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Home Neural Research Lyme Disease Quinine Chaga Mushroom Contact NeuralResearch Research began into Quinine as two current medical uses employed quinine as a Nerve Modulatorwhich blocked potassium channels in neurons of the sympathetic neural system.The quinine molecule's
ability to bind to the proteins that form channels
which allow potassium ions to flow in and out of a neuron, changing the voltage potential of the neuron,
effectively stops the neuron from creating an action potential. As potassium channels vary in structure and
protein components from one type of neuron to another, a potassium channel blocker can block quite
specifically. Quinine has been found to primarily block, causing a current decrease, in voltage gated
potassium channels of sympathetic neurons: Kv 1.5 and Kv 2.1 (Rolf S. et al. 2000).
Clinically this has been found to be effective in resolving heart arrhythmia and night leg cramping.
The same study identified propranolol as also blocking Kv 1.5 and Kv 2.1 channels but less effectively than quinine. Quinine has well known and tested exhaustivly tested photosensitivity (Onoue and Tsuda,.2005)
and the degredation of quinie resulting from exposure to UV light has numerous documented case histories of
the unpleasant side effects. Many of these adverse effects may centre on the release of a super oxide
radical created by the quinine molecular structure on exposure to UV light.( Agnew and Jha 2014).
and ..
similarity in channel Blocking capacity of Propranolol ,
It was determined that the comparative channel blocking ability of these two molecules could be tested
by exposing muscle tissue to both chemicals. Leech Nephalopsis obscura was chosen as a suitable
test species and so testing was initiated exposing leeches to 1 mg doses of both
quinine and propranolol. The effects were similar with quinine having a more profound effect.
The leeches recovered from the treatment in 10-15 minutes and began to swim and step normally.
They did remain sluggish for 2-3 hours but were lively and interested in food after eight hours.
Propranolol and the Leptin Pathway to Sympathetic Neurons Recent research has discovered that leptin released by adipocytes and carried to the Hypothalmus causes the release of signal molecules that promote bone resorbtion. Early clues to this understanding were derived from reports that leptin deficient ob/ob mice had relitively high bone mass. The same high bone mass
was also seen in low weight mice who were deficient in receptors for leptin, leading to the belief that
leptin itself was the signal as opposed to any response to high body mass. This leptin signalling
pathway interacts with the sympathetic nervous system via the supression of neuropeptide Y
(Baldock P. et al 2002). Thus bone mass decreased when mice were treated with the adrenergic agonist isoproterenol and then increased when treated with adrenergic antagonist propranolol. These results were not affected by complimentary infusions of leptin(Takeda S. et al.2002). The same mesenchymal
precursor cells that form the osteoblasts which create bone mass also give rise to chondrocytes that form cartilage, and myoblasts,that form muscle tissue and tendon cells, so connecting the regulation of all these tissue types.
But of course leptin is released by adipocytes throughout life and bone mass, cartilage,muscle mass and
tendons remain healthy because the messengers that are released are countered by regulatory systems.
In this case the regulator is blood estrogen levels which regulate the expression of osteoprotegrin on the
undiferentiated cells in the bone marrow. Osteoprotegrin acts as an antagonist to the
ligand messanger called RANKL and stops it from binding to the receptor on the undifferentiated
mesenchymal cell by offering itself ad a 'decoy' receptor so that the messanger does not bind to the activating site ( Li J. et al.2000) . Osteoprotegrin is produced by the precursor cell itself in response to available estrogen levels. Too much osteoprotegrin stops the production of bone resorbing osteoclasts (Udagawa N. et al. 2000). This then connects the estrogen levels and osteoporosis in the aging human and surely by extrapolation changes to cartilage , muscle and tendon that also occur as the human ages and estrogen levels fall.
cases
This begs the following questions :
' Will treatment with propranolol affect the osteoporosis ? '
' Will treatment with propranolol affect the bone remodelling of osteoarthritis ? '
' Will treatment with propranolol affect the muscle wasting ? '
A Personal Anecdote
I have been affected by osteoarthritis and severe muscle wasting.
I used 1mg doses of propranolol rubbed into my skin at the tightened and
wasting deltoid muscle near the attachment points.(I was informed by a local veteranarian that
propranolol ointment is rubbed into the dermal tissue of the ear to help with arthritis in both
dogs and cats {1-5mg per Kg animal Merk} )
To my surprise, even this small dose had an immediate effect, including reduced pain.
I developed a routine of applying 2ml applications
to each shoulder twice a day. Each ml contained 10mg propranolol.
I have added the propranolol to a coconut oil based / distilled water emulsion for ease of application .
Pain was decreased, mobility increased and most importantly muscle wasting was reversed.
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