Experimental Diabetes Attenuates Cerebral Cortical−Evoked Forelimb Motor Responses

Abstract

Poorly controlled diabetes leads to debilitating peripheral complications, including retinopathy, nephropathy, and neuropathy. Chronic diabetes also impairs the central nervous system (CNS), leading to measurable deficits in cognition, somatosensory, and motor function. The cause of diabetes-associated CNS impairment is unknown. In this study, sustained hyperglycemia resulting from insulin deficiency was shown to contribute to CNS motor dysfunction. Experimental diabetes was induced in rats by streptozotocin (STZ) injection. CNS motor function was assessed by intracortical microstimulation of the sensorimotor cortex. Experimental diabetes significantly (P < 0.01; n ‫؍‬ 14) attenuated the number of motor cortical sites eliciting forelimb movements. The net area of the motor cortex representing the forelimb in diabetic rats was significantly reduced

Forced‐exercise delays neuropathic pain in experimental diabetes: effects on voltage‐activated calcium channels

“…1a). Subcutaneous implantation of insulin pellets at 4 weeks reversed the observed hyperglycemic effects of STZ and normalized blood glucose levels to near physiological concentrations in sedentary rats (Emerick et al 2005), consistent with the experimental induction of insulin-dependent diabetes. By comparison, control rats receiving an equal volume of citrate buffer (100 mmol/L; pH 4.5) maintained non-fasting blood glucose levels near 6 mmol/L (Fig.…”

“…The effect of forced‐exercise on peripheral nerve function in vehicle‐ and STZ‐treated rats was quantified by evoke‐response electrophysiology (Emerick et al. 2005; Sarkey et al.…”

“…Forced-exercise protects against diabetes-associated peripheral nerve conduction deficits The effect of forced-exercise on peripheral nerve function in vehicle-and STZ-treated rats was quantified by evokeresponse electrophysiology (Emerick et al 2005;Sarkey et al 2007). Despite exhibiting marked and sustained hyperglycemia, STZ-treated rats (8 weeks) maintained near normal evoke-response sciatic/tibial nerve conduction amplitudes when compared with vehicle-treated non-diabetic controls or pre-treatment (baseline) measures (Table 2).…”

Insulin and IGF-I prevent brain atrophy and DNA loss in diabetes

“…Evoked potentials (Ozkaya et al, 2007), centrally evoked forelimb motor responses (Emerick et al, 2005), and excitatory postsynaptic potentials (Kamal et al, 2006) are abnormal. Cognitive deficits are associated with abnormal long-term potentiation and long-term depression (Biessels et al, 1996; Biessels et al, 1998).…”

Cortical Evoked Potentials in Children of Diabetic Mothers

“…Cortical dysfunctions could be related to poor metabolic control, as suggested by clinical and experimental studies, with subtle negative effects on the offspring's CNS [24–26]. …”