At first, the mice showed an irregular smattering of neural impulses when they heard the baby's cries. Then, as the oxytocin kicked in, the signal evolved into a more orderly pattern typical of a maternal brain. The study showed in unusual detail how the hormone changed the behaviour of neurons1. “Oxytocin is helping to transform the brain, to make it respond to those pup calls,” Froemke says.

The short half-life (<2h)[16] of 5-HTP may inherently limit the therapeutic potential of 5-HTP,[17] as the systemic 5-HTP exposure levels will fluctuate substantially, even with relatively frequent dosing. Such exposure fluctuations are usually associated with increased adverse event burden, resulting from Cmax drug spikes, and decreased clinical efficacy resulting from sub-therapeutic exposure for large parts of the day. It has been proposed that 5-HTP dosage forms achieving prolonged delivery would be more effective,[17] as is generally the situation with short-acting active pharmaceutical ingredients.[18]
To investigate whether the newborn neurons generated in the DG are capable of projecting their axons into the CA3 region of the hippocampus after TBI, we stereotactically injected a fluorescent tracer, 1,1″-dioleyl-3,3,3″,3″-tetramethylindocarbocyanine methanesulfonate (Dil, Delta 9-DiI; AnaSpec, San Jose, CA) into the ipsilateral CA3 region (stereotaxic coordinates AP, -3.6 mm bregma, ML, 3.6 mm, DV, 3.0 mm, Paxinos and Watson, 1994) at day 28 after TBI. BrdU (100mg/kg, ip) was injected i.p. daily starting at day 1 after TBI for 10 days to label newly generated cells. One week after DiI injection (i.e., 35 days after TBI), the animals were anesthetized and sacrificed. Their brains were fixed in 4% paraformaldehyde. The brain was cut into seven equally spaced 2-mm coronal blocks using a rat brain matrix. The brain blocks containing the hippocampus were processed for vibratome sections (100 μm) followed by BrdU staining. BrdU and DiI labeling in the hippocampus on brain sections was analyzed with a Bio-Rad MRC 1024 (argon and krypton) laser-scanning confocal imaging system mounted onto a Zeiss microscope (Bio-Rad, Cambridge, MA). Co-localization of BrdU-positive nuclei within retrogradely DiI-labeled granule cells was found, indicating that newborn granule neurons extend axons into the CA3 region that are capable of retrogradely transporting DiI from the CA3 to their cell bodies within the DG after TBI (Fig.2). This finding suggests that newborn granule neurons may be incorporated into functional hippocampal circuitry after TBI.
To prevent adverse effects, always consult your physician and pharmacist before taking any drug or supplement. Inform your doctor and pharmacist about all drugs you take, whether they are prescription, non-prescription, vitamins, supplements, or herbs. Be sure to read and understand the Drug Facts section of the product label before taking any medication, and never take more than what is specified by your doctor. Dietary supplements are drugs, so be sure to keep them out of sight and reach of children and pets.
Johansson, A., Westberg, L., Sandnabba, K., Jern, P., Salo, B., & Santtila, P. (2012). Associations between oxytocin receptor gene (OXTR) polymorphisms and self-reported aggressive behavior and anger: Interactions with alcohol consumption [Abstract]. Psychoneuroendocrinology 37(9), 1546-56. Retrieved from
Oxytocin produces antidepressant-like effects in animal models of depression,[81] and a deficit of it may be involved in the pathophysiology of depression in humans.[82] The antidepressant-like effects of oxytocin are not blocked by a selective antagonist of the oxytocin receptor, suggesting that these effects are not mediated by the oxytocin receptor.[17] In accordance, unlike oxytocin, the selective non-peptide oxytocin receptor agonist WAY-267,464 does not produce antidepressant-like effects, at least in the tail suspension test.[83] In contrast to WAY-267,464, carbetocin, a close analogue of oxytocin and peptide oxytocin receptor agonist, notably does produce antidepressant-like effects in animals.[83] As such, the antidepressant-like effects of oxytocin may be mediated by modulation of a different target, perhaps the vasopressin V1A receptor where oxytocin is known to weakly bind as an agonist.[84][85]
An interesting concept that has emerged from initial findings is that regeneration and fibrosis are competing events in the vertebrate heart. That is, if there is a capacity for injury-stimulated cardiomyocyte hyperplasia beyond a certain threshold, regenerative mechanisms will overcome scarring. Results consistent with this idea came from experiments with zebrafish possessing a ts mutation in the cell-cycle checkpoint kinase Mps1 (Poss et al., 2002b). As mentioned earlier, mps1 mutants were initially identified based on their defects in caudal fin regeneration. Serendipitously, mps1 mutants also showed defects in cardiac regeneration at a temperature restrictive for the mutation (Poss et al., 2002b). Instead of regenerating muscle in response to ventricular resection injury, mps1 mutants repaired wounds by forming large, collagen-rich scars. Inhibition of Fgf signaling also stunts cardiac regeneration and causes scarring (Lepilina et al., 2006). These results indicate that even vertebrates with high cardiac regenerative capacity have a default scarring mechanism; normally, regeneration somehow restricts this pathway (Fig. 8). The implication is exciting; perhaps by stimulating regeneration in a poorly-regenerative system like the mammalian heart, scarring events characteristic of myocardial infarction would be restricted by new muscle formation. Similarly, deterring cardiac scarring mechanisms would perhaps favor regeneration in mammals.
About three months after quitting, I did have a major relapse, which was falling back into old habits for about two weeks. And the whole time I knew what was happening, I knew how dangerous it was, but I couldn't stop myself. I felt like I couldn't connect to anyone without drinking. I couldn't talk to my friends, I couldn't be open and honest with anybody in my life without already having had a few drinks. It was a really disconnected, really unpleasant feeling. That's what I couldn't sit with and I couldn't cope with that feeling, so I went back to drinking.
"By understanding the oxytocin system's dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions," said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.

In a landmark 1979 study3, Cort Pedersen and Arthur Prange at the University of North Carolina in Chapel Hill showed that giving oxytocin to virgin rats could trigger maternal behaviours: the animals would build nests, lick or crouch over unfamiliar pups and even return lost pups to the nest. Researchers went on to show that oxytocin signalling in the brains of prairie voles (Microtus ochrogaster) helps the animals to form lifelong pair bonds4 — a rarity among mammals. In 2012, researchers even found a version of oxytocin in the tiny roundworm Caenorhabditis elegans, where it helps the animals find and recognize mates5.

I went to a neurologist, He said it was just in my head because I have depression–the exact reason why I took 5HTP. Not satisfied with that doctor, I went to an immunologist. He said I got myositis. Eosinophilic Myositis. From my blood test, I got positive ANA IF, very high number of IgE, elevated Creatine Kinase, and very low Vitamin D 25(OH)D. But my ANA Profile test showed negative.

5-HTP is sometimes taken by people coming down from MDMA to relieve post-MDMA dysphoria.[8] As 5-HTP is a necessary precursor for the brain to produce more serotonin, and MDMA use depletes a person's natural serotonin levels, it is believed that taking 5-HTP after consuming MDMA will speed up serotonin production. DanceSafe claims that the anecdotal evidence is widespread and that the theory is physiologically reasonable.[9] Backing up this approach is research conducted by Wang, et al.  in 2007, which observed that MDMA-induced depletions of 5-HT (serotonin) were restored in rats after administration 5-HTP, and suggested that this approach might be clinically useful in abstinent MDMA users.[8]