Related Experiment Videos
Long-term synaptic depression in the striatum: physiological and pharmacological characterization
1Clinica Neurologica, Dip. Sanità, II Università di Roma, Italy.
Summary
Tetanic stimulation induces long-term synaptic depression (LTD) in the striatum, requiring membrane depolarization, metabotropic glutamate receptors, and coactivation of D1 and D2 dopamine receptors for expression.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Basal Ganglia Function
Background:
- The striatum plays a crucial role in motor control and habit formation.
- Synaptic plasticity, particularly long-term depression (LTD), in the striatum is vital for regulating neural circuit function.
- The precise physiological and pharmacological conditions governing striatal LTD remain incompletely understood.
Purpose of the Study:
- To investigate the conditions required for tetanic stimulation-induced long-term synaptic depression (LTD) in corticostriatal pathways.
- To elucidate the roles of membrane potential, glutamate receptors, and dopamine receptors in striatal LTD.
- To understand how striatal LTD influences basal ganglia circuitry and motor activity.
Main Methods:
- Extracellular and intracellular recording techniques in rat striatal slices.
- Tetanic stimulation of corticostriatal glutamatergic fibers.
- Pharmacological manipulation using receptor antagonists (NMDA, metabotropic glutamate, GABA(A), muscarinic, D1, D2) and agonists.
- Lesioning of the nigrostriatal dopamine system.
Main Results:
- Tetanic stimulation induced long-term synaptic depression (LTD) (> 2 h) of field potentials and EPSPs, independent of intrinsic membrane properties.
- LTD expression was dependent on postsynaptic membrane depolarization during tetanic stimulation and required activation of glutamate metabotropic receptors.
- LTD was blocked by antagonists of D1 and D2 dopamine receptors and was absent in dopamine-depleted slices, but could be restored by co-application of D1 and D2 receptor agonists.
Conclusions:
- Striatal LTD requires membrane depolarization, action potential discharge, glutamate metabotropic receptor activation, and coactivation of D1 and D2 dopamine receptors.
- Dopamine signaling is essential for the expression of striatal LTD.
- Striatal LTD, influenced by these conditions, may modulate the output of the striatum and impact motor control.