Curcumin Rescues Aging-Related Loss of Hippocampal Synapse Input Specificity of Long Term Potentiation in Mice

• Published in: Neurochemical research 2013-01, Vol.38 (1), p.98-107
• Main Authors: Cheng, Yue-Fa, Guo, Lan, Xie, Yue-Sheng, Liu, Ying-Shuo, Zhang, Jun, Wu, Qing-Wen, Li, Jian-Min
• Format: Article
• Language: English
• Subjects: 2-Amino-5-phosphonovalerate - pharmacology; Aging - physiology; Animals; Antioxidants - pharmacology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Calcium Channel Blockers - pharmacology; Cell Biology; Curcumin - pharmacology; Electric Stimulation; Excitatory Amino Acid Antagonists - pharmacology; Excitatory Postsynaptic Potentials - drug effects; Glutathione - metabolism; Hippocampus - drug effects; Hippocampus - growth & development; Hippocampus - metabolism; Long-Term Potentiation - drug effects; Male; Mice; Mice, Inbred C57BL; Neurochemistry; Neurology; Neuroprotective Agents - pharmacology; Neurosciences; Nimodipine - pharmacology; Original Paper; Oxidation-Reduction; Patch-Clamp Techniques; Synapses - drug effects; Synaptic Transmission - drug effects; Thiobarbituric Acid Reactive Substances - metabolism
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-012-0894-y

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.