Postsynaptic endocannabinoid release is critical to long-term depression in the striatum

@article{Gerdeman2002PostsynapticER,
  title={Postsynaptic endocannabinoid release is critical to long-term depression in the striatum},
  author={Gregory L. Gerdeman and Jennifer A. Ronesi and David M. Lovinger},
  journal={Nature Neuroscience},
  year={2002},
  volume={5},
  pages={446-451}
}
The striatum functions critically in movement control and habit formation. The development and function of cortical input to the striatum are thought to be regulated by activity-dependent plasticity of corticostriatal glutamatergic synapses. Here we show that the induction of a form of striatal synaptic plasticity, long-term depression (LTD), is dependent on activation of the CB1 cannabinoid receptor. LTD was facilitated by blocking cellular endocannabinoid uptake, and postsynaptic loading of… 
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References

SHOWING 1-10 OF 52 REFERENCES
Decreased probability of neurotransmitter release underlies striatal long-term depression and postnatal development of corticostriatal synapses.
  • S. Choi, D. Lovinger
  • Biology, Psychology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1997
TLDR
Interestingly, LTD maintenance appears to involve a decrease in the probability of neurotransmitter release from presynaptic terminals as evidenced by increases in paired-pulse facilitation and the coefficient of variation of synaptic responses that are tightly associated with LTD expression.
Activation of group I mGluRs is necessary for induction of long-term depression at striatal synapses.
TLDR
Both group I mGluR subtypes contribute to the induction of LTD at corticostriatal synapses, according to the results of this study.
Regional and postnatal heterogeneity of activity-dependent long-term changes in synaptic efficacy in the dorsal striatum.
TLDR
Heterogeneous activity-dependent changes in the direction of synaptic strength in subregions of the developing rat striatum suggests mechanisms by which this brain region plays pivotal roles in the acquisition or encoding of some forms of motor sequencing and stereotypical behaviors.
Dopamine-dependent synaptic plasticity in striatum during in vivo development.
TLDR
It is suggested that a major role of DA in the striatum is to initiate mechanisms that regulate the efficacy of excitatory striatal synapses, producing a decrease in glutamate release.
Selective involvement of mGlu1 receptors in corticostriatal LTD
Short- and long-term synaptic depression in rat neostriatum.
TLDR
It is shown that glutamatergic synapses in neostriatum are capable of expressing a form of synaptic depression that may involve decreased glutamate release and was blocked by treatments that increase transmitter release including increased extracellular Ca2+, application of 4-aminopyridine, or application of phorbol ester.
CB1 cannabinoid receptor inhibits synaptic release of glutamate in rat dorsolateral striatum.
TLDR
Findings support the interpretation that CB1 activation leads to a decrease of glutamate release from afferent terminals in the striatum and may suggest CB1-targeted drugs as potential therapeutic agents in the treatment of Parkinson's disease and other basal ganglia disorders.
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.
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.
...
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