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Role of the opioid system in the behavioral deficit observed after uncontrollable shock

Spinal cord neurons can support a simple form of instrumental learning that can
be used to assess behavioral potential (plasticity) within this system. In this paradigm,
subjects completely transected at the second thoracic vertebra learn to minimize shock
exposure by maintaining a hindlimb in a flexed position. Preexposure to uncontrollable
shock (shock independent of leg position) disrupts this learning.
Activation of opioid receptors seems to contribute to the expression of the
behavioral deficit observed after uncontrollable shock. Intrathecal application of
naltrexone, a nonselective opioid receptor antagonist, blocked the expression, but not the
induction, of the deficit. Treatment with nor-BNI, a kappa receptor antagonist, prior to
testing had a similar effect, whereas mu (CTOP) and delta (naltrindole) receptor
antagonists did not block the deficit. These findings suggest that prior exposure to
uncontrollable shock induces a kappa opioid mediated event that inhibits learning. The
current study examined the role of the kappa receptor in the behavioral deficit. Only
GR89696, a selective kappa-2 receptor agonist, inhibited learning. This impairment was
dose-dependent and, at the highest dose (30 nmol), inhibited learning for 96 hours.
However, GR89696 and uncontrollable shock did not interact in an additive fashion.
Instead, an intermediate dose attenuated the induction of the deficit. These findings
suggest that activation of kappa receptors, specifically the kappa-2 subtype, inhibit
instrumental learning and block the induction of the learning deficit. Both effects may
be linked to the inhibition of NMDA-mediated plasticity.
Date16 August 2006
CreatorsWashburn, Stephanie Nicole
ContributorsGrau, James W.
PublisherTexas A&M University
Source SetsTexas A and M University
Detected LanguageEnglish
TypeBook, Thesis, Electronic Thesis, text
Format256309 bytes, electronic, application/pdf, born digital

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