Rapid communicationAn antagonist of glutamate metabotropic receptors, (RS)-α-methyl-4-carboxyphenylglycine, prevents the LTP-related increase in postsynaptic AMPA sensitivity in hippocampal slices
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Cited by (51)
Effects of pre-natal alcohol exposure on hippocampal synaptic plasticity: Sex, age and methodological considerations
2016, Neuroscience and Biobehavioral ReviewsCitation Excerpt :In addition to NMDAR-dependent forms of LTP, studies have shown that metabotropic glutamate receptors (mGluRs) are involved in LTP (Bashir et al., 1993; Nosyreva and Huber, 2005; Riedel et al., 1995; Riedel et al., 1996). Particularly the mGluR1, which is linked to activation of phosphoinositide hydrolysis and the subsequent release of intracellular Ca2+ stores, has been shown to contribute to the induction and maintenance of some forms of LTP both in vivo and in vitro (Riedel et al., 1996; Sergueeva et al., 1993; Martin and Morris, 1997). Recently, it has been suggested that the number of pulses used for the induction of LTP regulate the competition between NMDA- and mGluR dependent LTP highlighting the mechanistic complexity underlying synaptic plasticity (Hsu et al., 2011).
Involvement of inositol-1,4,5-trisphosphate receptors in the bidirectional synaptic plasticity induced in hippocampal CA1 neurons by 1-10 Hz low-frequency stimulation
2010, NeuroscienceCitation Excerpt :Considering the results shown in Fig. 2, it is possible that LFS with a pulse number between 80 and 1000 at frequencies between 1 and 10 Hz induces bidirectional synaptic plasticity depending on the frequency or duration of LFS and that PKC is involved in the increase in potentiation and IP3 is involved in the decrease in potentiation and/or in the increase in depression. Previous studies on CA1 neurons have shown that co-activation of mGluRs and NMDARs is involved in the mechanism of activity-dependent LTP (Behnisch and Reymann, 1993; Bortolotto and Collingridge, 1993; Brown et al., 1994; Segueeva et al., 1993; Fujii et al., 2003). In this study, perfusion with AP5 or MCPG during 10 Hz LFS inhibited LTP induction (Figs. 2A–C and 4B), showing that the LTP induced by 10 Hz LFS at CA1 synapses involves both NMDARs and mGluRs.
Early Increase in Extrasynaptic NMDA Receptor Signaling and Expression Contributes to Phenotype Onset in Huntington's Disease Mice
2010, NeuronCitation Excerpt :Upon subsequent transient application of TBOA, ifenprodil eliminated the difference between YAC128 and WT INMDA decay TauW (Figures 6E and 6F, p = 0.6). Contrastingly, the broad spectrum group I/II mGluR antagonist S-MCPG (250 μM; Sergueeva et al., 1993) had no significant effect upon TBOA-induced increase in Ex-INMDA TauW in WT or YAC128 MSNs (Figure 6F), demonstrating that mGluR activity is not required. Collectively, the data suggest that elevated Ex-INMDA in YAC128 MSNs is carried by a distinct extrasynaptic population of NR2B-containing NMDARs.
The late maintenance of hippocampal LTP: Requirements, phases, 'synaptic tagging', 'late-associativity' and implications
2007, NeuropharmacologyCitation Excerpt :Following tetanization, a slowly developing increase in AMPA-sensitivity was detected, which paralleled the conversion from STP to early-LTP. If a NMDA or group I mGluR antagonists or a PKC inhibitor was added to the perfusion medium during or immediately after tetanization, STP was not sustained and there was no increase in AMPA sensitivity (Davies et al., 1989; Reymann et al., 1988b; Sergueeva et al., 1993). This implies that the mGluR-PKC pathway is required to generate but not to maintain both the increase in AMPA receptor function and LTP1.
Function of the hippocampus in memory formation: Desperately seeking resolution
2001, Progress in Neuro-Psychopharmacology and Biological Psychiatry