There are several the other neurotransmitter as etiologies of mood disorders for continue explanation about biogenic amines factors. We will find that neurotransmitter as etiologies of mood disorders below.
Dopamine
What is an imbalance dopamine cause mood disorders?. Although norepinephrine and serotonin are the biogenic amines most often associated with the pathophysiology of depression, dopamine has also been theorized to play a role. The data suggest that dopamine activity may be reduced in depression and increased in mania. The discovery of new subtypes of the dopamine receptors and an increased understanding of the presynaptic and postsynaptic regulation of dopamine function have further enriched research into the relation between dopamine and mood disorders.
Drugs that reduce dopamine concentrations for example, reserpine (Serpasil) and diseases that reduce dopamine concentrations (e.g., Parkinson's disease) are associated with depressive symptoms. In contrast, drugs that increase dopamine concentrations, such as tyrosine, amphetamine, and bupropion (Wellbutrin), reduce the symptoms of depression. Two recent theories about dopamine and depression are that the mesolimbic dopamine pathway may be dysfunctional in depression and that the dopamine D1 receptor may be hypoactive in depression.
Other Neurotransmitter Disturbances
Acetylcholine (ACh) is found in neurons that are distributed diffusely throughout the cerebral cortex. Cholinergic neurons have reciprocal or interactive relationships with all three monoamine systems. Abnormal levels of choline, which is a precursor to ACh, have been found at autopsy in the brains of some depressed patients, perhaps reflecting abnormalities in cell phospholipid composition. Cholinergic agonist and antagonist drugs have differential clinical effects on depression and mania (in Bipolar mood disorders). Agonists can produce lethargy, anergia, and psychomotor retardation in healthy subjects, can exacerbate symptoms in depression, and can reduce symptoms in mania. These effects generally are not sufficiently robust to have clinical applications, and adverse effects are problematic. In an animal model of depression, strains of mice that are super- or subsensitive to cholinergic agonists have been found susceptible or more resistant to developing learned helplessness (discussed below). Cholinergic agonists can induce changes in hypothalamic-pituitary adrenal (HPA) activity and sleep that mimic those associated with severe depression. Some patients with mood disorders in remission, as well as their never-ill first-degree relatives, have a trait-like increase in sensitivity to cholinergic agonists.
γ-Aminobutyric acid (GABA) has an inhibitory effect on ascending monoamine pathways, particularly the mesocortical and mesolimbic systems. Reductions of GABA have been observed in plasma, CSF, and brain GABA levels in depression. Animal studies have also found that chronic stress can reduce and eventually can deplete GABA levels. By contrast, GABA receptors are upregulated by antidepressants, and some GABAergic medications have weak antidepressant effects.
The amino acids glutamate and glycine are the major excitatory and inhibitory neurotransmitters in the CNS. Glutamate and glycine bind to sites associated with the N-methyl-D-aspartate (NMDA) receptor, and an excess of glutamatergic stimulation can cause neurotoxic effects. Importantly, a high concentration of NMDA receptors exists in the hippocampus. Glutamate, thus, may work in conjunction with hypercortisolemia to mediate the deleterious neurocognitive effects of severe recurrent type of mood disorders in depression. Emerging evidence suggests that drugs that antagonize NMDA receptors have antidepressant effects.
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