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Glutamate-triggered events inducing corticostriatal long-term depression
P Calabresi1, D Centonze, P Gubellini
1Clinica Neurologica, Università di Roma Tor Vergata, 00133 Rome, Italy.
Summary
Long-term depression (LTD) in corticostriatal pathways, crucial for motor learning, requires postsynaptic depolarization, metabotropic glutamate receptor activation, dopamine receptor activation, and nitric oxide release. These factors are essential for inducing LTD in the striatum.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Motor Learning
Background:
- Corticostriatal long-term depression (LTD) is implicated in motor learning and memory.
- Understanding the induction mechanisms of striatal LTD is crucial.
Purpose of the Study:
- To investigate the critical factors involved in inducing corticostriatal LTD.
- To elucidate the roles of glutamate receptors, dopamine, and nitric oxide in synaptic plasticity.
Main Methods:
- Intracellular recordings from rat corticostriatal slice preparations.
- Pharmacological activation of glutamate receptors (AMPA, t-ACPD, quisqualate).
- High-frequency stimulation (HFS) of corticostriatal fibers and electrical depolarization.
Main Results:
- LTD induction requires simultaneous activation of ionotropic and metabotropic glutamate receptors.
- Dopamine (DA) and nitric oxide (NO) are necessary for LTD induction during electrical depolarization.
- LTD induction is blocked by D2 dopamine receptor antagonist and NO synthase inhibitor.
Conclusions:
- Corticostriatal LTD induction necessitates a combination of postsynaptic depolarization, metabotropic glutamate receptor activation, dopamine receptor activation, and nitric oxide release.
- These findings highlight a complex interplay of signaling pathways in regulating striatal synaptic plasticity.
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