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Neuroanatomical And Cellular Substrates Of Opioid-Induced Sensitization.

Overview

Repeated exposure to opioids induces sensitization, which is a behavioral consequence of adaptations that occur in the adult brain. Changes at the neuronal level leads to altered function of the underlying neurocircuitry, thus it is important that we identify the neuroanatomical and cellular substrates that contribute to this phenomenon. The ventral pallidum (VP) is situated in the mesocorticolimbic circuit and integrates inputs from the ventral tegmental area (VTA), nucleus accumbens (NAc) and medial prefrontal ...
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Overview

Repeated exposure to opioids induces sensitization, which is a behavioral consequence of adaptations that occur in the adult brain. Changes at the neuronal level leads to altered function of the underlying neurocircuitry, thus it is important that we identify the neuroanatomical and cellular substrates that contribute to this phenomenon. The ventral pallidum (VP) is situated in the mesocorticolimbic circuit and integrates inputs from the ventral tegmental area (VTA), nucleus accumbens (NAc) and medial prefrontal cortex (mPFC). The first part of this dissertation project provided a detailed behavioral assessment of the contribution of VP mu-opioid receptors (MORs) in morphine-induced sensitization. Toward that end, we demonstrated that MORs in the VP were necessary for morphine-induced sensitization by treating rats with intra-VP CTOP, a selective MOR antagonist, prior to administration of systemic morphine. We also demonstrated that local infusion of morphine into the VP induced sensitization, indicating that MORs in the VP were sufficient for this phenomenon. Additional studies revealed that sensitization induced by systemic administration of morphine can be expressed upon local infusions of morphine, verifying that the VP is sensitized during systemic morphine treatment. Ionotropic glutamate receptors are critical for opiate-induced sensitization. Specifically, the AMPA receptor mediates fast excitatory neurotransmission in the brain, and changes in the surface levels of these receptors (where they are functional) contribute to the neuronal plasticity that occurs following exposure to abused drugs. AMPA receptors are heteromeric complexes that include subunits GluR1-4; trafficking of GluR1-containing receptors is regulated and occurs in an activity-dependent manner. Thus, the second part of this dissertation project investigated the changes in the cellular distribution of GluR1-containing AMPA receptors in brain regions that contribute to opioid-induced sensitization - the VP, NAc and mPFC. We used a membrane-impermeable cross-linking agent to distinguish between surface and intracellular GluR1 protein in morphine-sensitized rats. We revealed that morphine treatment decreased surface expression of GluR1 in the mPFC without affecting levels in the VP or NAc. Overall, the work presented in this dissertation identifies the VP as a critical neuroanatomical substrate of opoid-induced sensitization, and changes in excitatory neurotransmission from the mPFC may contribute to this process.
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Product Details

  • ISBN-13: 9781244045460
  • Publisher: BiblioLabsII
  • Publication date: 9/11/2011
  • Pages: 78
  • Product dimensions: 7.44 (w) x 9.69 (h) x 0.16 (d)

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