PMID- 26224288
OWN - NLM
STAT- MEDLINE
DCOM- 20160719
LR  - 20181113
IS  - 1573-6903 (Electronic)
IS  - 0364-3190 (Linking)
VI  - 40
IP  - 9
DP  - 2015 Sep
TI  - Effect of Melatonin on Glutamate: BDNF Signaling in the Cerebral Cortex of 
      Polychlorinated Biphenyls (PCBs)-Exposed Adult Male Rats.
PG  - 1858-69
LID - 10.1007/s11064-015-1677-z [doi]
AB  - Various epidemiological survey suggests that the central nervous system is the 
      target for many environmental contaminants. One among them is Aroclor 1254, a 
      mixture of polychlorinated biphenyls (PCBs) which explore a spectrum of 
      biochemical and neurotoxic responses in humans and laboratory animals. Learning 
      and motor coordination deficits are the profound effects of PCBs which may be 
      related to cerebral dysfunction. The aim of the study is to elicit the protective 
      effect of melatonin (Mel), a potent, blood brain permeable antioxidant against 
      the effect of Aroclor 1254 on the signaling of glutamate-principal excitatory 
      neurotransmitter and brain derived neurotrophic factor (BDNF) in the cerebral 
      cortex of adult rats which plays a key role in brain functions. Adult male Wistar 
      rats were grouped into four and treated intraperitonealy (i.p) Group I with corn 
      oil (Control), Group II with PCBs (2 mg/kg/bwt), Group III with PCBs + Mel 
      (2 mg/kg/bwt + 5 mg/kg/bwt) and Group IV with Mel (5 mg/kg/bwt). The protein 
      expression of glutamate signaling molecules and mRNA expressions of GLAST, BDNF 
      signaling molecules were analyzed. The results suggest that simultaneous 
      melatonin treatment significantly attenuated the NMDA receptor mediated glutamate 
      excitotoxicity and protects the inhibition of BDNF signaling caused by PCBs 
      exposure in cerebral cortex of adult male rats. Schematic pathway illustrating 
      the proposed mechanism by which melatonin protects against A1254 mediated 
      glutamate induced neurodegeneration in the cerebral cortex of adult male rats. 
      PCBs induced neurodegeneration is caused by the overactivation of NMDAR, followed 
      by the activation of voltage dependent calcium channels leading to the increase 
      in intracellular Ca(2+) that stimulates calpain. Calpain inturn inhibits the PKA 
      alpha and neurtrophin BDNF, its receptor and downstream signaling MAPK pathway 
      leading to neurodegeneration. Melatonin had scavenged the ROS produced by PCBS 
      and decreased the NMDAR expression which inturn protected the cells from 
      neurodegeneration.
FAU - Bavithra, S
AU  - Bavithra S
AD  - Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical 
      Sciences, University of Madras, Chennai, 600 113, India.
FAU - Sugantha Priya, E
AU  - Sugantha Priya E
FAU - Selvakumar, K
AU  - Selvakumar K
FAU - Krishnamoorthy, G
AU  - Krishnamoorthy G
FAU - Arunakaran, J
AU  - Arunakaran J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150730
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calcium Channels, N-Type)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Glutamate)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 3.4.22.- (Calpain)
RN  - JL5DK93RCL (Melatonin)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Calcium Channels, N-Type/metabolism
MH  - Calpain/metabolism
MH  - Cerebral Cortex/*drug effects/enzymology/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/genetics
MH  - Cyclic AMP-Dependent Protein Kinases/metabolism
MH  - Glutamic Acid/*metabolism
MH  - Male
MH  - Melatonin/*pharmacology
MH  - Polychlorinated Biphenyls/*toxicity
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Receptors, Glutamate/metabolism
MH  - Signal Transduction
EDAT- 2015/08/01 06:00
MHDA- 2016/07/20 06:00
CRDT- 2015/07/31 06:00
PHST- 2015/05/08 00:00 [received]
PHST- 2015/07/21 00:00 [accepted]
PHST- 2015/07/17 00:00 [revised]
PHST- 2015/07/31 06:00 [entrez]
PHST- 2015/08/01 06:00 [pubmed]
PHST- 2016/07/20 06:00 [medline]
AID - 10.1007/s11064-015-1677-z [doi]
PST - ppublish
SO  - Neurochem Res. 2015 Sep;40(9):1858-69. doi: 10.1007/s11064-015-1677-z. Epub 2015 
      Jul 30.