High impact information on Long-Term Depression (Physiology)

• Modulation of H1 binding activity is thought to be an important step in the potentiation/depotentiation of chromatin structure for transcription [1].
• The depotentiation seen in both L-DOPA-treated non-dyskinetic rats and intact controls was prevented by activation of the D1 subclass of dopamine receptors or inhibition of protein phosphatases [2].
• Activation of group 1 metabotropic glutamate receptors (mGluRs) stimulates dendritic protein synthesis and long-term synaptic depression (LTD), but it remains unclear how these effects are related [3].
• Cerebellar long-term synaptic depression requires PKC-mediated activation of CPI-17, a myosin/moesin phosphatase inhibitor [4].
• Hippocampal N-methyl-D-aspartate (NMDA) receptor-dependent long-term synaptic depression (LTD) is associated with a persistent dephosphorylation of the GluR1 subunit of AMPA receptors at a site (Ser-845) phosphorylated by cAMP-dependent protein kinase (PKA) [5].

Biological context of Long-Term Depression (Physiology)

• Remoxipride itself did not influence basal synaptic transmission or depotentiation [6].
• This study tested the hypothesis that endogenous adenosine, a neuromodulator which is known to modify long-term potentiation (LTP), might also affect other forms of long-lasting synaptic plasticity, namely long-term depression (LTD) and depotentiation, in the hippocampus [7].
• Here, we have examined the effects of N-methyl-D-aspartate receptor (NMDAR) blockade on the induction of LTD, LTP, and depotentiation of field potentials evoked in sensorimotor cortex by stimulation of the white matter in the adult, freely moving rat [8].

Anatomical context of Long-Term Depression (Physiology)

• A selective role of calcineurin aalpha in synaptic depotentiation in hippocampus [9].
• To investigate whether all of these forms of synaptic plasticity require the same isoforms of calcineurin, we have examined LTD, depotentiation, and LTP in mice lacking the predominant calcineurin isoform in the central nervous system, Aalpha-/- mice [9].
• In addition, we find that MCPG fails to block the NMDA receptor-dependent forms of LTP, LTD, and depotentiation in visual cortex [10].
• Depotentiation in the dentate gyrus of freely moving rats is modulated by D1/D5 dopamine receptors [11].
• Activation of group II metabotropic glutamate receptors induces depotentiation in amygdala slices and reduces fear-potentiated startle in rats [12].

Associations of Long-Term Depression (Physiology) with chemical compounds

• Brief bath application of N-methyl-D-aspartate (NMDA) to hippocampal slices produces long-term synaptic depression (LTD) in CA1 that is (1) sensitive to postnatal age, (2) saturable, (3) induced postsynaptically, (4) reversible, and (5) not associated with a change in paired pulse facilitation [13].
• Lithium treatment blocks long-term synaptic depression in the striatum [14].
• We show that homosynaptic depression is fully developed in the juvenile and that 5-HT reliably induces synaptic facilitation at depressed synapses [15].
• This NMDA-induced depotentiation was blocked by adenosine A(1) receptor antagonist [16].
• This LFS-induced depotentiation was specifically prevented by protein phosphatase (PP)1 inhibitors, okadaic acid, and calyculin A but not by the PP2A or PP2B inhibitors [16].

Gene context of Long-Term Depression (Physiology)

• LY341495 also blocked NMDA receptor-independent depotentiation and setting of a molecular switch involved in the induction of LTP; effects which have previously been shown to be blocked by the mGlu receptor antagonist (S)-MCPG [17].
• Surprisingly another form of LTD, depotentiation, requires activation of NR2A-containing NMDARs [18].
• We have combined pharmacologic and genetic approaches to demonstrate that PKA activity is required for both homosynaptic LTD and depotentiation and that a specific neuronal isoform of type I regulatory subunit (RI beta) is essential [19].
• In addition, Mas-/- mice show alterations in the onset of depotentiation [20].
• Here we show that although induction of LTP is unaffected by either pharmacological activation or inhibition of 5-HT4, application of the 5-HT4 receptor agonist, RS67333, completely blocks learning-induced depotentiation of LTP in the hippocampal CA1 region of freely moving rats, suggesting a role for 5-HT4 receptors in behavioural metaplasticity [21].

Analytical, diagnostic and therapeutic context of Long-Term Depression (Physiology)

• Perfusion of the mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) for a prolonged period (20 min) induced long-term depression (LTD) of field excitatory postsynaptic field potentials (epsps) from the baseline level and also depotentiation (DP) from the long-term potentiated level [22].

References