The uterine-contracting properties of the principle that would later be named oxytocin were discovered by British pharmacologist Sir Henry Hallett Dale in 1906,[125][46] and its milk ejection property was described by Ott and Scott in 1910[126] and by Schafer and Mackenzie in 1911.[127] In the 1920s, oxytocin and vasopressin were isolated from pituitary tissue and given their current names. The word oxytocin was coined from the term oxytocic, Greek ὀξύς, oxys, and τοκετός , toketos, meaning "quick birth".
Who is 5-HTP best for? Emotional eaters stand to benefit greatly, of course. So do carb addicts. Carbs help the body make 5-HTP — so when 5-HTP or serotonin are low, carb cravings kick in. Boosting 5-HTP with a supplement has been shown to slash carb cravings by more than 50 percent. And if a “fat gene” runs in your family, early evidence hints that this genetic tendency toward obesity is linked to “decreased activity of an enzyme that helps turn tryptophan into 5-HTP,” explains Michael T. Murray, ND, author of 5-HTP: The Natural Way to Overcome Depression, Obesity and Insomnia ($14.77, Amazon). Though more human research is needed, Dr. Murray believes 5-HTP supplements are a quick fix for the genetic glitch.
Recent preclinical studies by us and others have revealed that endogenous neurorestoration is present after TBI, including neurogenesis, axonal sprouting, synaptogenesis, and angiogenesis, which may contribute to the spontaneous functional recovery.13-18 In addition, treatments that promote these neurorestorative processes have been demonstrated to improve functional recovery after brain injury.19,20 However, clinical trials in TBI have primarily targeted neuroprotection, and trials directed specifically at neurorestoration have not been conducted. The essential difference between neuroprotective and neurorestorative treatments is that the former target the lesion that is still not irreversibly injured and the latter treat the intact tissue.19 Thus, neurorestorative treatments can be made available for a larger number of TBI patients.
Social behavior[66][111] and wound healing: Oxytocin is also thought to modulate inflammation by decreasing certain cytokines. Thus, the increased release in oxytocin following positive social interactions has the potential to improve wound healing. A study by Marazziti and colleagues used heterosexual couples to investigate this possibility. They found increases in plasma oxytocin following a social interaction were correlated with faster wound healing. They hypothesized this was due to oxytocin reducing inflammation, thus allowing the wound to heal more quickly. This study provides preliminary evidence that positive social interactions may directly influence aspects of health.[112] According to a study published in 2014, silencing of oxytocin receptor interneurons in the medial prefrontal cortex (mPFC) of female mice resulted in loss of social interest in male mice during the sexually receptive phase of the estrous cycle.[113] Oxytocin evokes feelings of contentment, reductions in anxiety, and feelings of calmness and security when in the company of the mate.[101] This suggests oxytocin may be important for the inhibition of the brain regions associated with behavioral control, fear, and anxiety, thus allowing orgasm to occur. Research has also demonstrated that oxytocin can decrease anxiety and protect against stress, particularly in combination with social support.[114] It is found, that endocannabinoid signaling mediates oxytocin-driven social reward.[115]

To determine the effects of Tβ4 peptide and H2O2 on cytotoxicity, its cell viability was evaluated. A 48-h exposure to 0.1–5 μg/mL Tβ4 peptide did not affect H2O2-mediated cell viabilities (Fig 2A). In order to examine whether Tβ4 peptide suppressed ROS-induced inflammatory mediators, the ability of Tβ4 peptide on production of NO and PGE2, and expressions of COX-2 and iNOS were measured by RT-PCR, Western blot, and ELISA. Pretreatment with Tβ4 peptide dose-dependently inhibited H2O2-induced mRNA and protein expressions of COX-2 and iNOS, and NO and PGE2 production (Fig 2B–2E).
When combined with antidepressants of the MAOI or SSRI class, very high parenteral doses of 5-HTP can cause acute serotonin syndrome in rats.[23][24] It is unclear if such findings have clinical relevance, as most drugs will cause serious adverse events or death in rodents at very high doses. In humans 5-HTP has never been clinically associated with serotonin syndrome, although 5-HTP can precipitate mania when added to an MAOI.[25]
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