The third group of modifiers in Table 1 included the PEO/PPO monoamines
. The cation exchange ratio of the PEO-based monoamines
again was much lower than the n/CEC of the PPO-based monoamines
, which were comparable to the n/CEC of the alkylammonium modifiers of the first group in Table 1.
Moreover, when measured 2 weeks after the end of exposure, the levels of various monoamines
and the numbers of tyrosine hydroxylase-positive (T[H.sup.+]) and -negative (T[H.sup.-]) cells measured using unbiased stereology were reduced in both dopaminergic tracts.
Although existing antidepressant medications increase levels of monoamines
in the brain, there is a delay between measured increases in monoamines
and corrections in mood.
Today's antidepressant drugs enhance the levels of monoamines
in the brain (particularly in the synaptic gaps between neurons), by either preventing their degradation by enzymes or blocking their reabsorption into the neurons that released them.
The effects of two chronic intermittent stressors on brain monoamines
. Pharmaology, Biochemistry, and Behavior, 53(3): 517-523.
The knowledge of how much exercise it takes to stimulate the production of endorphins, their chemical structure and the location of their secretory centers will provide a teleologic clue as to why increased endorphin output (along with monoamines
, e.g., serotonin, norepinephrine) contributes to psychophysiologic benefits for the exerciser.
VMAT2 is a protein concentrated in the human brain that is primarily responsible for re-packaging and transporting monoamines
(dopamine, norepinephrine, serotonin, and histamine) in pre-synaptic neurons.
hypothesis of depression postulates that symptoms originate from underactivity of monoamines
, such as serotonin, norepinephrine, and dopamine, in the brain.
Therefore, this is the first report which identified the anti-stress activity of novel Ocimumoside A and B at the level of central monoamines
and antioxidant properties, implicating their therapeutic importance in the prevention of stress-related disorders.
Writing about their work in the the Journal of Clinical Psychopharmacology, the researchers point out that placebos are thought to act by stimulating the brain's central reward pathways by releasing a class of neurotransmitters called monoamines
, specifically dopamine and norepinephrine.
Tetrabenazine is a centrally acting drug that reversibly inhibits vesicular monoamine
transporter-2, depletes monoamines
presynaptically, and depletes dopamine preferentially over norepinephrine and 5-hydroxytryptamine, according to Prestwick Pharmaceuticals.
They are located on mitochondrial membranes and have functions that pertain to regulation of the synaptic availability of monoamines