The brain monoamine data are presented in Table 2.
Brain monoamine concentrations were measured using high-performance liquid chromatography (HPLC) coupled to fluorometry.
Brain monoamine concentrations were determined using high-performance liquid chromatography coupled to fluorometry.
Even more recently, compounds that enhance the influence of brain monoamine neurotransmitters are being used to restore the functional integrity of multiple neuroendocrine axes and thereby to better protect against the ravages of advancing age.
Changes in brain monoamines were measured by HPLC with electrochemical detection, and serum corticosterone and leptin were monitored using radioimmunoassay.
Age-related declines of brain monoamines in mice were restored to levels observed in young mice by SQDB treatment [31].
In this study, the antidepressant effects of orally administered LEO were evaluated in mice by tail suspension test (TST) and their influence on the brain monoamines was determined.
Scarce data are available regarding its toxicity, pharmacokinetics and effects on brain monoamines.
This data is consistent with previous work that the potency of cocaine in inhibiting sodium channels is roughly 100 fold lower than those for the monoamine transporters [5].
Additionally, levels of brain monoamines and their metabolites were determined in the striatum, hippocampus and cortex of some of the experimental groups.
One possible source of increased oxidative stress are elevations in brain monoamine oxidase B (MAO-B) levels, which have been demonstrated to increase with age and in association with neurodegenerative disease both in humans and in mice [ 12, 13].
