Bi-directional changes in synaptic plasticity induced at corticostriatal synapses in vitro

Area of Science:

• Neuroscience
• Synaptic Plasticity

Background:

• Long-term changes in synaptic efficacy at corticostriatal synapses are crucial for basal ganglia function, impacting motor learning and cognition.
• Previous research indicated long-term depression (LTD) as the primary plasticity mechanism at these synapses.

Purpose of the Study:

• To investigate the conditions under which long-term potentiation (LTP) can be induced at corticostriatal synapses.
• To clarify the mechanisms underlying synaptic plasticity in the corticostriatal pathway.

Main Methods:

• Utilized a sagittal slice preparation of the corticostriatal pathway.
• Applied tetanic stimulation to white matter and direct stimulation within the striatum.
• Investigated the role of NMDA receptors and dopamine receptors (D1 and D2) in synaptic plasticity.

Main Results:

• Tetanic stimulation of white matter readily induced LTP at corticostriatal synapses without pharmacological agents.
• NMDA receptor activation was essential for corticostriatal LTP.
• Striatally induced LTD required dopamine receptor blockade and NMDA receptor blockade, suggesting involvement of local striatal circuits.
• Pairing white matter and striatal stimulation significantly enhanced LTP magnitude.

Conclusions:

• Corticostriatal LTP can be induced under physiological conditions, contrary to previous assumptions.
• Striatally induced LTD likely involves local striatal circuits and dopaminergic inputs.
• These findings offer new insights into the regulation of basal ganglia function and its role in motor learning and cognition.