sensitized neuron, outputs are no longer coupled to the intensity or duration and many inputs may be combined. Circuit Potentiation During high frequency stimulation synapses conveying nociceptive information may become hyper efficient in a process that is similar although not identical to long-term potentiation. Molecules such as substance P may be involved in potentiation via neurokinin receptors. NMDA activation also triggers a change in the post synapse, it activates receptor kinases that increase receptor trafficking and post-translationally modify receptors causing changes in their excitability. Cellular The phenomena described above are dependent on changes at the cellular and molecular levels. Altered expression of ion channels, changes in neurotransmitters and their receptors, as well as altered gene expression in response to neural input, are at play. Neuropathic pain is associated with changes in sodium and calcium channel subunit expression resulting in functional changes. In chronic nerve injury, there is redistribution and alteration of subunit compositions of sodium and calcium channels resulting in spontaneous firing at ectopic sites along the sensory pathway. See also Cranial nerves Nerve Neuralgia Neuritis Neuropathy References External links Pain