Abstract
Since the discovery of NMDA receptor (NMDAR) dependent long-term potentiation (LTP) in the hippocampus, many studies have demonstrated that NMDAR dependent LTP exists throughout central synapses, including those involved in sensory transmission and perception. NMDAR LTP has been reported in spinal cord dorsal horn synapses, anterior cingulate cortex and insular cortex. Behavioral, genetic and pharmacological studies show that inhibiting or reducing NMDAR LTP produced analgesic effects in animal models of chronic pain. Investigation of signalling mechanisms for NMDAR LTP may provide novel targets for future treatment of chronic pain.
Highlights
Hippocampal long-term potentiation (LTP) is a well investigated form of synaptic plasticity in the central nervous system
We found that postsynaptic calcium is important for the induction of post-LTP, since the postsynaptic application of BAPTA completely blocked the induction of LTP. Ca2+-activated AC subtype 1 (AC1) is required for potentiation
Since N-methyld-aspartic acid (NMDA) receptor (NMDAR) play an important role in activity-dependent plasticity in the anterior cingulate cortex (ACC), we suggest that GluN2B may be regulated through NMDA–calcium–CaMdependent signaling pathways
Summary
Hippocampal long-term potentiation (LTP) is a well investigated form of synaptic plasticity in the central nervous system. NMDAR LTP in Spinal Dorsal Horn intervals) of the dorsal root induces long-lasting enhancement of synaptic responses to presynaptic stimulation [8, 9]. Postsynaptic depolarization of dorsal horn neurons is critical for the induction of spinal LTP. Pairing postsynaptic depolarization with synaptic activity induces long-lasting enhancement of synaptic responses. Glutamate is a major transmitter between primary afferent fibers and spinal dorsal horn neurons, whereas neuropeptides (e.g., SP and NKA) mediate slow excitatory postsynaptic potentials (EPSPs) at synapses between small-myelinated Aδ and unmyelinated C fibers and dorsal horn neurons [3,4,5,6]. While transgenic mice and wild-type mice were indistinguishable in tests of acute nociception, GluN2B transgenic mice exhibited enhanced behavioral responses after peripheral inflammation These findings provide the first genetic evidence that forebrain NMDARs play a critical role in chronic pain
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