Biochemical Factors That Lead to Depression – Ssris and the Effects on the Chemical Make-Up of the Brain
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Over the past decade there have been many breakthroughs in the medical community regarding depression and how the roots of it stem from biochemical factors. While a large population in the medical communities dispute biochemical causes of depression versus cognitive behavior it has been found that the effect of certain medicinal compounds are proven effective in treating major depressive disorders. This paper will address how these compounds such as SSRIs and SNRIs play a part in the recovery or treatment of major depressive disorders.
This paper will describe how certain medications affect the serotonin levels in the brain, the catecholamine systems in the brain and the glutamate receptors in the brain. While it is has been proven that certain traumatic events experienced during childhood or adolescents can cause major depressive symptoms later in life, evidence has shown that when certain medications intervene, it often results in the person willing to pursuit treatment such as cognitive behavioral therapies more aggressively.
SSRIs and the Effects on the Chemical Make-Up of the Brain
SSRIS are the most widely prescribed anti-depressants in many countries to aid patients suffering from major depressive disorders. While the efficacy of SSRIs is currently disputed by many medical professionals a 2010-meta-analysis indicates that “The magnitude of benefit of anti depressant medication compared with placebo may be minimal on average in patients with mild or moderate symptoms. For patients however suffering from severe depression, the benefit of medications over placebo was found to be extremely substantial.”(Drevet, W. 2008). Another adaptive process provoked by SSRIs is the down regulation of postsynaptic serotonin 5-HT receptors. After the use of an SSRI, since there is more serotonin available, the response is to decrease the number of postsynaptic receptors over time and in the long run, this modifies the serotonin/receptor ratio. This down regulation of 5-HT2A occurs when the anit-depressant effects of SSRIs become apparent (www.en.wikipedia.//wiki/selective_serotonin_reputake_inhibitor). Also, deceased suicidal and otherwise depressed patients have had more 5-HT2A receptors than normal patients. These considerations suggest that 5- HT2A over activity is involved in the pathogenesis of depression.
The Function of the Catecholamine System Related to Depression
The other chemical system that has been associated with major depressive disorder is the Catecholamine System. This system consists of norepinephrine and dopamine in the brain. Norepinephrine or nor adrenaline is a catecholamine with multiple roles including as a hormone and neurotransmitter. Differences in the norepinephrine systems are implicated in depression. Serotonin-nor epinephrine reuptake inhibitors are anti-depressants that treat depression by increasing the amount of serotonin and norepinphrine available to postsynaptic cells in the brain (www.en.wikipedia./wiki/norepinephrine). There is some recent evidence implying that SNRIs may also increase dopamine transmission. This is because SNRIs work by inhibiting reuptake, i.e. preventing the serotonin and nor epinephrine transporters from taking their respective neurotransmitters back to their storage vesicles for later use. If the norepinephrine transporter normally recycles some dopamine too, then SSRIs will also enhance dopaminergic transmission. Therefore, the anti-depressant effects associated with increasing norepinephrine levels may also be partly or largely due to the concurrent increase in dopamine particularly in the prefrontal cortex of the brain. (Fishbain, D. 2007).
The Glutamate Receptors in the Brain in Relation to Depression
Recently studies as of late point to another