Dr James Schaller
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Advanced Autism & PDD Treatment
Part 2

As mentioned in part 1, it is surprising aMSH is not tested for by autism experts. Below is a sample of the role MSH has on healing neurons. I have yet to see one Autism expert discuss this material, and some think 10 million American's have an MSH deficiency due to over six causes.

1: J Neurotrauma. 1999 Jun;16(6):543-53.

Alpha-melanocyte stimulating hormone promotes regrowth of injured axons in the adult rat spinal cord.

Joosten EA, Majewska B, Houweling DA, Bar PR, Gispen WH.

Peptides related to melanotropin (alphaMSH) and corticotropin (ACTH), collectively termed melanocortins, are known to improve the postlesion repair of injured peripheral nerves. In addition, melanocortins exert trophic effects on the outgrowth of neurites from central nervous system neurons in vitro. Here we report, for the first time, the stimulation by alpha-MSH of spinal neurite outgrowth in vivo after injury. In the in vivo model, spinal cord trauma was produced at lower thoracic spinal levels of adult rats. Under a surgical microscope a laminectomy was performed exposing the dorsum of the spinal cord. Then the dura was cut longitudinally and the dorsal columns were identified. Iridectomy scissors were used to transect the dorsal half of the spinal cord bilaterally, thereby completely lesioning the main corticospinal tract component. Then the lesion gap was immediately filled with a solid collagen matrix. Ingrowth of fibers was quantified using an advanced image analyser using a video image of sections transmitted by a camera. In the control situation virtually no ingrowth of sprouting injured fibers into the collagen implant in the lesion gap was seen. However, when the collagen matrix contained 10(-8) M alpha-MSH, a profound and significant stimulation of fiber ingrowth into the implant was observed (alpha-MSH, 21.5 +/- 2.9%; control, 1.4 +/- 0.6% p < 0.01). A small percentage of these ingrowing fibers was CGRP-immunoreactive (17.0 +/- 4%), whereas no serotonergic ingrowth was observed. Furthermore, we found that local application of alpha-MSH directs a substantial amount of lesioned anterogradely labelled corticospinal tract axons to regrow into the collagen implant (alpha-MSH, 15.2 +/- 5.2%; control, 0.5 +/- 0.3%, p < 0.01). The observed fiber ingrowth is not accompanied by an invasion of astroglial or reactive microglial cells into the implant. In conclusion, inclusion of alpha-MSH in the collagen implant stimulates the regrowth of injured axons in the adult rat spinal cord.

2: Brain Res Mol Brain Res. 1999 Jan 8;63(2):276-86.

Expression of melanocortin receptors and pro-opiomelanocortin in the rat spinal cord in relation to neurotrophic effects of melanocortins..

van der Kraan M, Tatro JB, Entwistle ML, Brakkee JH, Burbach JP, Adan RA, Gispen WH.

Although neurotrophic [nerve growth] effects of alpha-melanocyte-stimulating hormone (alpha-MSH) are well established, the mechanism underlying these effects is unknown. To identify candidate components of the signaling system that may mediate these effects, in the present study rat spinal cord, dorsal root ganglia, sciatic nerve and soleus muscle were analysed for the expression of the neural MC3, MC4 and MC5 receptors and for the expression of the melanocortin precursor pro-opiomelanocortin (POMC). In rat lumbar spinal cord, the MC4 receptor was the only MC receptor subtype for which mRNA was detectable using RNAse protection assays. In situ binding studies using 125I-NDP-MSH, a synthetic alpha-MSH analogue, demonstrated MC receptor protein in the rat spinal cord, predominantly localised in substantia gelatinosa and area X, surrounding the central canal. Furthermore, POMC mRNA was demonstrated in rat spinal cord and dorsal root ganglia. These findings suggest a functional melanocortin system in the rat spinal cord, that might be involved in peripheral nerve repair. Regulation of POMC or MC receptor transcripts does not appear to be involved in the response to peripheral nerve crush in rats, since no change in mRNA expression patterns was detected after sciatic nerve crush, using quantitative RNAse protection assays. Nevertheless, subtle changes in melanocortin receptor binding did occur postsurgically in several regions of the spinal cord in both sham-operated and sciatic nerve-lesioned rats. The robust expression of MC receptor protein in spinal cord regions that are generally associated with nociception suggests a potentially broader involvement of endogenous melanocortins in spinal pathways which mediate the responses to peripheral injury [more receptors mean MSH can help heal more in injured spinal nerves] , in addition to any direct melanocortin [MSH] effects on sprouting and neurite outgrowth.

3: Peptides. 1995;16(5):979-93.

ACTH-related peptides: receptors and signal transduction systems involved in their neurotrophic and neuroprotective actions.

Hol EM, Gispen WH, Bar PR.

Department of Neurology, Rudolf Magnus Institute for Neurosciences, Utrecht University, The Netherlands.

ACTH-related peptides [like MSH] are promising neurotrophic and neuroprotective agents, as demonstrated in many in vivo and in vitro studies. They accelerate nerve repair after injury, improving both sensor and motor function. Furthermore, ACTH-related peptides have neuroprotective properties against cisplatin- and taxol-induced [chemical] neurotoxicity, they improve neuronal function in animals with neuropathy due to experimental diabetes, and they prevent degeneration of myelinated axons in rats suffering from experimental allergic neuritis, a model of peripheral demyelinating neuropathy. Studies in neuronal cultures have corroborated these clinical observations and serve to investigate the mechanism of action of the ACTH-related peptide effects. This paper reviews both in vitro and in vivo effects and emphasizes the mechanism of action. Recent data on melanotrophic receptors and signal transduction systems will be discussed in this context.

[All bolding and italics are mine. My thanks to all these researchers for their hard work!]

Dedicated to Loving Parents!

Dr. J


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