title: Curcumin rescues aging-related loss of hippocampal synapse input specificity of long term potentiation in mice.
abstract: Curcumin has neuroprotective effect and could enhance memory. However, the mechanisms underlying the protection of curcumin on aging-related memory decline are not well understood. In this study, high frequency stimulation (HFS)-induced long term potentiation (LTP) was evaluated by a cellular model of memory formation. A two-input stimulation paradigm was used to record the potentiation as well as synapse input specificity. The data suggested that an N-Methyl-D-aspartate receptors (NMDAR) -dependent LTP was inducible in adult hippocampal slices with a characteristic of synapse input specificity. It also indicated that aging resulted in a reduction in LTP but more importantly a loss of synaptic input specificity. The reason behind the above conclusions is that LTP induction is more dependent on the calcium channel. This is due to a switch of the dependence of LTP induction to voltage-dependent calcium channel (VDCC) compared to NMDA receptors. Curcumin administration recovers input specificity by re-establishing NMDA receptor dependence of induction. In addition, curcumin administration ameliorated aging-related increase of brain thiobarbituric acid-reactive substances and elevated aging-related decrease of glutathione in hippocampus. It is then concluded that curcumin modulates hippocampal redox status and restores aging-related loss of synapse input specificity of HFS-induced LTP by switching VDCC calcium source into NMDA receptor-dependent one.
authors.affiliation: Jitang College of Hebei United University, Tangshan 063000, People's Republic of China. chengyuefa@hotmail.com
authors.forename: Yue-Fa
authors.initials: YF
authors.lastname: Cheng
authors.forename: Lan
authors.initials: L
authors.lastname: Guo
authors.forename: Yue-Sheng
authors.initials: YS
authors.lastname: Xie
authors.forename: Ying-Shuo
authors.initials: YS
authors.lastname: Liu
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.forename: Qing-Wen
authors.initials: QW
authors.lastname: Wu
authors.forename: Jian-Min
authors.initials: JM
authors.lastname: Li
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000375:Aging / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003474:Curcumin / Q000494:pharmacology*; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000254:growth & development* / Q000378:metabolism; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009553:Nimodipine / Q000494:pharmacology; D010084:Oxidation-Reduction; D018408:Patch-Clamp Techniques; D013569:Synapses / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D002121:Calcium Channel Blockers; D018691:Excitatory Amino Acid Antagonists; D018696:Neuroprotective Agents; D017392:Thiobarbituric Acid Reactive Substances; D009553:Nimodipine; D015763:2-Amino-5-phosphonovalerate; D005978:Glutathione; D003474:Curcumin