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

Inhibitory Potential Changes of Fluoxetine (Prozac)Over the past some(prenominal) decades many scientists consume 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 particular 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 linked 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 major metabolite, 5-hydroxyndoleacetic acid (5-HIAA) consistently indicate that 5-HIAA levels are low in the cerebrospinal fluid of dep ressed patients (Davison, Neale and Kring, 2004). Because serotonin does not cross the blood-brain barrier, it must 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 re-uptake into nerve terminals done 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 being 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 i nactivation (Tollefson and Rosenbalum, p. 32, 2001).Low levels of serotonin have been most 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 inhibition 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 prosecution was the development 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