Depression adrenergic receptors

The original monoamine hypothesis of depression states that depressions are associated with a deficiency of catecholamines, particularly norepinephrine, at functionally important adrenergic receptor sites in the brain. Elation conversely may be associated with an excess of such amines. The hypothesis was articulated in 1966 only after the mechanism of action of the tricyclic antidepressant desipramine and of the psychostimulants... 

Low-dose dopamine is not without adverse reactions and most studies have failed to evaluate its potential toxicities. Adverse reactions that may be associated with low-dose dopamine include tachycardia, arrhythmias, myocardial ischemia, depressed respiratory drive, and gut ischemia. Low-dose dopamine has also been postulated to impair resistance to infection through a reduction in prolactin concentrations.21 Furthermore, significant overlap in receptor activation occurs. Therefore, doses considered to activate only dopamine receptors may increase cardiac output and blood pressure through dopamine s effect on 3- or a-adrenergic receptors. 

Trazodone routinely causes sedation, which is why it is used far more often as an adjunct with other antidepressants for sleep than as a primary agent for the treatment of depression. Priapism is a rare but serious adverse effect in males who take trazodone. In addition, orthostatic hypotension and dizziness are more common with trazodone than with nefazodone because the latter agent has a weaker effect at a-adrenergic receptors and also has a balancing of adrenergic effects owing... 

Price, L. H., Charney, D. S., Rubin, A. L. and Heninger, G. R. Alpha 2-adrenergic receptor function in depression. The cortisol response to Yohimbine. Arch. Gen. Psych. 43 849-858,1986. 

Some failures will be due to the presence of variants in drug handling. Patients who are rapid acetylators of isoniazid have a slower antituberculous response than slow acetylators (Evans and Clarke, 1961). Asthmatics who do not respond well to (32-agonist bronchodilators may have fewer functioning p2-adrenergic receptors (Drysdale et al., 2000). Variations in the synthesis or structure of the serotonin transporter protein, which is involved in selective reuptake of serotonin by presynaptic neurons, may explain why some patients with depressive disorders respond to selective serotonin reuptake inhibitors and others do not (Steimer et al., 2001). 

Binds to DNA and prevents separation of the helical strands Affects neuronal transmissions Binds to opiate receptors and blocks pain pathway Acts as central nervous system depressant Inhibits Na/K/ATPase, increases intracellular calcium, and increases ventricular contractibility Blocks the actions of histamine on Hi receptor Blocks ai-adrenergic receptor, resulting in decreased blood pressure Inhibits reuptake of 5-hydroxytryptamine (serotonin) into central nervous system neurons Inhibits cyclooxygenase, inhibition of inflammatory mediators Inhibits replication of viruses or tumor cells Inhibits HIV reverse transcriptase and DNA polymerase Antagonizes histamine effects... 

Abdulla D, Renton KW. 2005. Beta-adrenergic receptor modulation of the LPS-mediated depression in CYPIA activity in astrocytes. Biochem Pharmacol 69 741-750. 

Schramm NL, McDonald MP, Limbird LE (2001) The alpha(2a)-adrenergic receptor plays a protective role in mouse behavioral models of depression and anxiety. J Neurosci 21 4875-4882... 

Schmidt P, Holsboer F, Spengler D (2001) Beta(2)-adrenergic receptors potentiate glucocorticoid receptor transactivation via G protein beta gamma-subimits and the phospho-inositide 3-kinase pathway. Mol Endocrinol 15 553-564 Schramm NL, McDonald MP, Limbird LE (2001) The alpha(2a)-adrenergic receptor plays a protective role in mouse behavioral models of depression and anxiety. J Neurosci 21 4875-4882... 

The directly acting vasodilators, with the exception of calcium channel antagonists and sympathetic nervous system depressants, receive the bulk of attention in this chapter. Other chapters offer additional information on diuretics (see Chapter 21), the renin-angiotensin system (see Chapter 18), adrenergic receptor antagonists (see Chapter 11), and the calcium channel antagonists (Chapter 19). 

Mecfianism of Action A tetracyclic compound that acts as an antagonist at presynap-tic alphaj-adrenergic receptors, increasing both norepinephrine and serotonin neurotransmission. Flas low anticholinergic activity. Therapeutic Effect Relieves depression and produces sedative effects. 

Mechanism of Action Exact mechanism is unknown. Appears to inhibit neuronal uptake of serotonin and norepinephrine and to antagonize alpha -adrenergic receptors. Therapeutic Effect Relieves depression. 

Other effects Drowsiness occurs due to CNS depression, usually during the first 2 weeks of treatment. Confusion is sometimes encountered.The neuroleptics often produce dry mouth, urinary retention, constipation, and loss of accommodation. They block a-adrenergic receptors, resulting in lowered blood pressure and orthostatic hypotension. The neuroleptics depress the hypothalamus, causing amenorrhea, galactorrhea, infertility, and impotence. 

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