You got my curiosity up, so I did some reading at PubMed myself. What I found in the time that has elapsed since I read your post is that the helium-neon diode lasers, which produce light in the red region (600-700nm) of the electromagnetic spectrum, have been found to be useful for treating open wounds in the first few days of healing. I have not found anything that would indicate to me that one would find any benefit in aiming one at a pwpsp's brain stem in an attempt to produce acetylcholine.
The abstract that I have copied below sums up the problem pretty well. This sentence in particular points to the source of difficulty for the pwpsp: "Normal cholinergic transmission <u>requires the presence of intact cholinergic neurons</u> capable of releasing sufficient acetylcholine"...
So, there would be two difficulties, as least as I see it, to the laser approach in stimulating the release of acetylcholine. First, you would not be able to penetrate to the depth needed to reach the cells. Second, the neurons that release acetylcholine are not functional.
Personally, I would save my money. It's 2AM so I haven't read anything about the Photonic Therapy device offered online by the vet, but I am interested in knowing if it is used for open wounds, or if he is advertising it for use in curing internal problems.
I hope more opinions will be offered here.
1: Brain. 2005 Feb;128(Pt 2):239-49. Epub 2005 Jan 13. Links
Cholinergic systems in progressive supranuclear palsy.Warren NM, Piggott MA, Perry EK, Burn DJ.
Institute for Ageing and Health, University of Newcastle upon Tyne, UK. firstname.lastname@example.org
Progressive supranuclear palsy (PSP) is a progressive neurodegenerative disease characterized by akinetic-rigid features, falls, a supranuclear gaze palsy and subcortical dementia. Pathologically, there is abnormal accumulation of tau protein. Cholinergic deficits are thought to underlie the postural instability and cognitive impairment of PSP, but trials of cholinergic agonists and cholinesterase inhibitors have failed to show improvement in motor function, quality of life and cognitive impairment. The five cortico-basal ganglia loops, linking functionally related areas of the brain, are damaged in PSP, leading to specific clinical deficits. Cholinergic dysfunction is related to loss of cholinergic interneurons in the striatum, compounded by reduced inputs into the circuits from other cholinergic nuclei, such as the pedunculopontine nucleus and nucleus basalis of Meynert. Normal cholinergic transmission requires the presence of intact cholinergic neurons capable of releasing sufficient acetylcholine, and functional muscarinic and nicotinic receptors. Whilst there is evidence from autopsy and in vivo studies of loss of cholinergic neurons in PSP, the receptor status is unknown. This may be critical to understanding the basis for the poor therapeutic response to cholinomimetics. Symptomatic treatment using cholinergic drugs may thus be improved by more specific targeting of cholinergic receptors or nuclei. There is also evidence that cholinergic agents may have disease-modifying effects. This article reviews the key clinical features of PSP, along with normal basal ganglia anatomy and cholinergic transmission. Cholinergic deficits based on clinical and neurochemical parameters are then discussed, before concluding with suggested future directions for cholinergic treatments.
PMID: 15649952 [PubMed - indexed for MEDLINE]
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