αCaMKII overexpressions enhance excitatory synaptic transmission in insular cortex of mice
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摘要: 为了研究CaMKII在小鼠前脑过量表达对岛叶皮层兴奋性锥体细胞基本电生理特性和突触传递的影响,利用脑片膜片钳技术研究CaMKII-F89G转基因小鼠岛叶皮层锥体细胞的基本电生理性质及突触传递.结果显示:野生型和CaMKII-F89G转基因型小鼠岛叶皮层锥体细胞在静息膜电位,动作电位及电流电压曲线方面没有显著性差异;在突触传递中,野生型鼠与转基因鼠的自发兴奋性突触后电流和微小兴奋性突触后电流的幅度差异显著,而频率没有显著性差异;此外,两组小鼠的双脉冲易化(PPF)曲线也没有显著性差异.由此得出结论,CaMKII在前脑特异性过量表达可能不改变岛叶皮层锥体细胞基本电生理特性和突触前递质释放能力;CaMKII过量表达提高自发兴奋性突触后电流幅度可能是通过突触AMPA 和(或)NMDA受体介导的.Abstract: The experiment was designed to study basic electrophysiological characteristics and basal synaptic transmission of insular pyramidal cells in CaMKII forebrain overexpression mice by patch clamping. The basic electrophysiological results showed that there were no significant differences in the resting membrane potential, action potential and I-V curve of pyramidal cells in insular cortex between wild type and transgenic mice. No significant difference was measured in the frequency of sEPSCs and mEPSCs. However, compared to the wild type mice, transgenic mice exhibited augmented amplitude of sEPSCs and mEPSCs. There was also no significant difference in PPF curve. The results suggested that forebrain specific overexpression of CaMKII did not change the basic electrophysiological characteristics and presynaptic transmitter release in insular cortex. The influence of CaMKII overexpression on the amplitude of EPSCs may be mediated by postsynaptic receptors.
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Key words:
- αCaMKII /
- Insular cortex /
- EPSCs
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[1] [1] WANG H, SHIMIZU E, TANG Y P. Inducible protein knockout reveals temporal requirement of CaMKII reactivation for memory consolidation in the brain [J]. PNAS, 2003, 100(7): 4287-4292.[2] AUGUSTINE J R. Circuitry and functional aspects of the insular lobe in primates including humans [J]. Brain Research Reviews, 1996, 22: 229-244.[3] SHELLEY B P, TRIMBLE M R. The insular lobe of Reil-its anatamico-functional, behavioural and neuropsychiatric attributes in humans-a review [J]. World J Biol Psychiatry, 2004, 5(4): 176-200.[4] DUFFAU H, TAILLANDIER L, GATIGNOL P. The insular lobe and brain plasticity: Lessons from tumor surgery [J]. Clinical Neurology and Neurosurgery, 2006, 108: 543-548.[5] BURES J,FEDERICO B R, YAMAMOTO T. Conditioned Taste Aversion: Memory of a Special Kind [M]. Oxford: Oxford University Press, 1998: 1-13.[6] FEDERICO B R, LETICIA R L, RANIER G. Molecular signals into the insular cortex and amygdala during aversive gustatory memory formation [J]. Cell Mol Neurobiol, 2004, 24(1): 25-36.[7] BRAUN J J, SLICK T B, LORDEN J F. Involvement of gustatory neocortex in the learning of taste aversions [J]. Physiol Behav, 1972, 9(4): 637-641.[8] ROMAN C, REILLY S. Effects of insular cortex lesions on conditioned taste aversion and latent inhibition in the rat [J]. European Journal of Neuroscience, 2007, 26: 2627-2632.[9] ESCOBAR M L,BERMUDEZ-RATTONI F. Long-term potentiation in the insular cortex enhances conditioned taste aversion retention [J]. Brain Res, 2000, 852(1): 208-212.[10] ESCOBAR M L,CHAO V, BERMUDEZ-RATTONI F. In vivo long-term potentiation in the insular cortex: NMDA receptor dependence [J]. Brain Research, 1998, 779: 314-319.[11] RODRIGUES S M, FARB C R, BAUER E P, et al. Pavlovian fear conditioning regulates Thr286 autophosphorylation of Ca2+/calmodulin-dependent protein kinase Ⅱ at lateral amygdala synapses [J]. J Neurosci, 2004, 24(13): 3281-3288.[12] BENNETT M K, ERONDU N E, KENNEDY M B. Purification and characterization of a calmodulin-dependent protein kinase that is highly concentrated in brain [J]. Biol Chem, 1983, 258: 12735-12744.[13] MALINOW R, SCHULMAN H, TSIEN R W. Inhibition of postsynaptic PKC or CaMKII blocks induction but not expression of LTP [J]. Science, 1989, 245: 862-866.[14] SILVA A J, STEVENS C F, TONEGAWA S, et al. Deficient hippocampal long-term potentiation in a-calcium-calmodulin kinase Ⅱ mutant mice [J]. Science, 1992, 257: 201-206.[15] SILVA A J, PAYLOR R, WEHNER J M, et al. Impaired spatial learning in alpha-calcium-calmodulin kinase Ⅱ mutant mice [J]. Science, 1992: 257, 206-211.[16] HANSON P I, SCHULMAN H. Inhibitory autophosphorylation of multifunctional Ca2+/calmodulin-dependent protein kinase analyzed by site-directed mutagenesis [J]. Annu Rev Biochem, 1992, 61: 559-601.[17] BACH M E, HAWKINS R D, OSMAN M, et al. Impairment of spatial but not contextual memory in CaMKII mutant mice with a selective loss of hippocampal LTP in the range of the theta frequency [J]. Cell, 1995, 81: 905-915.[18] MAYFORD M, BACH M E, HUANG Y Y, et al. Control of memory formation through regulated expression of a CaMKII transgene [J]. Science, 1996, 274: 1678-1683.[19] MALENKA R C, NICOLL R A. Long-term potentiation-a decade of progress [J] . Science, 1999, 285: 1870-1874.[20] FRANKLAND P W, O’BRIEN C, OHNO M, et al. Alpha-CaMKII-dependent plasticity in the cortex is required for permanent memory [J]. Nature, 2001, 411: 309-313.[21] LISMAN J, SCHULMAN H, CLINE H. The molecular basis of CaMKII function in synaptic and behavioural memory [J]. Nat Rev Neurosci, 2002, 3(3): 175-190.[22] IRVINE E E, VON HERTZEN L S, PLATTNER F, et al. Alpha-CaMKII autophosphorylation: a fast track to memory [J]. Trends Neurosci, 2006, 29(8): 459-465.[23] IRVINE E E, VERNON J, GIESE K P. Alpha-CaMKII autophosphorylation contributes to rapid learning but is not necessary for memory [J]. Nat Neurosci, 2005(8): 411-412.[24] CAO X, WANG H, MEI B. Inducible and selective erasure of memories in the mouse brain via chemical-genetic manipulation [J]. Neuron, 2008, 60(2): 353-366.[25] BELELOVSKY K, ELKOBI A, KAPHZAN H, et al. A molecular switch for translational control in taste memory consolidation [J]. European Journal of Neuroscience, 2005, 22: 2560-2568[26] LI Y X, ZHANG Y, LESTER H A, et al. Enhancement of neurotransmitter release induced by brain-derived neurotrophic factor in cultured hippocampal neurons [J]. J Neuroscience, 1998, 18: 10231-10240.[27] LIU Z W, YANG S, ZHANG Y X, et al. Presynaptic alpha-7 nicotinic acetylcholine receptors modulate excitatory synaptic transmission in hippocampal neurous [J]. Acta Physiol Sin, 2003, 55: 731-735.[28] DEBANNE D, GUERINEAU N C, GAHWILER B H, et al. Paired-pulse facilitation and depression at unitary synapses in rat hippocampus: quantal fluctuation affects subsequent release [J]. J Physiol, 1996, 491: 163-176.[29] MERRILL M A, CHEN Y, STRACK S, et al. Activity-driven postsynaptic translocation of CaMKII [J]. Trends Pharmacol Sci, 2005, 26(12): 645-653.[30] TAN S E, WENTHOLD R J, SODERLING T R. Phosphorylation of AMPA-type glutamate receptors by calcium/calmodulin-dependent protein kinase Ⅱ and protein kinase C in cultured hippocampal neurons [J]. J Neurosci, 1994, 14(3 Pt 1): 1123-1129. [31] BARRIA A, DERKACH V, SODERLING T. Identification of the Ca2+/calmodulin-dependent protein kinase Ⅱ regulatory phosphorylation site in the α-amino-3-hydroxyl-5-methyl4- isoxazole-propionate-type glutamate receptor [J]. J Biol Chem, 1997, 272: 32727-32730.[32] THIAGARAJAN T C, PIEDRAS-RENTERIA E S, TSIEN R W. α- and βCaMKII: inverse regulation by neuronal activity and opposing effects on synaptic strength [J]. Neuron, 2002, 36: 1103-1114.[33] SONG I, HUGANIR R L. Regulation of AMPA receptors during synaptic plasticity [J]. Trends Neurosci, 2002, 25: 578-588.[34] LOWETH J A, SINGER B F, BAKER L K, et al. Transient Overexpression of α-Ca2+/Calmodulin-Dependent Protein Kinase Ⅱ in the Nucleus Accumbens Shell Enhances Behavioral Responding to Amphetamine [J]. J Neurosci, 2010, 30(3): 939-949.[35] COLONNESE M T, SHI J, CONSTANTINE-PATON M. Chronic NMDA receptor blockade from birth delays the maturation of NMDA currents, but does not affect AMPA/kainate currents [J]. J Neurophysiol, 2003, 89(1): 57-68.[36] COLBRAN R J, BROWN A M. Calcium/calmodulin-dependent protein kinase II and synaptic plasticity [J]. Neurobiology, 2004, 14: 318-327.[37] OMKUMAR R V,KIELY M J, ROSENSTEIN A J, et al. Identification of a phosphorylation site for calcium/calmodulin-dependent protein kinase Ⅱ in the NR2B subunit of the N-methyl-D-aspartate receptor [J]. J Biol Chem, 1996, 271: 31670-31678.[38] LISMAN J, SCHULMAN H, CLINE H. The molecular basis of CaMKII function in synaptic and behavioural memory [J]. Nat Rev Neurosci, 2002, 3(3): 175-190.[39] BARRIA A, MALINOW R. NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII [J]. Neuron, 2005, 48: 289-301.[40] PARK C S, ELGERSMA Y, GRANT S G, et al. αCaMKII and PSD-95 differentially regulate synaptic expression of NR2A and NR2B-containing NMDA receptors in hippocampus [J]. Neuroscience, 2008, 151(1): 43-55.
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