Year: 2006
Type: dissertation
Abstract: Spinal cord neurons can support a simple form of instrumental learning that can\nbe used to assess behavioral potential (plasticity) within this system. In this paradigm,\nsubjects completely transected at the second thoracic vertebra learn to minimize shock\nexposure by maintaining a hindlimb in a flexed position. Preexposure to uncontrollable\nshock (shock independent of leg position) disrupts this learning.\nActivation of opioid receptors seems to contribute to the expression of the\nbehavioral deficit observed after uncontrollable shock. Intrathecal application of\nnaltrexone, a nonselective opioid receptor antagonist, blocked the expression, but not the\ninduction, of the deficit. Treatment with nor-BNI, a kappa receptor antagonist, prior to\ntesting had a similar effect, whereas mu (CTOP) and delta (naltrindole) receptor\nantagonists did not block the deficit. These findings suggest that prior exposure to\nuncontrollable shock induces a kappa opioid mediated event that inhibits learning. The\ncurrent study examined the role of the kappa receptor in the behavioral deficit. Only\nGR89696, a selective kappa-2 receptor agonist, inhibited learning. This impairment was\ndose-dependent and, at the highest dose (30 nmol), inhibited learning for 96 hours.\nHowever, GR89696 and uncontrollable shock did not interact in an additive fashion.\nInstead, an intermediate dose attenuated the induction of the deficit. These findings\nsuggest that activation of kappa receptors, specifically the kappa-2 subtype, inhibit\ninstrumental learning and block the induction of the learning deficit. Both effects may\nbe linked to the inhibition of NMDA-mediated plasticity.
Author: Stephanie N. Washburn
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2289556983