The effect of a nutritional source of tryptophan on dieting-induced
changes in brain 5-HT function.
Psychol Med. 2003.
Dieting in healthy women results in a decrease in the availability of tryptophan, the amino-acid precursor of serotonin, for brain serotonin synthesis. This is associated with increases in the prolactin response to serotonin drug challenge suggesting a 'supersensitivity' of serotonin neuroendocrine responses. The aim of the study was to assess whether increased tryptophan intake during dieting would prevent the changes in tryptophan availability and serotonin neuroendocrine function. Fifty female subjects underwent a 1000 kcal daily diet for 3 weeks. In the final week of the diet subjects were randomly allocated to receive either nutritionally-sourced tryptophan ( g daily) or placebo in a double-blind, parallel group, design. Tryptophan supplementation failed to modify the dieting-induced reduction in fasting tryptophan availability to the brain. However, in contrast to placebo-treated subjects, subjects receiving additional tryptophan did not show enhanced prolactin responses to intravenous tryptophan challenge. The decrease in tryptophan availability produced by dieting may be due to increased tryptophan metabolism rather than decreased tryptophan intake. While tryptophan treatment did not increase fasting tryptophan availability it may have modified the effect of dieting on brain serotonin function. Further studies will test the effect of tryptophan has consequences for the effectiveness of dieting as means of weight control.
In isolated synaptoneurosomes, Noopept (as well as the endogenous peptide cycloprolylglycine) appear to modulate neuronal membrane potential, causing depolarization but and being able induce hyperpolarization in a calcium-dependent manner (hyperpolarization abolished in calcium-free medium); Noopept was more effective than cycloprolylglycine in this regard but the two were competitive rather than additive.  The researchers noted this effect could be due to blocking calcium channels (noted previously in snail neurons  where 10nM Noopept as well as both Piracetam at 100mM and Vinpocetine at 30mM at inhibiting slow inactivating potassium channels without influencing calcium or fast acting potassium channels  ) and would result in increased excitatory potential of neurons. However, as Noopept is also associated with protection against stroke (a mechanism related to opening potassium channels) a modulatory effect was proposed. 
Everyone should take such nutritional supplements daily for a lifetime because of all the health benefits provided by nitric oxide. Since NO declines appreciably with age, I suggest that men and women begin taking such nutritional supplements at a relatively young age, such as between 20 and 35 years of age. The younger the better. Having indicated that, it’s never too late to begin at any age because you will still enjoy the health benefits of nitric oxide at any age. I recommend strongly that women take products to boost their nitric oxide, and they should begin many years prior to onset of menopause. The reason for this pertains to the levels of estrogen in women, which decline sharply during and after menopause. Estrogen is well known to stimulate the production of NO, and prior to the onset of menopause women produce more NO than do men of equivalent age. Consequently, prior to menopause, women are more protected than are men of equivalent age against cardiovascular disease associated with low levels of NO, such as stroke and heart attack. However, big changes occur in women after menopause. The sharp decline in estrogen causes a simultaneous decline in NO production and thereby increases the risk for stroke and heart attack in women compared with men of equivalent age. Therefore, I recommend that women begin boosting their nitric oxide levels between 20 and 35 years of age and continue to do so daily for a lifetime.