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Types and symptoms

Legality | Mechanisms and effects | Addiction | Serotonin/norepinephrine reuptake inhibitors, SNRIs | Antidepressants, Other | Tricyclic antidepressants, TCAs | Monoamine oxidase inhibitors, MAO Is | Summury | Глоссарий терминов и аббревиатур |


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Depending on the number and severity of symptoms, a depressive episode can be categorized as mild, moderate, or severe.

A key distinction is also made between depression in people who have or do not have a history of manic episodes. Both types of depression can be chronic (i.e. over an extended period of time) with relapses, especially if they go untreated.

 

 

Drugs used for the treatment of depression include the following:

· Selective serotonin reuptake inhibitors (SSRIs)

· Serotonin/norepinephrine reuptake inhibitors (SNRIs)

· Atypical antidepressants

· Tricyclic antidepressants (TCAs)

· Monoamine oxidase inhibitors (MAOIs)

· St. John’s wort (Hypericum perforatum)

 

All antidepressants on the market are potentially effective. Usually, 2-6 weeks at a therapeutic-dose level are needed to observe a clinical response. The choice of medication should be guided by anticipated safety and tolerability, which aid in compliance; physician familiarity, which aids in patient education and anticipation of adverse effects; and history of previous treatments. Often, treatment failures are caused not by clinical resistance but by medication noncompliance, inadequate duration of therapy, or inadequate dosing.

Antidepressants can have central and peripheral anticholinergic effects, as well as sedative effects, and can block the active reuptake of norepinephrine (NE), serotonin (5-HT), and dopamine. SSRIs are metabolized via the cytochrome P-450 system and may have drug interactions on that basis. The degree of enzyme inhibition varies among SSRIs. Effects on blood levels and bioavailability of coadministered drugs, as well as pharmacodynamic interactions, account for most clinically significant SSRI-drug interactions.

All available antidepressants appear to work via one or more of the following mechanisms :

· Presynaptic inhibition of uptake of 5-HT or NE

· Antagonist activity at presynaptic inhibitory 5-HT or NE receptor sites, thereby enhancing neurotransmitter release

· Antagonism of NE beta or serotonin 5-HT2 receptors

· N-Methyl-D-aspartate (NMDA) receptor antagonism

· Induction of brain-derived neurotrophic factor (BDNF)

· Inhibition of monoamine oxidase, thereby reducing neurotransmitter breakdown

 


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