iGluR Antibodies for Pain Research Explorer Kit

Ionotropic Glutamate receptors (AMPA, NMDA and Kainate) have significant potential for therapeutic research in several types of persistent pain such as neuropathic pain resulting from injury to peripheral or central nerves, inflammatory pain and joint pain. Symptoms associated with these types of pain include allodynia, spontaneous pain and hyperalgesia. It is hypothesized that all these forms of clinical presentations depend on long term increases in synaptic efficacy of glutamatergic signaling in nociceptive pathways. This causes phosphorylation-induced alterations in the biophysical properties of ionotropic glutamate receptors and their trafficking to the postsynaptic membrane.

Inflammation and hyperalgesia have been found to cause an increase in GluA1 (a gene encoding the AMPA receptor) expression in the rostral ventral medial medulla area. This area gives rise to descending inhibitory inputs to sensory neurons in the spinal cord. In addition, blocking of the AMPA (and Kainate) receptors prevents the development of persistent pain states after exposure to incision and first degree burns in animal models.

Activation of NMDA receptors with appropriate receptor agonists, injected to rat hind paws, causes nociceptive behavior suggesting that NMDA receptors are involved in peripheral pain signaling. NMDA receptors are also involved in spinal cord injury pain signaling causing increased thermal algesia and mechanical allodynia when activated.

Kainate receptors are mostly localized on neuronal dendrites, postsynaptic membranes, nerve fibers and synaptic terminals. The main Kainate receptor involved in spinal cord injury pain signaling is the GLUK5 receptor. Although it is not yet fully understood whether Kainate receptors are also involved in pain signaling in the brain their wide expression within different parts of the brain such as the amygdala and the sensory cortex suggests so¹.