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Contribution of the parafascicular nucleus to the suppression of pain affect in rats

Posted on:2006-12-22Degree:Ph.DType:Dissertation
University:Wayne State UniversityCandidate:Harte, Steven EFull Text:PDF
GTID:1454390008470628Subject:Psychology
Abstract/Summary:
The contribution of the parafascicular nucleus (PF) to the suppression of tailshock-elicited pain behaviors organized at spinal (spinal motor response, SMRs), medullary (vocalization during shock, VDSs), and forebrain (vocalization afterdischarges, VADs) levels of the neuraxis was evaluated. The first set of experiments examined the antinociceptive interaction between opioid and cholinergic receptor mechanisms within PF. The antinociceptive effects produced by morphine (opioid receptor agonist) administration into PF were challenged by the local administration of atropine (acetylcholine muscarinic receptor antagonist). Likewise, the antinociceptive effects produced by carbachol (acetylcholine agonist) administration into PF were challenged by the local administration of methylnaloxonium (mu-opioid receptor antagonist). The second set of experiments assessed the antinociceptive effects produced by PF-administered morphine and carbachol following suppression of glutamatergic transmission in the rostral anterior cingulate cortex (rACC).; Microinjection of morphine into PF produced increases in VDS and VAD thresholds, but failed to elevate SMR threshold. Carbachol administration into PF produced elevations in all three thresholds. Both treatments produced a preferential elevation in VAD threshold. Administration into PF of methylnaloxonium or atropine attenuated the morphine-induced increases in vocalization thresholds. Administration of atropine but not methylnaloxonium into PF blocked threshold increases generated by PF-administered carbachol. Administration into the rACC of AP-5 (NMDA receptor antagonist) or CNQX (AMPA/kainate receptor antagonist) also reversed, in a dose-dependent manner, morphine-induced increases in vocalization thresholds. However, administration of AP-5 and CNQX into the rACC failed to alter increases in vocalization thresholds generated by PF-administered carbachol. Results are discussed in terms of a proposed PF-rACC circuit that underlies the antinociceptive action of morphine and carbachol administered into the PF.
Keywords/Search Tags:Into PF, Suppression, Carbachol, Administration into, Antinociceptive effects produced, Receptor antagonist, Morphine
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