in the knockout mice is a strike against the argument that low levels of 5-HT cause an onset of depressive symptoms because these mice lack the ability to reuptake the 5-HT that is left in the extracellular space. The monoamine hypothesis was and still is a good starting point for needing to search for the biological basis of depression. It is now understood however, that this theory needs to be broadened and fill in the gaps that have opened up in the literature. It is important to consider an alternative view to this unsolved question.
Neurotrophic theory An alternative theory to the monoamine hypothesis is the neurotrophic theory which states that depression could be due to the reduced synthesis of proteins which are involved in neurogenesis …show more content…
Duman and Li (2012) describe findings of reduced limbic brain structures in brains of depressed patients in particular a reduction in mass of the hippocampus and PFC. They also described preclinical studies which found participants who were exposed to stress regularly, in the hippocampus and PFC of their brains there was evidence of neuronal atrophy as well as loss of glial cells and neuronal cells seem to contribute to mood disorders such as MDD. Duman and Li (2012) highlighted that brain-derived neurotrophic factor (BDNF) is one of the most studied neurotrophic factors and rodent models have found a correlation between various types of stress and a reduction in BDNF in the PFC and hippocampus. Duman and Li (2012) explained these findings had also been observed in the post-mortem studies of depressed human participants and further went on to explain that with antidepressant treatment such as SSRIs and SNRIs, BDNF had been observed to increase in expression in the before mentioned areas. Duman and Li (2012) reiterate however that these results are after the use of these antidepressants over a period of time and do not show any changes in the acute use of the …show more content…
Duman, Russell & (2007) looked at BDNF knock out mice who in the baseline condition behaved normally however, when placed in a stressful environment they exhibited depressive behaviour. A study by Casey, Glatt, Tottenham, Soliman, Bath, Amos and colleagues (2009) looked at human genetics specifically the BDNF gene and its resilience and susceptibility in relation to environmental factors. Casey et al (2009) wanted to focus not only on the polymorphism in terms of its importance in developmental processes but also what the impact across development it had. Casey et al (2009) used a genetic mouse model, utilising the Val66Met, a single nucleotide polymorphism of BDNF that was identified and observed to be responsible for the reduction in process and release of BDNF. Casey et al (2009) explained this allele played roles in executive function and episodic memory as well as was found to be partly responsible for the reduced hippocampal volume in not just depressed participants but the controls also. Casey et al (2009) looked at BDNFmet/met, a genotype that been associated with an anxious phenotype and found that in mice with BDNFmet/met, they tend to spend more time “frozen” in response to a conditioned stimulus even when the aversive stimulus is not present. Casey et al (2009) also demonstrated this