%0 Journal Article
%T Myosin Va but not nNOS¦Á is significantly reduced in jejunal musculomotor nerve terminals in diabetes mellitus
%A ARUN CHAUDHURY
%A Jacqueline N. Zanoni
%J Frontiers in Medicine
%D 2014
%I Frontiers Media
%R 10.3389/fmed.2014.00017
%X Nitric oxide (NO) mediated slow inhibitory junction potential (sIJP) and mechanical relaxation after electrical field stimulation is impaired in diabetes mellitus. Externally added NO donor restore nitrergic function, indicating that this reduction result from diminution of NO synthesis within the prejunctional nerve terminals. The present study aimed to investigate two specific aims that may potentially provide pathophysiological insights into diabetic nitrergic neuropathy. Specifically, alteration in nNOS¦Á contents within jejunal nerve terminals and a local subcortical transporter myosin Va was tested sixteen weeks after induction of diabetes by low-dose streptozotocin in male Wistar rats. The results show that diabetic rats, in contrast to vehicle treated animals, have (a) nearly absent myosin Va expression in nerve terminals of axons innervating smooth muscles and (b) significant decrease of myosin Va in neuronal soma of myenteric plexus. In contrast, nNOS¦Á staining in diabetic jejunum neuromuscular strips showed near intact expression in neuronal cell bodies. The space occupancy of nitrergic nerve fibers was comparable between groups. Normal concentration of nNOS¦Á was visualized within a majority of nitrergic terminals in diabetes, suggesting intact axonal transport of nNOS¦Á to distant nerve terminals. These results reveal the dissociation between presences of nNOS¦Á in the nerve terminals but deficiency of its transporter myosin Va in the jejunum of diabetic rats. This significant observation of reduced motor protein myosin Va within jejunal nerve terminals may potentially explain impairment of prejunctional nitric oxide synthesis during electrical field stimulation of diabetic gut neuromuscular strips despite presence of the nitrergic synthetic enzyme nNOS¦Á.
%K Axonal Transport
%K myosin Va
%K nNOS
%K diabetes
%K Neuropathy
%U http://www.frontiersin.org/Journal/10.3389/fmed.2014.00017/abstract