Secondary messenger systems

Abnormal G protein functioning dysregulates adenylate cyclase activity, phosphoinositide responses, sodiurrypotassiunVcalcium channel exchange, and activity of phospholipases. Abnormal cyclic adenosine monophosphate and phosphoinositide secondary messenger system activity. 

Normalizes or inhibits secondary messenger systems (e.g, inhibits phos-phoinositide and adenylate cyclase signaling normalizes guanine nucleotidebinding protein [G protein] signal transduction system) ... 

Increases choline in red blood cells and potentiates the cholinergic secondary messenger system. 

Figure 2.4. Relationship between the postsynaptic receptor and the secondary messenger system. GTP=guanosine triphosphate GDP=guanosine diphosphate ATP=adenosine triphosphate AMP=adenosine monophosphate.

At the postsynaptic level, lithium has been shown to reduce the function of beta adrenoceptors, presumably by affecting the coupling between the receptor and the secondary messenger system. This effect only becomes apparent following chronic treatment, which may help to explain the delay of several days, or even weeks, before an optimal beneficial effect is observed. All antidepressants are known to reduce the functional activity of postsynaptic beta receptors, which may explain why lithium has both an antimanic and an antidepressant effect in patients with manic-depression. 

With regard to its effect on neurotransmitter function, alcohol increases adenylate cyclase activity, possibly via the membrane-bound G protein complex. The effect of alcohol on the secondary messenger system appears to depend on its location the noradrenaline-linked cyclase in the cortex seems to be directly affected by the drug, whereas the dopamine-linked enzyme in the basal ganglia appears to be altered by a combination of changes in the membrane fluidity, together with those in the G protein-cyclase complex. 

Phosphatidylinositol system G protein linked secondary messenger system which,... 

Current research strongly suggests that lithium s actions inside neuronal cells explain therapeutic effects (Weber, Saklad, and Kastenholz 1992). Specifically, lithium inhibits receptor-induced overactivity of intracellular secondary messenger systems. These secondary messengers can be sent into overactive cycles by the action of various neurotransmitters at the receptor. Some neurotransmitters may induce manic symptoms others may induce depressive symptoms. Lithium s ability to interrupt these overactive pathways, regardless of the triggering neurotransmitter, may explain its action in both depression and mania. 

Bipolar disorder is likely caused by genetic factors, environmental triggers, and the dysregulation of neurotransmitters, neurohormones, and secondary messenger systems in the brain. 

This inhibition of tyrosine kinase, concerned with secondary messenger systems in cell growth and division, is an indicator of possible anticancer activity and the interesting activity shown by derivatives of rohitukine is discussed above. 

Potential modes of action of lead reproductive toxicity include disraption of the hypothalamic-pituitaiy-gonadal axis through reduced luteinizing hormone secretion and reduction in the expression of the steroidogenic acute regulatory protein (Crain et al. 2008 EPA 2012). Lead may also interfere with cation-dependent secondary messenger systems that mediate pituitary hormone release... 

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