Thalamic amplification of sensory input in experimental diabetes

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Abstract

Diabetic neuropathy is a common, and often debilitating, secondary complication of diabetes mellitus. As pain, hypersensitivity and paraesthesias present in a distal–proximal distribution, symptoms are generally believed to originate from damaged afferents within the peripheral nervous system. Increasing evidence suggests altered processing within the central nervous system in diabetic neuropathy contributes towards somatosensory dysfunction, but whether the accurate coding and relay of peripherally encoded information through the central nervous system is altered in diabetes is not understood. Here, we applied the strengths of the rodent whisker–barrel system to study primary afferent-thalamic processing in diabetic neuropathy. We found that neurons in the thalamic ventral posteromedial nucleus from rats with experimental diabetic neuropathy showed increased firing to precisely graded, multidirectional whisker deflection compared to non-diabetic rats. This thalamic hyperactivity occurred without any overt primary afferent dysfunction, as recordings from the trigeminal ganglion showed these primary afferents to be unaffected by diabetes. These findings suggest that central amplification can substantially transform ascending sensory input in diabetes, even in the absence of a barrage of ectopic primary afferent activity.

We investigate whether the accurate coding and relay of tactile stimulation through the CNS is altered in experimental diabetic neuropathy. We show that neurons in the thalamic VPM nucleus of rats with experimental diabetes show increased firing to precisely graded, multidirectional whisker deflection compared to control rats, while their primary afferents in the trigeminal ganglion do not. We suggest that central amplification can substantially transform ascending sensory input in diabetes.

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