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Taurine replacement attenuates hyperalgesia and abnormal calcium signaling in sensory neurons of STZ-D rats

Division of Endocrinology and Metabolism, Departments of ¹Internal Medicine and ²Physiology, Michigan Diabetes Research and Training Center, University of Michigan and Ann Arbor Veterans Administration Hospitals, Ann Arbor, Michigan; and ³Division of Nutrition and Chronic Disease, Louisiana State University, Baton Rouge, Louisiana

Submitted 13 April 2004 ; accepted in final form 18 August 2004

The etiology of painful diabetic neuropathy is poorly understood, but may result from neuronal hyperexcitability secondary to alterations of Ca²⁺ signaling in sensory neurons. The naturally occurring amino acid taurine functions as an osmolyte, antioxidant, Ca²⁺ modulator, inhibitory neurotransmitter, and analgesic such that its depletion in diabetes may predispose one to neuronal hyperexcitability and pain. This study reports the effects of taurine replacement on hyperalgesia and sensory neuron Ca²⁺ homeostasis in streptozotocin-diabetic (STZ-D) rats. Nondiabetic and STZ-D rats were treated with a 2% taurine-supplemented diet for 6–12 wk. Thermal hyperalgesia and mechanical allodynia were determined by measuring hindpaw withdrawal latency to radiant heat and the withdrawal threshold to the von Frey anesthesiometer. Intracellular Ca²⁺ signaling was explored in neurons from L₄–L₆ dorsal root ganglia (DRG), using fura 2 fluorescence. Taurine replacement of diabetic rats attenuated deficits of nerve conduction and prevented reductions of mechanical and thermal withdrawal threshold and latency, respectively. In small DRG sensory neurons from diabetic rats, recovery of intracellular Ca²⁺ concentration ([Ca²⁺]_i) in response to KCl was slowed and 73% corrected by taurine. The amplitudes of caffeine and ATP-induced [Ca²⁺]_i transients were decreased by 47 and 27% (P < 0.05), respectively, in diabetic rat DRG sensory neurons and corrected by 74 and 93% (P < 0.05), respectively, by taurine replacement. These data indicate that taurine is important in the regulation of neuronal Ca²⁺ signaling and that taurine deficiency may predispose one to nerve hyperexcitability and pain, complicating diabetes.

pain; diabetic neuropathy; allodynia

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