In vivo evidence of reduced nodal and XXXX in type 1 @entity6 .

@entity1 @entity3529 @entity4024 @entity66 @entity6 @entity713 @entity16 @entity3949
OBJECTIVES: @entity3949 is a debilitating complication of @entity6 . Animal models of type 1 @entity6 (T1DM) suggest that functional and structural changes, specifically axo-glial dysjunction, may contribute to @entity16 development. The present study sought to examine and characterise early sensory axonal function in T1DM @entity1 in the absence of clinical @entity16 . METHODS: Thirty @entity1 with T1DM (15M:15F) without @entity16 underwent median nerve sensory and motor axonal excitability studies to examine axonal function. A verified mathematical model of @entity1 motor and sensory axons was used to elucidate the underlying causes of observed alterations. RESULTS: Compared to controls (NC), T1DM @entity1 demonstrated significant @entity66 in sensory and motor axons. These included marked reductions in sensory and motor subexcitability during the recovery cycle (T1DM 7.9  0.4:10.4  0.6%, NC 10.4  0.7:15.4  1.2%, P<0.01) and during hyperpolarizing threshold electrotonus at 10-20ms (T1DM -75.5  0.8:-69.7  0.8%, NC -78.4  1:-72.7  0.9%, P<0.01). Mathematical modelling demonstrated that these changes were due to reduced nodal @entity4024 currents, nodal/paranodal @entity3529 conductances and @entity4024 / @entity3529 pump dysfunction, consistent with axo-glial dysjunction as outlined in animal models of T1DM. CONCLUSIONS: The study provided support for the occurrence of early changes in nodal and @entity713 in @entity1 with T1DM. SIGNIFICANCE: These data indicate that axonal excitability techniques may detect early changes in @entity6 @entity1 , providing a window of opportunity for prophylactic intervention in T1DM.
