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The pathogenetic mechanisms underlying gastrointestinal dysmotility in diabetic patients remain poorly understood, although enteric neuropathy, damage to interstitial cells of Cajal (ICC) and smooth muscle cell injury are believed to play a role.The aim of this study was to investigate the morphological and functional changes underlying intestinal dysmotility in RIP-I ⁄ hIFNb transgenic mice treated with multiple very low doses of streptozotocin (20 mg⁄ kg, i.p., 5 days). Compared with vehicle-treated mice, streptozotocin-treated animals developed type 1 diabetes mellitus, with sustained hyperglycaemia for 3.5 months, polyphagia, polydipsia and increased faecal output without changes in faecal water content (metabolic cages). Diabetic mice had a longer intestine, longer ileal villi and wider colonic crypts (conventional microscopy) and displayed faster gastric emptying and intestinal transit. Contractility studies showed selective impaired neurotransmission in the ileum and mid-colon of diabetic mice. Compared with controls, the ileal and colonic myenteric plexus of diabetic mice revealed ultrastructural features of neuronal degeneration and HuD immunohistochemistry on whole-mount preparations showed 15% reduction in neuronal numbers. However, no immunohistochemical changes in apoptosis-related markers were noted. Lower absolute numbers of neuronal nitric oxide synthase- and choline acetyltransferase-immunopositive neurons and enhanced vasoactive intestinal polypeptide and substance P immunopositivity were observed. Ultrastructural and immunohistochemical analyses did not reveal changes in the enteric glial or ICC networks. In conclusion, this model of diabetic enteropathy shows enhanced intestinal transit associated with intestinal remodelling, including neuroplastic changes, and overt myenteric neuropathy. Such abnormalities are likely to reflect neuroadaptive and neuropathological changes occurring in this diabetic model.

Electrophysiologic assessment of the blink reflex test and the muscle-evoked potentials evoked by stimulation of the facial nerve were performed in 15 healthy adult Beagles before and after supraorbital (trigeminal) and facial anesthetic nerve blocks performed by lidocaine injections. Unilateral electrical stimulation of the supraorbital nerve elicited 2 ipsilateral (R1 and R2) and a contralateral (Rc) reflex muscle potential in orbicularis oculi muscles. Electrical stimulation of the facial nerve elicited 2 muscle potentials (a direct response [D] and a reflex faciofacial response [RF]) in the ipsilateral orbicularis oculi muscle. Anesthetic block of the left supraorbital nerve resulted in bilateral lack of responses upon left supraorbital nerve stimulation, but normal responses in right and left orbicularis oculi muscles upon right supraorbital stimulation. Right facial anesthetic block produced lack of responses in the right orbicularis oculi muscle regardless the side of supraorbital nerve stimulation. Results of this study demonstrate that the blink reflex can be electrically elicited and assessed in dogs. Reference values for the blink reflex responses and for the muscle potentials evoked by direct facial nerve stimulation in dogs are provided. The potential usefulness of the electrically elicited blink reflex test in the diagnosis of peripheral facial and trigeminal dysfunction in dogs was demonstrated.