In years past, oxytocin had the reputation of being an "uncomplicated" hormone, with only a few well-defined activities related to birth and lactation. As has been the case with so many hormones, further research has demonstrated many subtle but profound influences of this little peptide, particularly in regards to its effects in the brain. Oxytocin has been implicated in setting a number of social behaviors in species ranging from mice to humans. For example, secretion or administration of oxytocin in humans appears to enhance trust and cooperation within socially-close groups, while promoting defensive aggression toward unrelated, competing groups.
Members agreed that the relevant matters under Section 52E(1) of the Therapeutic Goods Act 1989 included: (a) risks and benefits of the use of a substance; (b) the purpose for which a substance is to be used and the and extent of use; (c) the toxicity of a substance; (d) the dosage, formulation, labelling, packaging and presentation of a substance; (e) the potential for abuse of a substance; and (f) any other matters that the Secretary considers necessary to protect public health.
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.
Melanotan II is a synthetic hormone that speeds up the production of melanin, the pigment that absorbs ultraviolet radiation and gives skin its colour. It was originally developed as a potential treatment for female sexual dysfunction and erectile dysfunction, but this research ceased in 2003. In technical terms, Melanotan II is a synthetic analogue of the peptide hormone α-melanocyte-stimulating hormone (α-MSH). Today, there are numbers of sellers on the internet of unlicensed and untested powders sold as Melanotan II.
The CCI model we used causes cortical tissue loss. Traditionally, the target for neuroprotective treatment of TBI is to reduce the lesion volume.39,40 A major limitation of neuroprotection strategies is the short time window between injury and treatment. In the vast majority of preclinical TBI studies, the treatment compounds provide neuroprotection only when administered early (usually several hours after brain injury).11 The administration of a compound early in the clinical setting is not practical.41 The neuroprotective effects demonstrated in rodents may diminish if the treatment compounds are given in the clinical setting beyond the short neuroprotective window. We are able to stimulate recovery of neurological function without altering the lesion volume, which has also been demonstrated in our experimental studies of stroke,19,42,43 and is in essence, enhancement of neurorecovery.19 The extended 24-hour window for treatment which improves neurological recovery, without altering CCI cortical volume, is a major benefit of the neurorestorative therapy. Recently, we evaluated the efficacy of delayed Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by CCI.34 Briefly, TBI rats received Tβ4 at a dose of 6 mg/kg or a vehicle (saline) administered i.p. starting at 24 hours after injury and then every third day for 2 weeks. The dose of Tβ4 was selected based on our previous studies in animal models of stroke and EAE.25,27 Tβ4 did not alter lesion volume (14.2 ± 3.9% for saline treatment vs. 15.7 ± 3.6% for Tβ4 treatment). TBI caused neuronal cell loss in the ipsilateral CA3 and DG examined 35 days after injury compared to sham controls. Tβ4 treatment initiated 24 hours post injury significantly reduced cell loss in these two regions compared to saline controls. Tβ4-treated TBI rats showed significant improvement in spatial learning (MWM test) and sensorimotor (mNSS test) functional recovery compared to the saline-treated TBI rats.34
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