Abstract
We have previously found that spinal dorsal horn neurons from streptozotocin-diabetic rats, an animal model for diabetes mellitus, show the prominent changes in the mechanisms responsible for [Ca 2+] i regulation. The present study aimed to further characterize the effects of streptozotocin-induced diabetes on neuronal calcium homeostasis. The cytoplasmic Ca 2+ concentration ([Ca 2+] i) was measured in Fura-2AM-loaded dorsal horn neurons from acutely isolated spinal cord slices using fluorescence technique. We studied Ca 2+ entry through plasmalemmal Ca 2+ channels during potassium (50 mM KCl)-induced depolarization. The K +-induced [Ca 2+] i elevation was inhibited to a different extent by nickel ions, nifedipine and ω-conotoxin suggesting the co-expression of different subtypes of plasmalemmal voltage-gated Ca 2+ channels. The suppression of [Ca 2+] i transients by Ni 2+ (50 μM) was the same in control and diabetic neurons. On the other hand, inhibition of [Ca 2+] i transients by nifedipine (50 μM) and ω-conotoxin (1 μM) was much greater in diabetic neurons compared with normal animals. These data suggest that under diabetic conditions the activity of N-and L- but not T-type voltage-gated Ca 2+ channels substantially increased in dorsal horn neurons.
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