One of the most prominent discoveries of recent neuroscience is the finding that neurogenesis, the formation of new neurons, can occur in the adult brain. While it was previously thought that neurogenesis occurs only in developmental stages, recent breakthrough research has revealed novel analyses about the brain, specifically its inherent plastic nature. Plasticity is not just an attribute of the brain; many bodily mechanisms exhibit plastic properties, as well, including the pain pathway. Sensitization, or the lowered sensitivity threshold of pain-responsive receptors with increased stimulation, is one such example of plasticity in the pain response. Interestingly, mechanisms of pain and neurogenesis have been shown to be connected. Research indicates an inverse relationship between pain and neurogenesis: fewer neurons will form as pain is enhanced. Patients with Alzheimer’s disease, a disease in which adult neurogenesis occurs at a slower rate than normal, report a higher pain tolerance. The present study was designed to investigate if the administration of galantamine and nicotine, both of which are acetylcholine agonists but have opposing effects on neurogenesis, have effects on pain behavior associated with varying degrees of neurogenesis. We hypothesize that if neurogenesis increases with galantamine administration and decreases with administration of nicotine, the mice should display significantly more pain behavior in galantamine conditions when compared to both nicotine subjects and controls because of the increased number cells involved in the pain pathway that form in conjunction with new neurons. Such findings would establish a correlation between either increased pain threshold or analgesia and drug-induced neurogenesis. The general trend observed indicated that with increased neurogenesis, the subject exhibited more pain during the formalin test. Limitations and future research are discussed
To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.