Characterisation of LTP induced by the activation of glutamate metabotropic receptors in area CA1 of the hippocampus
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2022, NeuropharmacologyCitation Excerpt :As is the case with NMDAR-mediated synaptic plasticity, agonists have been employed extensively to study the mGluR-dependent forms of synaptic plasticity. For example, when we tested (1S,3R)-ACPD on CA3-CA1 synapses, we observed a robust slow-onset potentiation (Bortolotto and Collingridge, 1993, 1995). This effect was stereospecific since the (1R,3S)-enantiomer had no effect.
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2020, Journal of Chemical NeuroanatomyLong-term potentiation and the role of N-methyl-D-aspartate receptors
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2012, NeuropharmacologyCitation Excerpt :The activation of group 1 mGluRs and their involvement in tLTP induction in our study is interesting since mGluR activation has been implicated in both LTP and LTD. It has been suggested that mGluR activation is required for HFS-LTP induction in CA1 pyramidal neurons (Bashir et al., 1993), that it can enhance HFS-LTP (McGuinness et al., 1991a, b), and that application of mGluR agonist alone can induce LTP (Bortolotto et al., 1995; Bortolotto and Collingridge, 1993, 1995). In addition, prior activation of mGluRs, called “priming” was shown to facilitate LTP (Cohen and Abraham, 1996; Cohen et al., 1998) and mGluRs have been suggested to serve as a molecular switch for LTP induction (Bortolotto et al., 1994, 2005).
Early, time-dependent disturbances of hippocampal synaptic transmission and plasticity after in utero immune challenge
2011, Biological PsychiatryCitation Excerpt :This form of plasticity shares features with other nonclassical forms of LTP elicited by LFS in the CA1 area of the hippocampus (23,36,37) and of the amygdala (38). Most of these forms of LTP have been found dependent on mGlur and independent of NMDAr activation (36,38–40). Although the slow-onset LTP is only observed in LPS rats between 16 and 25 days old and not after 30 days of age, it might have a deep and delayed impact on learning capability, by promoting the formation of aberrant synaptic circuits at a crucial time of brain maturation (i.e., the second week of age in rodents).