Modulation of long-term potentiation of excitatory synaptic transmission in the spinal cord dorsal horn

Abstract

There is considerable interest in understanding long-term potentiation (LTP) of glutamatergic synaptic transmission because the molecular mechanisms involved in its induction and expression are thought to be essential for learning, memory and pain. The molecular mechanisms involved in induction and expression of LTP have been widely characterized, especially in the hippocampus and have been proposed to be cellular models of learning and memory. LTP in the spinal pain pathways has been considered as one of the cellular mechanisms of post-injury pain hypersensitivity (central sensitization). Extensive evidence has indicated that changes in both the presynaptic release of glutamate and postsynaptic response to glutamate are involved in expression of LTP. This chapter attempts a brief review of some of the postsynaptic mechanisms underlying induction, expression and modulation of the high frequency stimulation-induced LTP of excitatory synaptic transmission in the superficial dorsal horn of the spinal cord. It is becoming clear that the spinal LTP, which might contribute to hyperalgesia in animal models of pain, uses multiple mechanisms involving protein phosphorylation, similar to the processes associated with hippocampal LTP. Modulation of postsynaptic AMPA and NMDA receptor function caused by phosphorylation may play an important role in the induction and expression of synaptic plasticity at dorsal horn excitatory synapses.