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Transient incorporation of native GluR2-lacking AMPA receptors during hippocampal long-term potentiation
TLDR
It is demonstrated that long-term potentiation in CA1 hippocampal pyramidal neurons causes rapid incorporation of GluR2-lacking calcium-permeable (CP)-AMPARs, which are physiologically expressed at CA1Pyramidal cell synapses during LTP, and may be required for LTP consolidation.
Review: Cholinergic mechanisms and epileptogenesis. The seizures induced by pilocarpine: A novel experimental model of intractable epilepsy
TLDR
The amygdala, thalamus, olfactory cortex, hippocampus, neocortex, and substantia nigra are the most sensitive regions to epilepsy‐related damage following convulsions produced by pilocarpine.
Kainate receptors are involved in synaptic plasticity
TLDR
It is found that LY382884 is a selective antagonist at neuronal kainate receptors containing the GluR5 subunit, which has no effect on long-term potentiation (LTP) that is dependent onNMDA receptors but prevents the induction of mossy fibre LTP, which is independent of NMDA receptors.
Induction of LTP in the hippocampus needs synaptic activation of glutamate metabotropic receptors
TLDR
(RS)-α-methyl-4-carboxyphenylglycine is a specific mGluR antagonist in the hippocampus and this compound is used to examine the nature of the involvement ofmGluRs in LTP, and it is shown that synaptic activation of mGLURs is necessary for the induction of both NMDA receptor-dependent and NMDA receptors-independent forms of LTP inThe hippocampus.
A molecular switch activated by metabotropic glutamate receptors regulates induction of long-term potentiation
TLDR
The role of mGluRs in the induction of LTP is fundamentally different from that of NMDA receptors and this work shows that the molecular switch is a new feature of LTB which has fundamental consequences for the understanding of synaptic plastic mechanisms.
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