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J Neurophysiol 80: 1236-1244, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 3 September 1998, pp. 1236-1244
Copyright ©1998 The American Physiological Society

Serum From Diabetic BB/W Rats Enhances Calcium Currents in Primary Sensory Neurons

Helen Ristic1, Shanthi Srinivasan1, Karen E. Hall1, Anders A. F. Sima2, and John W. Wiley1

1 Department of Internal Medicine and 2 Department of Pathology, University of Michigan Medical Center and the Ann Arbor Veterans Affairs Medical Center, Ann Arbor, Michigan 48105

Ristic, Helen, Shanthi Srinivasan, Karen E. Hall, Anders A. F. Sima, and John W. Wiley. Serum from diabetic BB/W rats enhances calcium currents in primary sensory neurons. J. Neurophysiol. 80: 1236-1244, 1998. We examined the hypothesis that exposure of nondiabetic rat dorsal root ganglion (DRG) neurons to sera from diabetic BB/W rats would produce an increase in calcium currents associated with impaired regulation of the inhibitory G protein-calcium channel complex. Acutely dissociated rat DRGs were incubated for 18-24 h in medium supplemented with sera (10% vol/vol) from either diabetic rats with neuropathy or age-matched, nondiabetic controls. Exposure of DRG neurons to sera from diabetic BB/W rats resulted in a surface membrane immunofluorescence pattern when treated with an anti-rat light-chain antibody that was not observed in neurons exposed to control sera. Calcium current density (IDCa) was assessed with the use of the whole cell variation of the patch-clamp technique. IDCa in neurons exposed to diabetic sera was significantly increased compared with neurons exposed to control sera. Guanine nucleotide-binding (G) protein regulation of calcium channel function was examined with the use of a two-pulse "facilitation" or IDCa enhancement protocol in the presence of activators [guanosine 5'-O-(3-thiotriphosphate) (GTPgamma S)] or antagonists [guanosine 5'-O-(2-thiodiphosphate) (GDPbeta S) and pertussis toxin (PTX)] of G protein function. Facilitation was significantly decreased in neurons exposed to diabetic sera. Intracellular diffusion of neurons with GDPbeta s blocked facilitation, whereas dialysis with GTPgamma s increased facilitation to a similar magnitude in neurons exposed to either diabetic or control sera. Treatment with PTX resulted in a significant increase in IDCa and ~50% decrease in facilitation in neurons treated with control sera but no significant changes in neurons exposed to diabetic sera. We conclude that serum from diabetic BB/W rats with neuropathy contains an autoimmune immunoglobulin that impairs regulation of the inhibitory G protein-calcium channel complex, resulting in enhanced calcium influx. Regulation of the inhibitory G protein-calcium channel complex involves PTX-sensitive and -insensitive G proteins.




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