Objective: 

Diabetes mellitus (DM), particularly due to its neurologic complications, is among the major public health problems globally. Oxytocin (OX) has been on the agenda recently, owing to its non-endocrine features, implicating neuroprotection and behavioral serenity. We aimed to identify the development of diabetic peripheral neuropathy (DPN) in the streptozocin (STZ)-induced DPN rat, and then test the possibility of reversing it by OX.

Methods: 

Having received Ege-University-Animal-Ethics-Committee's consent, 6-8 w.o. 30 male Sprague Dawley rats were used and 24 were administered a single dose of 60 mg/kg STZ(Sigma-Aldrich), i.p for inducing DM. After 2 days, tail vein blood was drawn to determine plasma glucose levels (PGL). Rats presenting PGL>=250mg/dL were included as DM and allowed 20 days for development of DPN;no insulin was applied.At day 0, 20 and 50,all rats were anesthetized(40mg/kg ketamine+ 4mg/kg xylasine,ip), their right hind leg sciatic nerve was stimulated (30–45V; 0.03s) at popliteal muscle and Achilles tendons for submaximal response, and EMG was recorded from 2.-3.interdigital muscles. The latency of M response (compound muscle action potentials=CMAP) and nerve conduction velocity (NCV) were calculated promptly. Inclined plane (IP) and tail flick (TF) tests were also performed.Five groups(n=6/g) were categorized accordingly: G-I) naive control (n=6);G-II) DPN+vehicle/placebo/sham(saline); and G-III),G-IV) and G-V that were administered OX(Synpitan, i.p) 20, 40 and 80 U/kg/day, respectively for 28 days.

Results: 

NCV; A) %25 decrease in the DPN rats (36.57±3.2m/sn), compared to naives (50.12±1.36m/s); B)47.7±2.7m/sn in the OX-treated DPN groups, indicating very significant (p<0.0001;G-V) improvement in dose dependent manner.

Behavioral assessment: A) IP; profound disfunction in DPN rats (69.75±2.5°) (p<0.005) compared to naives(75.25±2.37°); significant (p<0.005; G-V) reversal; and B) TF: significant deficiency in DPN rats (11.6±0.81s) compared to naives (7.83±0.75s), and significant (p<0.001) improvement in the G-V(8.2± 0.83s).

Conclusions: 

Our results proved the nerve protecting/restoring effect of OX despite post-deterioration application. Thus, OX may be a potent candidate to restore the sensory and motor features of peripheral nerves following neurodegenerative processes. Histopathological evaluation will also be correlated.