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Figure 2 | Molecular Pain

Figure 2

From: Understanding LTP in pain pathways

Figure 2

Potential mechanisms of potentiation, prevention and de-potentiation at synapses between C-fibres and spinal cord projection neurons. Conditioning electrical nerve stimulation or natural noxious stimulation triggers release of glutamate and substance P which causes opening of NMDA receptor channels and T-type voltage-gated Ca2+ channel and Ca2+ release from intracellular stores. This activates Ca2+-dependent signal transduction pathways including protein kinases and transcription factors. Synaptic strength is probably increased by phosphorylation of synaptic proteins including AMPA receptor channels [55], altered trafficking of synaptic proteins, e.g. increased insertion of AMPA receptors into the sub-synaptic membrane [56] and de-novo protein synthesis. According to this model, LTP can be prevented if release of glutamate and/or substance P is inhibited, for example by activation of pre-synaptic, G-protein-coupled μ-opioid receptors, or if opening of voltage sensitive and Ca2+ permeable ion channels is blocked, e.g. via postsynaptic inhibition by an opioid. Depotentiation could result from de-phosphorylation of synaptic proteins, changes in receptors trafficking and degradation of synaptic proteins.

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