Depression is one of the most discussed and research topic in psychology and psychiatry. In earlier ages, depression, like many other mental diseases, was diagnosed as a form of demonic possession and a sickness from evil spirits. Again, like many other mental illnesses, the measures that were deemed appropriate to drive out the ‘evil spirits and demons’ were very extreme and ranged from lashings, use of restraints, imposed isolation and imposed starvation (History Today, 2012). Slowly, it started being linked to physiological illnesses and in the 4th century, depression was described as ‘melancholia’-attributed to an imbalance in the fluids of the four humours: blood, black bile, yellow bile and phlegm. It was suggested by Hippocrates that
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The research was done to how on what serotonin actually does in the brain and what it has to do with depression. A mouse brain was used because it is quite similar to human brain and a working mouse brain is easier to access than a working human brain. Mouse models were genetically modified to have varying levels in serotonin availability and the effects these differences had on their neurogenesis and overall mood were observed. Synthesis of serotonin is activated by amino acid tryptophan hydroxylase (TPH) and is inhibited by para-chlorophenylalanine (p-CPA). Some of the genetically modified mouse models were made with genes that serotonin receptor subtypes (5-HT1A), some with a tryptophan hydroxylase subtype (TPH2), some with gene subtypes that affect vesicular packaging (VMAT2) and serotonin re-uptake (SERT). In the transgenic mouse models were these modified genes caused lower levels of serotonin by inhibiting serotonin and serotonin receptor binding, inhibiting TPH2, inhibiting VMAT2 or inhibiting serotonin reuptake, behaviours like exaggerated aggressiveness, lowered anxiety and higher impulsivity were observed. They perceived that these serotonin deficient mice did not display the expected ‘depression model’ model phenotype suggested by Fernandez et al, 2012. This resulted in their conclusion that there is not necessarily a connection between depression and serotonin levels (Alenina et al, 2015). This research was quite efficient, but more research needs to be done because while mouse brain is really similar to human brain, there are still some differences and these differences might affect whether or not serotonin levels have an effect in causing depression so this experiment should be repeated more times on an animal like primates who have brains more similar to
The research was done to how on what serotonin actually does in the brain and what it has to do with depression. A mouse brain was used because it is quite similar to human brain and a working mouse brain is easier to access than a working human brain. Mouse models were genetically modified to have varying levels in serotonin availability and the effects these differences had on their neurogenesis and overall mood were observed. Synthesis of serotonin is activated by amino acid tryptophan hydroxylase (TPH) and is inhibited by para-chlorophenylalanine (p-CPA). Some of the genetically modified mouse models were made with genes that serotonin receptor subtypes (5-HT1A), some with a tryptophan hydroxylase subtype (TPH2), some with gene subtypes that affect vesicular packaging (VMAT2) and serotonin re-uptake (SERT). In the transgenic mouse models were these modified genes caused lower levels of serotonin by inhibiting serotonin and serotonin receptor binding, inhibiting TPH2, inhibiting VMAT2 or inhibiting serotonin reuptake, behaviours like exaggerated aggressiveness, lowered anxiety and higher impulsivity were observed. They perceived that these serotonin deficient mice did not display the expected ‘depression model’ model phenotype suggested by Fernandez et al, 2012. This resulted in their conclusion that there is not necessarily a connection between depression and serotonin levels (Alenina et al, 2015). This research was quite efficient, but more research needs to be done because while mouse brain is really similar to human brain, there are still some differences and these differences might affect whether or not serotonin levels have an effect in causing depression so this experiment should be repeated more times on an animal like primates who have brains more similar to