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[Abstract Title]. - Society for Neuroscience

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glutamate transporter EAAT2 is the main mediator of glutamate<br />

clearance to terminate glutamate-mediated responses. Transgenic mice<br />

over-expressing human EAAT2 (EAAT2 mice), which exhibited a 1.4-2.5<br />

fold enhanced glutamate uptake, showed 30% less writhing response to<br />

intraperitoneal acetic acid than nontransgenic littermates. Moreover,<br />

EAAT2 mice showed a 50-63% reduction in visceromotor response (VMR) to colo-rectal<br />

distension (CRD) when assessing the response to 15- 60<br />

mmHg pressures. Corroborating the involvement of enhanced glutamate<br />

uptake, wild-type mice treated <strong>for</strong> 1 week with ceftriaxone (200mg/kg<br />

daily), a stimulator of EAAT2 expression, showed a 52-70% reduction in<br />

VMR to graded increases in colo-rectal distension. The data suggest<br />

that enhanced glutamate uptake provides protective effects against<br />

mechanical distension-induced pain. Future studies will explore 1) the<br />

physiological site and mechanism by which enhanced glutamate transport<br />

activity mediates the antinociceptive effect and 2) enhanced glutamate<br />

transport effects on inflammogen-augmented visceral pain response.<br />

Disclosures: Y. Lin, None; J. Travers, None; R. Stephens, None; G. Lin, None.<br />

Poster<br />

269. Pain: Visceral Pain II<br />

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

Program#/Poster#: 269.3/GG18<br />

Topic: D.08.n. Visceral pain<br />

Support: Science Foundation Ireland<br />

GlaxoSmithKline<br />

IDA Ireland<br />

<strong>Title</strong>: Altered spinal expression of the astrocytic glutamate transporter EAAT1 in the rat<br />

maternal separation model of visceral hypersensitivity<br />

Authors: *R. D. GOSSELIN, N. DWYER, P. FITZGERALD, T. G. DINAN, J. F. CRYAN;<br />

Univ. Col. Cork, Cork, Ireland<br />

<strong>Abstract</strong>: Alterations in gastrointestinal function and elevations in visceral pain in adulthood<br />

represent one of the most troublesome consequences of early-life stress. However, the molecular

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