Inhibitory Potential Changes of Fluoxetine (Prozac) :: Biology Medicine Research Papers

Inhibitory Potential Changes of Fluoxetine (Prozac)Over the past several decades more scientists have explored the various possible links between the function of neurotransmitters in the brain and mood disorders. The neurotransmitter serotonin, found widely in plants, animals and humans has been a contingent focus. Scientists who specialize in examining the function and effect of serotonin on the mind and body argue that imbalances in the levels and function of serotonin can be joined to disturbances in mood, anxiety, satiety, cognition, aggression and sexual drives (Tollefson and Rosenbalum, 2001). More specifically, these scientists suggest that this decreased serotonergic neurotransmission plays an important role in the etiology of depression (Xia, Gopal, and Gross, p. 157, 2002). Indeed studies that have examined serotonin via its study metabolite, 5-hydroxyndoleacetic acid (5-HIAA) consistently indicate that 5-HIAA levels are low in the cerebrospinal fluid of depressed pat ients (Davison, Neale and Kring, 2004). Because serotonin does not cross the blood-brain barrier, it must(prenominal) be synthesized locally. That is, it must be synthesized from within neurons in the brain. Once it is synthesized is then released into the synapse from the cytoplasmic and vesicular reservoirs. Following release, serotonin is principally inactivated by reuptake into nerve terminals through a sodium/potassium (Na+/K+) adenosine triphosphatase (ATPase) dependent carrier. (Tollefson and Rosenbalum, p. 27, 2001). Problems arise when too much serotonin is recaptured in the reuptake process during synapse or when to little serotonin is creation locally manufactured in the central nervous system. As a result, too few serotonin neurotransmitters are able to make it across the synaptic cleft to stimulate postsynaptic receptors. Moreover, in the absence of pharmacological manipulation, the reuptake of serotonin into the presynaptic nerve terminal typically leads to its inactivation (Tollefson and Rosenbalum, p. 32, 2001).Low levels of serotonin have been approximately commonly linked to depression. For this reason, there have been many attempts by neuroscientists to develop antidepressant drugs that can interfere with the enzymes that eliminate serotonin neurotransmitters from the synapse. Indeed, though reuptake banning scientists hoped to be able to increase levels of serotonin in the CNS and thus ameliorate the negative affects of depression. One of the most recent breakthroughs in this pursuit was the exploitation of the antagonist drug, fluoxetine. Fluoxetine (or Prozac) is a selective serotonin reuptake inhibitor, and functions by acting as a barrier in the serotonin synaptic