Posted by Kizzie2 on October 16, 2011, at 12:09:54
Hi - I just wondered if anyone can explain what any if this actually means. It's taken from CNS forum. I am long term ad user and trying to find out effects (paxil then anafranil). Thanks for any help x. CNS Image Bank:
Depression - Long term antidepressant treatmentThe consequences of long term antidepressant treatment
Chronic administration of antidepressants can cause a number of changes in the brain, depending on the particular drug type: (1) SSRIs and MAOIs desensitize inhibitory 5-HT1A somatodendritic receptors and inhibitory pre-synaptic 5-HT1D autoreceptors. They can also prevent the uptake of 5-HT into the nerve terminal by binding to the imipramine binding site (2) TCA, electroconvulsive therapy (ECT) and other non-SSRI antidepressants can sensitize inhibitory post-synaptic 5-HT1A receptors and can reduce the expression of stimulatory 5-HT2A receptors. (3) Experimental evidence suggests that chronic antidepressant treatment can also affect post-receptor signalling mechanisms, such as G-proteins.
Changes in gene expression following administration of antidepressants: noradrenaline transporter
Tricyclic antidepressants and selective noradrenaline re-uptake inhibitors rapidly bind to and block the action of noradrenaline re-uptake transporters (NARTs). Chronic administration of these antidepressants leads to changes in NART gene expression. A significant increase in NART expression is seen in the hippocampus and the in cingulate, frontal, parietal, perirhinal, entorhinal and insular cortices in response to chronic antidepressant treatment. A decrease in NART expression is seen in the temporal cortex.
Changes in gene expression following administration of antidepressants: serotonin transporter
Tricyclic antidepressants and selective serotonin re-uptake inhibitors rapidly bind to and block the action of serotonin re-uptake transporters (SERTs). Chronic administration of these types of antidepressants leads to changes in SERT gene expression. A significant increase in SERT expression is seen in the hippocampus and the cingulate, insular, perirhinal and parietal cortices in response to chronic antidepressant treatment.
The effects of chronic antidepressant treatment on gene expression in the brain
Although the acute action of antidepressant treatment is associated with monoamine re-uptake inhibition, the molecular adaptations underlying the therapeutic action of these agents have still to be determined. Chronic administration of desipramine, fluoxetine and tranylcypromine has been shown to up-regulate the cAMP signal transduction cascade resulting in increased expression and function of the transcription factor CRE binding protein (CREB), in various regions of the brain, particularly the cerebral cortex and hippocampus. In turn, enhanced CREB expression leads to an upregulation in cAMP response element (CRE )-mediated gene transcription in these areas. For example, brain-derived neurotrophic factor (BDNF) expression is increased in the hippocampus. Studies have also demonstrated that expression of other transcription factors (NGF1-A, mineralocorticoid receptor (MR), glucocorticoid receptor (GR), c-Fos) is increased following treatment with a similar range of antidepressant drugs. Decreases in mRNA of corticotrophin-releasing factor (CRF) and its receptor CRF-R1 have been detected in the hypothalamus and amygdala, respectively, following chronic amitriptyline administration. Moclobemide causes decreased expression of the transcription factor NGF1-B in the hippocampus.
poster:Kizzie2
thread:999894
URL: http://www.dr-bob.org/babble/20111016/msgs/999894.html