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Effects of Antidepressants on Specific Neurotransmitters: Are Such Effects Relevant to Therapeutic Actions?
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
The precise mechanism of action of antidepressants still remains an enigma. Nevertheless, evidence from both clinical and experimental studies suggests that all effective antidepressants, regardless of their presumed selectivity of action determined by acute experimental studies, ultimately bring about adaptive changes in both monoaminergic and nonaminergic systems. This raises some important and fundamental questions. If, for example, the SSRI antidepressants do not inhibit serotonin reuptake into platelets from depressed patients (despite their proven effect in healthy volunteers and in rat brain), their classification as selective serotonin reuptake inhibitors is a misnomer [47]. Similarly, SNRI antidepressants affect the turnover of serotonin following their chronic administration and also normalize the defective reuptake of 3H serotonin into platelets from depressed patients, thereby losing their presumed selectivity. Such findings lend support to the hypothesis that the neural network of interconnected neurotransmitter systems is malfunctioning in depression and that all antidepressants, by initially acting at different parts of the network, eventually bring the system back to homeostasis. Clearly, the monoamine hypothesis of depression, despite its value in the past, needs to be radically restructured or even replaced to take into account the latest research emanating from molecular biology. The increasingly important contribution of molecular biology to our understanding of the mode of action of antidepressants, and indirectly to the biology of depression, has helped to focus attention on the changes that occur in the secondary and tertiary messenger systems and, ultimately, in gene expression. These intracellular changes only occur following the chronic administration of antidepressants and are independent of the type of antidepressant. From experimental studies, it appears that specific neurotrophic factors provide the final common pathway that leads to changes in synaptic plasticity and improved neuronal contacts.
Olfactory bulbectomy and raphe nucleus relationship: a new vision for well-known depression model
Published in Nordic Journal of Psychiatry, 2020
Halil Ozcan, Nazan Aydın, Mehmet Dumlu Aydın, Elif Oral, Cemal Gündoğdu, Sare Şipal, Zekai Halıcı
In this study, we hypothesized that the damage in OBs leading to depressive symptoms might be related to neuronal destruction leading to neurotransmission loss in DRNs. We think that the data expressing the biology of how OBX leads to depression might shed light on the biology of depression.
Neurobiology of depression: A neurodevelopmental approach
Published in The World Journal of Biological Psychiatry, 2018
Juan M. Lima-Ojeda, Rainer Rupprecht, Thomas C. Baghai
Numerous candidate genes for depression have been suggested (Kato 2007; Lohoff 2010; Utge et al. 2010). Also, to date, several studies have revealed a correlation between gene–environment interactions and depression (Uher 2014; Lopizzo et al. 2015). It is interesting to note that genes involved in the neurodevelopmental process also play a role in the biology of depression. The brain-derived neurotrophic factor gene (BDNF gene) appears to be important in neurodevelopment (Mitchelmore & Gede 2014). The protein encoded by this gene has been linked with events such as synaptic maturation during early development (Sallert et al. 2009) and neuronal survival (Lipsky & Marini 2007). Furthermore, Hall et al. (2000) observed an association between the BDNF gene and hippocampal long-term potentiation (LTP). Interactions between early-life stressful events, such as the loss of a parent, childhood maltreatment and a complicated parental environment, and BDNF gene polymorphism increase the risk of developing a depressive syndrome later in life (Kim et al. 2007; Gatt et al. 2009; Carver et al. 2011). Another candidate gene with implications in development of depression is the one that encodes the type 1 corticotropin-releasing hormone receptor (CRH-R1). Koutmani et al. (2013) reported that CRH, particularly though its type 1 receptor (R1), plays an important role in early neurogenesis and neuroprotection. Also, CRH participates in the adaptive response to stress (Rogers et al. 2013). The effects of maltreatment on children may be associated with CRH-R1 polymorphism and adult depression (Bradley et al. 2008). The evidence suggests that serotonin (5-hydroxytryptamine or 5-HT) plays a key role as a developmental signal modulating neurogenesis (Gaspar et al. 2003). Genes related to serotonin, such as the serotonin 2A receptor gene (HTR2A) (Zhao et al. 2014), the solute carrier family 6 member A4 gene (SLC6A4) (Caspi et al. 2003) and the tryptophan hydroxylase 2 gene (TPH2) (Haghighi et al. 2008) have been associated with depression, where early-life stress has the capacity to produce a genetic moderation of these genes (Caspi et al. 2003; Shinozaki et al. 2013; Van der Auwera et al. 2014). In general, the above-mentioned interactions seem to show a robust link with both neurodevelopment and depression. However, the list of gene–environment interactions in depression is substantial with a large number of candidate genes (Lopizzo et al. 2015; Uher 2014).