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Expression of ectonucleotidase CD39 by Foxp3+ Treg cells: hydrolysis of extracellular ATP and immune suppression.
TLDR
In humans CD39 is a marker of a Treg subset likely involved in the control of the inflammatory autoimmune disease and Notably, patients with the remitting/relapsing form of multiple sclerosis have strikingly reduced numbers of CD39(+) Treg cells in the blood. Expand
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. Expand
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. Expand
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. Expand
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. Expand
Re-emergence of striatal cholinergic interneurons in movement disorders
TLDR
A review of recent experimental and clinical studies on striatal cholinergic interneurons in Parkinson's disease and dystonia places them within the context of the pathogenesis of movement disorders. Expand
Acetylcholine-mediated modulation of striatal function
TLDR
It is proposed that endogenous ACh exerts a complex modulation of striatal synaptic transmission, which produces both short-term and long-term effects and might be of crucial importance in processing the cortical inputs to the striatum. Expand
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. Expand
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. Expand
Receptor Subtypes Involved in the Presynaptic and Postsynaptic Actions of Dopamine on Striatal Interneurons
TLDR
Immunohistochemical analyses in both wild-type and D1R-/- mice confirmed the expression of D5 receptors in both cholinergic and parvalbumin-positive interneurons of the striatum, and in mice lacking D2 receptors, the DA-dependent inhibition of GABA transmission was lost in both interneuron populations. Expand
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