PMID- 23832486
OWN - NLM
STAT- MEDLINE
DCOM- 20140623
LR  - 20211021
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 51
IP  - 3
DP  - 2013 Nov
TI  - Diabetes impairs synaptic plasticity in the superior cervical ganglion: possible 
      role for BDNF and oxidative stress.
PG  - 763-70
LID - 10.1007/s12031-013-0061-1 [doi]
AB  - The majority of diabetics develop serious disorders of the autonomic nervous 
      system; however, there is no clear understanding on the causes of these 
      complications. In this study, we examined the effect of streptozocin 
      (STZ)-induced diabetes on activity-dependent synaptic plasticity, associated 
      levels of brain-derived neurotrophic factor (BDNF) and antioxidant biomarkers in 
      the rat sympathetic superior cervical ganglion. Diabetes (STZ-induced) was 
      achieved by a single intraperitoneal injection of streptozocin 
      (55 mg/kg).Compound action potentials were recorded from isolated ganglia before 
      (basal) and after repetitive stimulation, or trains of paired pulses to express 
      ganglionic long-term potentiation (gLTP) or long-term depression (gLTD). The 
      input/output curves of ganglia from STZ-treated animals showed a marked rightward 
      shift along most stimulus intensities, compared to those of ganglia from control 
      animals, indicating impaired basal synaptic transmission in ganglia from 
      STZ-induced diabetic animals. Repetitive stimulation induced robust gLTP and gLTD 
      in ganglia isolated from control animals; the same protocols failed to induce 
      gLTP or gLTD in ganglia from STZ-induced diabetic animals, indicating impairment 
      of activity-dependent synaptic plasticity in these animals. Molecular analysis 
      revealed significant reduction in the levels of BDNF and the ratio of 
      glutathione/oxidized glutathione. Additionally, the activity of glutathione 
      peroxidase, glutathione reductase, catalase, and the levels of thiobarbituric 
      acid-reactive substances were increased in ganglia from STZ-treated animals. In 
      conclusion, impaired basal synaptic transmission and synaptic plasticity are 
      associated with reduced BDNF and altered oxidative stress biomarkers in the 
      sympathetic ganglia from STZ-induced diabetic animals, suggesting a possible 
      correlation of these factors with the manifestations of STZ-induced diabetes in 
      the peripheral nervous system.
FAU - Alzoubi, K H
AU  - Alzoubi KH
AD  - Faculty of Pharmacy, Department of Clinical Pharmacy, Jordan University of 
      Science and Technology, Irbid, Jordan.
FAU - Khabour, O F
AU  - Khabour OF
FAU - Alhaidar, I A
AU  - Alhaidar IA
FAU - Aleisa, A M
AU  - Aleisa AM
FAU - Alkadhi, K A
AU  - Alkadhi KA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130706
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Action Potentials
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Diabetes Mellitus, Experimental/*metabolism/physiopathology
MH  - Glutathione/metabolism
MH  - *Long-Term Potentiation
MH  - Male
MH  - *Oxidative Stress
MH  - Rats
MH  - Rats, Wistar
MH  - Superior Cervical Ganglion/*metabolism/physiopathology
EDAT- 2013/07/09 06:00
MHDA- 2014/06/24 06:00
CRDT- 2013/07/09 06:00
PHST- 2013/05/20 00:00 [received]
PHST- 2013/06/23 00:00 [accepted]
PHST- 2013/07/09 06:00 [entrez]
PHST- 2013/07/09 06:00 [pubmed]
PHST- 2014/06/24 06:00 [medline]
AID - 10.1007/s12031-013-0061-1 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2013 Nov;51(3):763-70. doi: 10.1007/s12031-013-0061-1. Epub 2013 
      Jul 6.