Metabotropic glutamate receptors are required for the induction of long-term potentiation

Zheng, Fang; Gallagher, Joel P.

doi:10.1016/0896-6273(92)90231-2

Cited by 142 publications

(59 citation statements)

References 48 publications

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“…A relatively fast onset LTP of intracellular EPSPs (peak attained in 30 min) induced by ACPD has also previously been observed in the dorsolateral septal nucleus, although tetanically induced LTP is not dependent on NMDAR activation in that nucleus (Zheng and Gallagher, 1992).…”

Section: Discussionmentioning

confidence: 96%

Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors

1995

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Whole-cell patch-clamp recordings of evoked excitatory postsynaptic currents (EPSCs) were made from granule cells of the rat dentate gyrus in vitro. Tetanic stimulation in control media evoked a statistically identical long-term potentiation (LTP) of both the AMPA and NMDA receptor-mediated components of the dual component EPSC (AM-PAR and NMDAR EPSCs), as shown by a similar percentage increase in both components when measured at a holding potential of -30 mV, and also by an identical time course of the pre- and post-LTP induced EPSC at -30 mV and -70 mV. Application of the selective metabotropic glutamate receptor (mGluR) agonist 1S,3R-ACPD induced a transient depression followed by a rapid onset LTP of both the AMPAR and the NMDAR components of the dual component EPSC. The ACPD- and tetanically induced LTP of the AMPAR EPSC was NMDAR dependent, being abolished by the NMDAR antagonist AP5. Tetanic stimulation, and application of ACPD, also induced a relatively rapid onset LTP of the pharmacologically isolated NMDAR EPSC. Such tetanically and ACPD-induced LTP of the isolated NMDAR EPSC was also dependent on NMDAR activation, being strongly inhibited by AP5. The tetanically and the ACPD-induced LTP of the NMDAR EPSC were dependent on protein kinase C (PKC) stimulation, being strongly inhibited by the PKC inhibitor PKCI (19–31). The studies suggest that coactivation of the mGluR and NMDAR are required for induction of LTP of both the AMPAR- and NMDAR-mediated synaptic transmission. Moreover, LTP of the NMDAR-mediated synaptic transmission appears to be dependent on coincident activation of the NMDAR and mGluR.

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Section: Discussionmentioning

confidence: 96%

Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors

1995

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“…For example, the application of the mGluR agonist (1S,3R)Ϫ1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) was reported to potentiate NMDA-and AMPA-mediated currents directly, and its application during tetanus enhanced LTP (O'Connor et al, 1995). When ACPD was combined with subthreshold tetanic stimulation, or when NMDA and ACPD were co-applied, LTP was induced in the hippocampus (Zheng and Gallagher, 1992). Conversely the mGluR, antagonist ( R, S)-␣-methyl-4-carboxylphenylglycine (MCPG) inhibited tetanus-induced LTP in both the CA1 region and at the perforant pathway in the dentate gyrus (Bashir et al, 1993;Riedel and Reymann, 1993;Richter-Levin et al, 1994).…”

Section: Abstract: Hippocampus; Gene Targeting; Long-term Potentiatimentioning

confidence: 99%

Mice Lacking Metabotropic Glutamate Receptor 5 Show Impaired Learning and Reduced CA1 Long-Term Potentiation (LTP) But Normal CA3 LTP

et al. 1997

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Class I metabotropic glutamate receptors (mGluRs) have been postulated to play a role in synaptic plasticity. To test the involvement of one member of this class, we have recently generated mutant mice that express no mGluR5 but normal levels of other glutamate receptors. The CNS revealed normal development of gross anatomical features. To examine synaptic functions we measured evoked field EPSPs in the hippocampal slice. Measures of presynaptic function, such as paired pulse facilitation in mutant CA1 neurons, were normal. The response of mutant CA1 neurons to low concentrations of (1S,3R)Ϫ1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) was missing, which suggests that mGluR5 may be the primary high affinity ACPD receptor in these neurons. Long-term potentiation (LTP) in mGluR5 mutants was significantly reduced in the NMDA receptor (NMDAR)-dependent pathways such as the CA1 region and dentate gyrus of the hippocampus, whereas LTP remained intact in the mossy fiber synapses on the CA3 region, an NMDAR-independent pathway. Some of the difference in CA1 LTP could lie at the level of expression, because the reduction of LTP in the mutants was no longer observed 20 min after tetanus in the presence of 2-amino-5-phosphonopentanoate. We propose that mGluR5 plays a key regulatory role in NMDAR-dependent LTP. These mutant mice were also impaired in the acquisition and use of spatial information in both the Morris water maze and contextual information in the fear-conditioning test. This is consistent with the hypothesis that LTP in the CA1 region may underlie spatial learning and memory.

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“…This observation has been considered particularly important for the understanding of the overall function of glutamatergic synapses and the role that mGluRs may play in the mechanisms of synaptic potentiation and neuronal plasticity (Nicholls, 1992). In fact, the importance of mGluR activation for the stimulation of neurotransmitter release and for the induction and maintenance of long term potentiation has been repeatedly stressed (Anwyl, 1991;Bortolotto & Collingridge, 1992;Zheng & Gallagher, 1992). However, using electrophysiological approaches, it has also been shown that IS,3R-ACPD and quisqualic acid (Quis), a non-selective mGluR agonist, cause a synaptic inhibition that has been ascribed to the decrease of transmitter release from glutamatergic terminals (Lovinger, 1991;Calabresi et al, 1992;Rannie & Shinnick-Gallagher, 1992).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological characterization of the metabotropic glutamate receptor inhibiting d‐[³H]‐aspartate output in rat striatum

Lombardi

Alesiani

Leonardi

et al. 1993

British J Pharmacology

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Metabotropic glutamate receptors are required for the induction of long-term potentiation

Cited by 142 publications

References 48 publications

Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors

Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors

Mice Lacking Metabotropic Glutamate Receptor 5 Show Impaired Learning and Reduced CA1 Long-Term Potentiation (LTP) But Normal CA3 LTP

Pharmacological characterization of the metabotropic glutamate receptor inhibiting d‐[³H]‐aspartate output in rat striatum

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Metabotropic glutamate receptors are required for the induction of long-term potentiation

Cited by 142 publications

References 48 publications

Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors

Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors

Mice Lacking Metabotropic Glutamate Receptor 5 Show Impaired Learning and Reduced CA1 Long-Term Potentiation (LTP) But Normal CA3 LTP

Pharmacological characterization of the metabotropic glutamate receptor inhibiting d‐[3H]‐aspartate output in rat striatum

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Pharmacological characterization of the metabotropic glutamate receptor inhibiting d‐[³H]‐aspartate output in rat striatum