If you suffer from severe depression which is interfere with your ability to function, the drug may be good for you. Thus, while many people use antidepressants when therapy strategies, exercise, or self-help might work as well or better, least side effects citalopram 20 . Therapy strategies and self-help can help you get to the root of your underlying issues and to develop the tools necessary to beat depression for good. Thus, while drug treatment may be beneficial, it is by no means the only answer. There are other effective treatment methods that can be taken in addition to or instead of drug. This is up to you to evaluate your options and decide what is best for you. However, few studies have examined the possibility that citalopram has other molecular mechanisms of action. We examined the effect of citalopram on delayed rectifier outward K+ current in mouse cortical neurons. Citalopram extracellular reversibly inhibited IK in a dose – dependent and significantly altered both steady-state activation and inactivation curves to hyperpolarizing. Neither the 5-HT itself or antagonists of 5-HT and dopamine receptor could abolish the citalopram-induced inhibition of IK. In addition, intracellular application of S- GTPγ the same failed to prevent the inhibition of IK by citalopram. When applied intracellularly, citalopram had no effect on indigenous knowledge and has no influence on the reduction of IK induced by extracellular citalopram. The effect of citalopram was use to load, but not frequency dependent, and there does not need to opening of the channel. Electrophysiological recordings in the acute cortical slice demonstrated that citalopram significantly reduced the action potential firing rate of cortical neurons and increased action potential duration . The blocker of Kv2.1 subunit selectively Jingzhaotoxin- III did not abolish the citalopram inhibition induced by KI. Transfection of HEK293 cells with Kv2.1 and Kv2.2 constructs indicated that citalopram mainly inhibited Kv2.2 current. We suggest that citalopram -induced inhibition of IK in mouse cortical neurons is independent of G- protein coupled receptors and may exert its antidepressant effects by enhancing synaptic efficacy.
‘And since this cell (MPC travel from the bone marrow) is coming from the periphery of the body, we would not need to use drugs may have adverse effects on the brain.’
The conclusion focuses on a key question in mental health research: the differences in people’s responses to antidepressant drugs, supposed to be based in part on differences in their genes. Some patients respond at the first attempt, they antidepressants, but most do not. Dose dependent on takes weeks to exert its full effect, and depression patient can worsen while they look for a drug that helps. Genetic studies, such as the one described here, can lead to a better understanding of which treatments are likely to work for each patient. Researchers studied DNA provided earlier by patients participating in a clinical trial recently completed NIMH. The study showed that depressed patients who do not benefit from the first medication they try to have a fair opportunity of being helped by others.