Hyperglycaemia is the main factor leading to the development of neural and vascular damage in diabetes. Excessive blood glucose increases the metabolic flux of neurons, causing osmotic and oxidative stress, formation of advanced glycation end products, reduced neurotrophic input and it also initiates signalling cascades in response to cellular damage. The combination of these events is thought to be the underlying cause of the loss of neural function and decreased conduction velocity observed in diabetic neuropathy. The aim of this study was to examine the effect of diabetes on the neural code of peripheral sensory neurons. In order to do this, the whisker system of streptozotocin (STZ) induced diabetic rats was used as a model of the somatosensory system. Extracellular recordings of neural activity in response to whisker deflections were performed in the first order neurons of the trigeminal ganglion (TG) of diseased and healthy animals. Latency of first spike responses were calculated for both groups, but no significant difference was found between diabetic and healthy animals.