Abstract

This chapter focuses on the recent information derived from experiments done in vitro using spinal slice preparation and acutely isolated spinal dorsal horn (DH) neurons of young rats. The emphasis is placed on modulation of synaptic and excitatory amino acids (EAAs) responses of DH neurons by κ-opioid receptor-preferring ligands and their potential role in long-term changes in synaptic transmission related to pain. To understand how opioids produce these changes, the cellular mechanisms of opioid actions have to be known. There is increasing evidence for involvement of opioids in long lasting activity-dependent changes in the efficacy of synaptic transmission in the brain and spinal cord. Studies of long-term potentiation (LTP) implicate opioid peptides in the induction of LTP in the hippocampus. In contrast, two reports suggest that dynorphin may reduce LTP in the hippocampus in a naloxone-reversible manner, at least in part, by a presynaptic action. Understanding the cellular mechanisms underlying the κ 1 -agonist actions has implications both for the understanding of somatosensory processing in the spinal DH and for the development of novel analgesic strategies to prevent post-injury pain hypersensitivity.

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