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1 ry synaptic plasticity, and have accentuated long-term synaptic depression.
2 sential for certain types of both short- and long-term synaptic depression.
3 endent plasticity, including interference in long-term synaptic depression.
4 n the parameter space conducive for inducing long-term synaptic depression.
5 , which is an important mechanism underlying long-term synaptic depression.
6 -d-aspartate receptor activation causes both long-term synaptic depression and rapid internalization
7 tein O-GlcNAcylation induces a novel form of long-term synaptic depression at hippocampal CA3-CA1 syn
8 resveratrol blocked endocannabinoid-mediated long-term synaptic depression in VTA dopamine neurons.
9 apses onto inhibitory interneurons undergo a long-term synaptic depression (interneuron LTD; iLTD).
10 ) (FMRFa) can induce transcription-dependent long-term synaptic depression (LTD) in Aplysia sensorimo
11 ynthesis yields exaggerated mGluR5-dependent long-term synaptic depression (LTD) in area CA1 of the h
12 xamine long-term synaptic potentiation (LTP)/long-term synaptic depression (LTD) in brain slices of r
13 artate (NMDA) to hippocampal slices produces long-term synaptic depression (LTD) in CA1 that is (1) s
14 onic acid-type glutamate receptors caused by long-term synaptic depression (LTD) in cerebellar Purkin
15                    Here, we demonstrate that long-term synaptic depression (LTD) in hippocampal neuro
16 noid (eCB) signaling mediates short-term and long-term synaptic depression (LTD) in many brain areas.
17 regulated following induction of presynaptic long-term synaptic depression (LTD) in O-LM interneurons
18                                   Cerebellar long-term synaptic depression (LTD) is a model system of
19                                   Cerebellar long-term synaptic depression (LTD) is a model system of
20 methyl-D-aspartate (NMDA) receptor-dependent long-term synaptic depression (LTD) is associated with a
21 to characterize the dependence of cerebellar long-term synaptic depression (LTD) on postsynaptic Ca(2
22                                  Presynaptic long-term synaptic depression (LTD) plasticity at glutam
23 campal long-term potentiation, their role in long-term synaptic depression (LTD) remains unclear.
24 icroanatomy instructs spine remodeling after long-term synaptic depression (LTD) remains unclear.
25 estigated the site of expression of striatal long-term synaptic depression (LTD) using analysis of Sr
26 ) stimulates dendritic protein synthesis and long-term synaptic depression (LTD), but it remains uncl
27                             M1 mAChRs induce long-term synaptic depression (LTD), but little is known
28 , including impaired group 1 mGluR-dependent long-term synaptic depression (LTD), reduced group 1 mGl
29 ptors (CB1Rs) are believed to participate in long-term synaptic depression (LTD).
30 aptic and postsynaptic spikes, we can induce long-term synaptic depression (LTD).
31 ation is necessary and sufficient to trigger long-term synaptic depression (LTD).
32 o G(i/o) protein, can mediate short-term and long-term synaptic depression (LTD).
33 ng that astrocytes are necessary elements in long-term synaptic depression (LTD).
34 s, which exhibit exaggerated mGlu1/5-induced long-term synaptic depression (LTD).
35 , long-term synaptic facilitation (LTF), and long-term synaptic depression (LTD).
36 on, ArcGFP+ neurons preferentially displayed long-term synaptic depression (mGluR-LTD) and robust inc
37 tor (mGluR)-stimulated protein synthesis and long-term synaptic depression (mGluR-LTD) are altered in
38 lutamate receptors (mGluRs) induce a form of long-term synaptic depression (mGluR-LTD) in area CA1 of
39 As supporting exaggerated mGlu(1/5) -induced long-term synaptic depression (mGluR-LTD) in the FX mous
40 n the dorsal striatum, inducing MOR-mediated long-term synaptic depression (MOR-LTD) or short-term de
41 binoid receptors (CB1Rs), mediate short- and long-term synaptic depression of neurotransmitter releas
42 d postsynaptic activity triggers associative long-term synaptic depression of visually evoked inhibit
43 etion did not rescue altered mGluR-dependent long-term synaptic depression or translational control o