Pain mediator glutamate

Figure 21.5 Mechanisms of opioid analgesia at the spinal level. Action potentials in nociceptive afferent fibres invade the terminal and by opening calcium channels (L, N and P-type) cause the release of glutamate and peptides that further transmit pain subsequent to activation of their postsynaptic receptors. Presynaptic opioid receptor activation (mu- and delta-mediated effects have been most clearly shown) opens potassium channels which hyperpolarise the terminal, so reducing transmitter release and inhibiting the postsynaptic neuron...

Schematic diagram of a primary afferent neuron mediating pain, its synapse with a secondary afferent in the spinal cord, and the targets for local pain control. The primary afferent neuron cell body is not shown. At least three nociceptors are recognized acid, injury, and heat receptors. The nerve ending also bears opioid receptors, which can inhibit action potential generation. The axon bears sodium channels and potassium channels (not shown), which are essential for action potential propagation. Synaptic transmission involves release of substance P, a neuropeptide (NP) and glutamate and activation of their receptors on the secondary neuron. Alpha2 adrenoceptors and opioid receptors modulate the transmission process.

Miyata M., Kashiwadani H., Fukaya M., Hayashi T., Wu D. Q., Suzuki T., Watanabe M., and Kawakami Y. (2003). Role of thalamic phospholipase C/S4 mediated by metabotropic glutamate receptor type 1 in inflammatory pain. J. Neurosci. 23 8098-8108. 

Chronic pain due to nerve injury results in sensitization of the central nervous system, maintained by a state of sensitization that is mediated in part by glutamate binding to the NMDA receptor (Dickenson, 1990 Coderre, 1993). A key step in the... 

Morita, K., Kitayama, T., Morioka, N., and Dohi, T. (2008). Glycinergic mediation of tactile allodynia induced by platelet-activating factor (PAF) through glutamate-NO-cyclic GMP signalling in spinal cord in mice. Pain 138, 525—536. 

Most often more than one neurotransmitter is released at the same time. Aspartate and glutamate are excitatory amino-acids (EAAs) involved in pain transmission [4,5]. Glutamate is the main excitatory CNS nem-otransmitter and mediates rapid, short-duration depolarization of second-order neurons. Peptides such as substance P and neurokinin are responsible for delayed long-lasting depolarization. EAAs act on various receptors, which principally include alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic... 

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