LTP and LTD An Embarrassment of Riches
Homosynaptic long-term depression in area CA1 of hippocampus and effects of N-methyl-D-aspartate receptor blockade.
The data suggest that synaptic depression can be triggered by prolonged NMDA receptor activation that is below the threshold for inducing synaptic potentiation, and it is proposed that this mechanism is important for the modifications of hippocampal response properties that underlie some forms of learning and memory.
The mGluR theory of fragile X mental retardation
Altered synaptic plasticity in a mouse model of fragile X mental retardation
- K. Huber, Sean M Gallagher, S. Warren, M. Bear
- BiologyProceedings of the National Academy of Sciences…
- 21 May 2002
It is shown that a form of protein synthesis-dependent synaptic plasticity, long-term depression triggered by activation of metabotropic glutamate receptors, is selectively enhanced in the hippocampus of mutant mice lacking FMRP.
Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity
It is shown that LTP and LTD reversibly modify the phosphorylation of the AMPA receptor GluR1 subunit, and that identical stimulation conditions recruit different signal-transduction pathways depending on synaptic history.
Learning Induces Long-Term Potentiation in the Hippocampus
It is found that one-trial inhibitory avoidance learning in rats produced the same changes in hippocampal glutamate receptors as induction of LTP with HFS and caused a spatially restricted increase in the amplitude of evoked synaptic transmission in CA1 in vivo.
Role for rapid dendritic protein synthesis in hippocampal mGluR-dependent long-term depression.
Local postsynaptic protein synthesis, triggered by synaptic activation of metabotropic glutamate receptors, was found to modify synaptic transmission within minutes.
BDNF Regulates the Maturation of Inhibition and the Critical Period of Plasticity in Mouse Visual Cortex
Ubiquitination Regulates PSD-95 Degradation and AMPA Receptor Surface Expression
A unified model of NMDA receptor-dependent bidirectional synaptic plasticity
This paper presents a mathematical embodiment of bidirectional synaptic plasticity that is able to explain diverse induction protocols with a fixed set of parameters and provides the foundation for a unified theory of N-methyl-d-aspartate receptor-dependent synaptic Plasticity.