A new drug, known as Q5, is generating some interesting data.
Q5 is 2-methyl-4-oxo-3H-quinazoline-3-acetyl piperidine. Kovacs et al have reported in Neurosci Lett. 2007 Jul 4 have reported that Q5 enhances the activity of brain inhibitory networks in pain areas. Q5 is classed as an anticonvulsant. Of course, MANY anticonvulsants are alreaady in use for central pain, so what makes Q5 any different.
Perhaps there is little new or different about the drug, but the severity of pain is theorized to be due to FREQUENCY of the discharge. With Q5, the number of discharges diminishes but NOT the frequency or duration. We are not speaking of individual action potentials but more along the lines of group or field discharges.
c-fos is a marker or measure of genetic activity seen in the intermediate early period after a stimulus and is supposed to represent heightened genetic manufacture, presumably toward the production of pain chemicals in neurons (and other cells).
Injection of Q5 causes signficant depletion of c-fos in the following areas: hypothalamic paraventricular nucleus, medial amygdaloid nucleus, piriform cortex, somatosensory cortex (SI), periventricular thalamic nucleus and periaqueductal central gray (PAG). These may be results or effects and not causative findings SI, the thalamus, and the PAG are important pain areas. Finding an anticonvulsant which more specifically targets pain areas is interesting. Perhaps better anticonvulsants will be developed for quieting the brain where we need it most.