Quoting from the book 'tuning the brain' written by Dr. J. Goldstein.
"Cannabinoids suppress central sensitization, a mechanism for chronic inflammatory pain. The endogenous cannabinoid anandamide is metabolized by fatty acid amidohydrolase. The action of the enzyme is blocked by nonsteroidal anti-inflammatory drugs (NSAIDs). If NSAIDs are effective in a neurosomatic patient, they may act by this mechanism."
"If excitatory inputs to the RTN are reduced (corticothalamic and collaterals from the ascending reticular activating system [ARAS]), the result will be large increases in receptive fields of thalamic neurons, a state that would worsen neurosomatic symptoms and increase central sensitization."
"IP3 increases intracellular Ca2+, and DAG activates PKC, which phosphorylates the NMDA receptor and removes the Mg2+ block. If this process can occur without first activating the AMPA receptor, the concomitant increase in SP and NR2B could produce depolarization and NMDA receptor-mediated events, including central sensitization."
"Other components of bee venom are serotonin (which is hyperalgesic), histamine, acetylcholine, and several kinins. There are also polypeptide toxins, such as melittin which damages cell membranes, mast cell degranulating protein, and apamin (a neurotoxin).
Tertiapin blocks muscarinic K+ channels. Enzymes include hyaluronidase, which helps the venom spread, and phospholipase A2, which is the major allergen. Many of these substances are arousal inducing, and most cause central sensitization."
"Diffusion of potentially algogenic transmitters may cause hyperalgesia and central sensitization in animals lacking (or perhaps with weakened)DNIC."
"Not only is the antihyperalgesic effect of GBP blocked by D-serine (and, therefore, cycloserine), but persistent activation of the NK1 receptor by SP removes the Mg2+ block of the NMDA-receptor channel (Urban L et al., 1994). This process contributes to postsynaptic central sensitization, as does a presynaptic hyperglutamatergic state."
"In addition to blocking Na+ channels, lidocaine inhibits the binding of SP to NK-1 receptors, altering central sensitization (TeradaHet al., 1999)."
"The patients may be more sensitive to potentially painful stimuli such as windup, increased pain sensation with each repetitive stimulus to a certain area (Staud R et al., 2001). Windup may be a manifestation of central sensitization of one or more wide dynamic range neurons as a result of long-term potentiation via NMDAreceptors (Gjerstad J et al., 2001). Neurosomatic patients often relapse after cognitive tasks."
