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.
Uterine contraction important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.[4]
Thank you for this important segment. i have read books that mention oxytocin along with other brain chemicals, if levels are low in the brain it will cause problems, of course, makes sense. low brain neurotransmitters can be restored by using amino acids (supplements) eg: tryptophan will increase serotonin and cure depression without the use toxic pharmaceutical drugs that don.t work.
In 19 obese females given either placebo or 8mg/kg (weight not actually given, only BMI between 30-40 for women) daily for 5 weeks without any concurrent dietary recommendations, 5-HTP treatment was associated with a decrease in appetite and food intake (resulting in weight loss) without significantly affecting mood state.[9] This study noted that food intake was reduced from an average of 2,903kcal to 1,819kcal (62% of baseline) while placebo only reduced calories to 80%, and the 0.5kg weight loss in placebo was outperformed by a near 1.5kg loss in 5-HTP. These weight loss effects have been noted with 750mg 5-HTP over 2 weeks in overweight diabetics[10] and over 12 weeks in obese persons given 900mg 5-HTP daily (58% of baseline intake); this latter study had a 6 week trial without a diet (in which significant weight loss was only noted at week 6) followed up by coadministration with a diet where weight loss proceeded to reach an additional 3.3kg over the subsequent 6 weeks;[11] this latter study is duplicated in Medline.[12]
In mammals, many mysteries remain. Oxytocin is difficult to measure reliably in the brain, making it hard to know exactly where, when and how much is normally released; nor do scientists understand precisely how it works to alter behaviour. “What we need to start thinking about is the more fundamental role that oxytocin plays in the brain,” Young says. The determination to find out has been strengthened by a growing move in neuroscience to characterize circuits that are important in brain operations. “That's the level that's critical for understanding how the brain is regulating behaviour,” says Thomas Insel, director of the US National Institute of Mental Health in Bethesda, Maryland, who has studied oxytocin in voles.
Researchers often investigate the effects of hormones on behavior in laboratory experiments with student subjects. Some studies show that when you give people oxytocin they become more generous and trusting. In others that administer testosterone to men, the opposite happens. The strength of such studies is that they can demonstrate cause and effect – the behavior change only occurs in subjects receiving hormones, not in those who get a placebo. But this research has weaknesses as well: it often focuses on single hormones, ignoring their potential interactions, and behavior is measured with highly artificial tasks.
Osteoclast differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) staining and activity. After 5 days of culture, cells were stained for TRAP kit using a leukocyte acid phosphatase kit (Sigma Aldrich, St Louis, MO, USA). Cells with three or more nuclei were counted as multinucleated mature osteoclasts. To measure TRAP activity, cells were fixed with 10% formalin for 10 min and 95% ethanol for 1 min, and then 100 μl of citrate buffer (50 mM, pH 4.6) containing 10 mM sodium tartrate and 5 mM p-nitrophenylphosphate (Sigma-Aldrich) was added to the wells containing fixed cells in the 48-well plates. After incubation for 1 h, enzyme reaction mixtures in the wells were transferred to new plates containing an equal volume of 0.1 N NaOH. Absorbance was measured at 410 nm using a microplate reader.

Oxytocin (Oxt; /ˌɒksɪˈtoʊsɪn/) is a peptide hormone and neuropeptide. Oxytocin is normally produced by the paraventricular nucleus of the hypothalamus and released by the posterior pituitary.[3] It plays a role in social bonding, sexual reproduction, and during and after childbirth.[4] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding.[5] This helps with birth, bonding with the baby, and milk production.[5][6] Oxytocin was discovered by Henry Dale in 1906.[7] Its molecular structure was determined in 1952.[8] Oxytocin is also used as a medication to facilitate childbirth.[9][10][11]

The RANKL and OPG have been identified as a key regulatory component of alveolar bone loss associated with inflammatory periodontal disease [52]. Moreover, PDLCs were shown to express several osteoclastogenic cytokines, including both OPG and RANKL [30, 31]. Our data demonstrated that Tβ4 peptide abolished H2O2-induced RANKL expression and restored OPG expression. Osteoclasts, bone-resorptive multinucleated cells derived from hematopoietic stem cells, are associated with osteolytic diseases. Furthermore, NFATc1, a master modulator of osteoclastogenesis, regulates target genes, such as cathepsin K and calcitonin receptor or Calcr [53]. In our in vitro study using BMMs, Tβ4 peptide directly and indirectly inhibited RANKL-induced osteoclast differentiation and expression of osteoclast markers, such as cathepsin-K, calcitonin receptor or Calcr, NFATc1, and RANK in BMM cells. These results indicated that Tβ4 was a key therapeutic target in controlling inflammation-induced bone loss.

To pursue the sexual dysfunction agent, melanotan-II was licensed by Competitive Technologies to Palatin Technologies.[9] Palatin ceased development of melanotan-II in 2000 and synthesized, patented, and began to develop bremelanotide, a likely metabolite of melanotan-II that differs from melanotan-II in that it has a hydroxyl group where melanotan-II has an amide.[6][13] Competitive Technologies sued Palatin for breach of contract and to try to claim ownership of bremelanotide;[13] the parties settled in 2008 with Palatin retaining rights to bremelanotide, returning rights to melanotan-II to Competitive Technologies, and paying $800,000.[14]


Eventually I found Dr Kristaps Paddock, a naturopathic doctor and 5-HTP expert from Maryland in the US. He said one benefit 5-HTP has over SSRIs is that it kicks in quickly for those with anxiety and depression. "Serotonin has a short metabolic half-life, so it metabolises very, very fast. It goes into the body and out at a great speed, unlike SSRIs, which take a while to take effect so a sufferer wouldn't be feeling good during that time, and in fact may be feeling more suicidal. SSRIs also then have to be weaned off slowly, whereas you can stop taking 5-HTP instantly." Another bonus, of course, is that it's natural rather than synthetic. "If you're seriously considering the supplement, you have to weigh the positives and negatives against each other. The toxicity with 5-HTP is lower than that of SSRIs, since it's natural. Also because it's metabolised much quicker, it'd get out of your system more quickly if there were any problems. On the other hand, the research basis for 5-HTP is dramatically lower, so it's important to think of that."
Studies demonstrate that TB-500 is a potent, naturally occurring wound repair factor with anti-inflammatory properties. Tß4 is different from other repair factors, such as growth factors, in that it promotes endothelial and keratinocyte migration. It also does not bind to the extracellular matrix and has a very low molecular weight meaning it can travel relatively long distances through tissues. One of TB-500 key mechanisms of action is its ability to regulate the cell-building protein, Actin, a vital component of cell structure and movement. Of the thousands of proteins present in cells, actin represents up to 10% of the total proteins which therefore plays a major role in the genetic makeup of the cell.
The PDLCs were pre-treated with Wnt5a siRNA (30 nM) or Wnt5 peptide (500 ng/mL) for 2 hours, post-incubated with Tβ4 peptide (1 μg/mL) and 200 μM H2O2 for 48 hours (A-E), and then conditioned medium (CM) was collected. The bar graph shows the fold increase in protein or mRNA expression compared with control. * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2-treated group. The data presented were representative of three independent experiments.
“Further analysis by gender revealed that females in the 5-HTP group had a significantly lower panic rate and intensity of cognitive symptoms whereas, in males, the effect of 5-HTP was limited to lowering the intensity of somatic panic symptoms. Thus, an increased availability of 5-HT may have a gender-dependent protective effect in CCK-4-induced panic.”
A Risk Quiz; Let’s say you are one of the volunteers to whom researchers gave $100, and this option: you can either keep the money, or give it to an anonymous trustee who will either invest it and double it to $200 and return half of the extra hundred bucks to you–$50–or keep all the money for herself. So you can either increase your money by 50%, or lose it all. What would you do? Would you trust that anonymous trustee? (Remember Loss Aversion from Chapter Two, where in a similar experiment most people decided to avoid the gamble and take the sure cash.)
But long before that, say researchers, oxytocin could use a rebranding. “It doesn't induce love; it doesn't induce massive amounts of trust,” Guastella says. “The problem we've got ourselves into is that we're trying to look for a simple answer: either oxytocin does or does not work in a patient population, or it does or does not enhance a certain social process.”

I am not sure if my original question posted…I was wondering if I could use TB-500 to regenerate thyroid tissue? My endocrinologist said that my Hashimoto’s Thyroiditis has almost completely destroyed my thyroid. If yes, then where do I inject?? Additionally, I was wonder if the BPC-157 would have any benefits on thyroid as I plan to take orally for leaky gut/digestive issues.
High and low oxytocin levels are possible, but research has not yet found any implications of these conditions. Men with high levels of oxytocin sometimes develop benign prostatic hyperplasia, or the enlarging of the prostate gland. This condition can cause urinary complaints. A lack of oxytocin can prevent the milk letdown reflex and make breastfeeding difficult. Low oxytocin levels have also been linked to depression, but using oxytocin to treat mental health conditions has not yet been studied sufficiently.
Our research mainly focusses on this early social experiences that people have that can be positive or negative, and that can really shape our developing brain. There have been some very interesting studies, for example, with children that grew up in Romanian orphanages. And we know that that early start, where it's really deprived from social contact and physical contact, had a massive impact. So we see that oxytocin levels, for example, are much lower than we would expect in other kids.
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]
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