation of NF-kB is<br />

involved in its enhancement of K currents.<br />

Disclosures: R. Yang, None; J.A. Strong, None; J. Zhang, None.<br />

Poster<br />

268. Neuropathic Pain Mechanisms: Ion Channels<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 268.17/GG14<br />

Topic: D.08.l. Neuropathic pain: Mechanisms<br />

Support: McMaster University<br />

<strong>Title</strong>: Increased excitability of dorsal root ganglion sensory neurones in an animal model of<br />

neuropathic pain<br />

Authors: Y. ZHU, Q. WU, *J. L. HENRY;<br />

Inst. <strong>for</strong> Pain Rese & Care, McMaster Univ., Hamilton, ON, Canada<br />

<strong>Abstract</strong>: Supportive evidence exists that pain following peripheral nerve injury is maintained<br />

by ectopic activity in primary sensory neurons, which is thought to arise from the dorsal root<br />

ganglion (DRG) somata, the axons and peripheral nerve terminals. Studies aimed at investigating<br />

the role of primary afferents in neuropathic pain (NeP) models have so far focused on small<br />

diameter neurones despite evidence of hyperexcitability of spinal neurones in response to both

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