Euphoria, Depression, Madness

The norepinephrine neurons living in your locus coeruleus project throughout your brain. This broad access allows them to influence your level of arousal and thus almost every aspect of your thinking and behavior. Consistent with this role, it has recently been discovered that schizophrenic patients who display a chronic state of hyperarousal have significantly more norepinephrine neurons in their brains. 

Another pair of dopamine pathways originates in a region of the midbrain near the substantia nigra and ascends upward into the brain. One pathway projects to brain regions that are 

The production of dopamine and norepinephrine in your brain begins with the amino acid tyrosine, which is obtained from your diet. Tyrosine is converted to the amino acid levodopa, or L-DOPA, by the en2yme tyrosine hydroxylase. One very important cofactor is iron. Without iron, tyrosine hydroxylase fails to function normally. People with anemia have reduced body levels of iron and, as consequently, may have reduced tyrosine hydroxylase activity and thus reduced production of norepinephrine and dopamine. The decreased brain levels of these important neurotransmitters may lead to a slight depression, although most likely only in people with severe anemia. Generally, in a normal healthy person, the production of these two neurotransmitters is not easily affected by the contents of the diet. 

Tyrosine can also be acted on by the enzyme tyrosinase and converted into a dark pigment. This enzyme is quite interesting to study because it is vulnerable to a genetic mutation that makes it heat labile (i.e., it only works correctly in the cooler areas of the body). The consequence of this mutation is a lack of pigmentation in humans (albinism) and, conversely, the characteristic pattern of dark pigmentation at the ends of the nose, 

The second critical enzymatic step in this pathway is the conversion of L-DOPA into dopamine. This conversion process is extremely efficient, which may explain why brain levels of L-DOPA tend to be very low and why providing exogenous L-DOPA to patients who lack sufficient dopamine—that is, those with Parkinson s disease—leads to a dramatic increase in the production of dopamine. The surviving dopamine neurons in these patients brains will quickly convert L-DOPA into additional dopamine, which is then released. 

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