a. Evidence implicating oxidative stress, altered neuronal calcium signaling and neuronal hyperexcitability in the development of painful diabetic neuropathy,

b. The emerging role of taurine as an important endogenous antioxidant, calcium regulator, neurotrophin, modulator of neuronal hyperexcitability and analgesic

c. Preclinical data implicating a critical role for taurine depletion and oxidative stress in the pathogenesis of experimental DN. 

d. Taurine replacement of diabetic rats attenuated deficits of nerve conduction and prevented reductions of mechanical and thermal withdrawal threshold and latency, respectively.

More details on:http://www.controlled-trials.com/mrct/trial/489967/

Taurine: preclinical evidence for analgesia

Taurine is not really a aminoacid, but it is close, and it serves as a inhibiting neurotransmitter in our brain, with antinoceptive properties. ^[1] To quote:  Taurine has been found in the central nervous system of rodents and humans, and among its potential therapeutic uses, it is interesting to remark its analgesic actions. ^[2] A neuropathic animal model also supported the anagesic effects of taurine. ^[3] In some preclinical models the analgesic effects of taurine could be reversed with the opiate antagonist naloxone. ^[4]

Taurine in the brain: GABA-ergic activity

We quote from a press release: http://www.medicalnewstoday.com/articles/94393.php

"We have discovered that taurine is a strong activator of what are known as GABA receptors in a regulatory area of the brain called the thalamus," says study senior author Dr. Neil L. Harrison, professor of pharmacology and pharmacology in anesthesiology at Weill Cornell Medical College. "We had discovered these receptors two years ago and showed that they interact with a neurotransmitter called gamma-aminobutyric acid (GABA) -- the brain's key inhibitory transmitter -- that is also involved in brain development. It seems that taurine shares these receptors." 

And: 

"Scientists have long questioned whether taurine might act on an as-yet-undiscovered receptor of its own," notes lead researcher Dr. Fan Jia, postdoctoral scientist in the Department of Anesthesiology. "But after some recent work in our lab, we ended up zeroing in on this population of GABA receptors in the thalamus."The thalamus, located deep in the brain's center, is involved in what neuroscientists call "behavioral state control," helping to regulate transitions between sleep and wakefulness, for example.

"It's like a railway junction, controlling information traffic between the brainstem, the senses and the executive functions in the cortex," Dr. Harrison explains. "When you're sleeping, the thalamus is discharging slowly and isolates the cortex from sensory input. But when you're awake, the thalamus allows information from the sensory system to activate the cortex."

Investigating further, the researchers exposed thin slices of thalamic tissue from the brains of mice to concentrations of taurine that were similar to what might be found in the human brain."We found that taurine is extraordinarily active on this population of GABA receptors in the thalamus," Dr. Harrison says.

"It came as a bit of a surprise that the same receptor was used by both taurine and GABA. Nevertheless, finding taurine's receptor has been like discovering the 'missing link' in taurine biology." 

Recent entry on taurine and(painful) diabetic neuropathy

On http://findarticles.com/p/articles/mi_m0FDN/is_4_11/ai_n27098210/pg_22/ we spotted the following summary on taurine and diabetic neuropathty, we quote in full:

Several animal studies indicate the amino acid taurine may provide some benefit for prevention or treatment of PN due to diabetes. Taurine is deficient in diabetes, particularly in the Schwann cells and vascular endothelium of nerves. (163) Taurine may act as an osmolytic agent and inhibitory neurotransmitter, resulting in modulation of pain perception. Theoretically, as high glucose results in sorbitol accumulation within the cell, taurine is depleted in the peripheral nerves, resulting in excitability and pain. One study of streptozotocin-diabetic rats found taurine levels decreased by 31 percent and myo-inositol levels by 37 percent. When sorbitol accumulation was decreased by an aldose reductase inhibitor, taurine levels increased by 22 percent. (164) In another animal study, diabetes resulted in abnormal calcium-ion signaling. Taurine repletion resulted in normalization of intracellular calcium concentrations, with resultant diminution of pain. (165) Other animal studies found taurine decreased diabetes-induced nerve conduction and nerve blood flow deficits, (166,167) and increased nerve growth factor and nerve ascorbate levels, (163) at least in part via antioxidant mechanisms. Clinical studies are indicated to determine whether taurine can provide benefit to individuals with diabetic PN. 

References taurine 

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Azuma, J., et al. "Beneficial effect of taurine on congestive heart failure induced by chronic aortic regurgitation in rabbits." Res Commun Chem Pathol Pharmacol 45(2): 261-70, August, 1984.

Fujita, T., Sato, Y. "Hypotensive effect of taurine. Possible involvement of the sympathetic nervous system and endogenous opiates." J Clin Invest 82(3): 993-97. September 1988.

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Foos TM, Wu JY. "The role of taurine in the central nervous system and the modulation of intracellular calcium homeostasis." Neurochem Res 2002 Feb;27(1-2):21-6.

Balakrishnan SD, Anuradha CV, Anitha Nandhini AT. "Taurine Modulates Antioxidant Potential and Controls Lipid Peroxidation in the Aorta of High Fructose-fed Rats." J Biochem Mol Biol Biophys 2002 Apr;6(2):129-33

Nandhini AT. "Anuradha CV.Taurine modulates kallikrein activity and glucose metabolism in insulin resistant rats." Amino Acids 2002;22(1):27-38

Dawson Jr R, Biasetti M, Messina S, Dominy J. "The cytoprotective role of taurine in exercise-induced muscle injury." Amino Acids 2002;22(4):309-24

Matsuzaki Y, Miyazaki T, Miyakawa S, Bouscarel B, Ikegami T, Tanaka N. "Decreased taurine concentration in skeletal muscles after exercise for various durations." Med Sci Sports Exerc 2002 May;34(5):793-7 

August 2010, Jan M. Keppel Hesselink, MD, PhD 

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