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Loss of bidirectional striatal synaptic plasticity in L-DOPA–induced dyskinesia
TLDR
Results indicate that abnormal information storage in corticostriatal synapses is linked with the development of L-DOPA–induced dyskinesia.
Long-term synaptic depression in the striatum: physiological and pharmacological characterization
TLDR
Data show that striatal LTD requires three main physiological and pharmacological conditions: (1) membrane depolarization and action potential discharge of the postsynaptic cell during the conditioning tetanus, (2) activation of glutamate metabotropic receptors, and (3) coactivation of D1 and D2 DA receptors.
Dopamine and cAMP-Regulated Phosphoprotein 32 kDa Controls Both Striatal Long-Term Depression and Long-Term Potentiation, Opposing Forms of Synaptic Plasticity
TLDR
Evidence is provided that the D1-like receptor-dependent activation of DA and cyclic adenosine 3′,5′ monophosphate-regulated phosphoprotein 32 kDa is a crucial step for the induction of both long-term depression (LTD) and long- term potentiation (LTP), two opposing forms of synaptic plasticity.
Long‐term Potentiation in the Striatum is Unmasked by Removing the Voltage‐dependent Magnesium Block of NMDA Receptor Channels
TLDR
The findings show that repetitive activation of cortical inputs can induce long‐term changes of synaptic transmission in the striatum and this structure may provide the cellular substrate for motor learning and underlie the physiopathology of some movement disorders.
Saccade preparation inhibits reorienting to recently attended locations.
TLDR
Manual reaction time in normal human subjects is measured to confirm that an eccentric visual signal has a biphasic effect on covert attention and eye movements and activation of return is activated by midbrain oculomotor pathways and may function as a location "tagging" mechanism to optimize efficiency of visual search.
Direct and indirect pathways of basal ganglia: a critical reappraisal
TLDR
A model in which intrastriatal connections are critical and the two pathways are structurally and functionally intertwined is proposed, in which all MSNs might either facilitate or inhibit movement depending on the form of synaptic plasticity expressed at a certain moment.
Abnormal Synaptic Plasticity in the Striatum of Mice Lacking Dopamine D2 Receptors
TLDR
This study indicates that D2Rs play a key role in mechanisms underlying the direction of long-term changes in synaptic efficacy in the striatum and shows that an imbalance between D2R and NMDA receptor activity induces altered synaptic plasticity at corticostriatal synapses.
Dopaminergic control of synaptic plasticity in the dorsal striatum
TLDR
Cortical glutamatergic and nigral dopaminergic afferents impinge on projection spiny neurons of the striatum, providing the most significant inputs to this structure, and the formation of LTD and LTP requires the activation of PKG and PKA in striatal projection neurons.
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