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When citing an abstract from the 2009 Annual - Society for ...

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Disclosures: R.H. Kline IV, None; R.G. Wiley, Adv<strong>an</strong>ced Targeting Sys, F.<br />

Consult<strong>an</strong>t/Advisory Board.<br />

Poster<br />

560. Opioids: Mech<strong>an</strong>ism of Action<br />

Location: South Hall A<br />

Time: Tuesday, October 20, <strong>2009</strong>, 8:00 am - 12:00 noon<br />

Program#/Poster#: 560.14/CC73<br />

Topic: D.08.bb. Opioids<br />

Support: DA-022599<br />

Title: Neurochemical alterations in <strong>the</strong> amygdala during opioid self-administration in nerveinjured<br />

rats<br />

Authors: *E. E. EWAN, N. L. BUECHLER, T. J. MARTIN;<br />

Wake Forest Univ., Winston-Salem, NC<br />

Abstract: The amygdala is a midbrain structure known to be involved in affective responses to<br />

noxious stimuli <strong>an</strong>d contains a dense population of mu opioid receptors (MOR’s). Previous work<br />

<strong>from</strong> our lab revealed that irreversible inhibition of MOR’s in <strong>the</strong> amygdala has a greater impact<br />

on heroin self-administration in rats with neuropathic pain compared to normal rats. This<br />

suggests that opioid pharmacology in <strong>the</strong> amygdala is altered following nerve injury, <strong>an</strong> effect<br />

that may be due to alterations in neuronal activity within this region. Microdialysis of <strong>the</strong><br />

amygdala was per<strong>for</strong>med in both normal <strong>an</strong>d nerve-injured rats during heroin self-administration<br />

<strong>an</strong>d revealed that glutamate levels were signific<strong>an</strong>tly increased only in nerve-injured rats during<br />

heroin self-administration. In rats with neuropathic pain, intra-amygdala administration of <strong>the</strong><br />

ampa/kainate <strong>an</strong>tagonist NBQX, <strong>the</strong> group II metabotropic glutamate agonist LY354740, <strong>an</strong>d <strong>the</strong><br />

group III metabotropic glutamate agonist LAP-4 failed to reverse mech<strong>an</strong>ical allodynia. These<br />

findings suggest that alterations in glutamatergic tr<strong>an</strong>smission in <strong>the</strong> amygdala may modulate <strong>the</strong><br />

rein<strong>for</strong>cing effects of opioids in <strong>the</strong> presence of neuropathic pain me<strong>an</strong>while producing no<br />

effects on hypersensitivity.<br />

Disclosures: E.E. Ew<strong>an</strong>, None; N.L. Buechler, None; T.J. Martin, None.<br />

Poster

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