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Corticostriatal glutamate mechanisms underlying beta synchrony and motor deficits via striatal NMDA receptors in Parkinson’s disease
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DOI：10.1016/j.ebiom.2026.106418.png)
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Abstract
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Beta-band (13–30 Hz) oscillations in the cortico-basal ganglia-thalamic (CBT) network strongly correlate with motor deficits in Parkinson’s disease (PD), yet their synaptic origins remain unclear. Given that dopamine (DA) loss is necessary but not sufficient to produce sustained beta rhythms, we hypothesised that corticostriatal glutamatergic overdrive may function as a significant non-dopaminergic amplifier of pathological synchrony.
Keywords:
Parkinson’s disease
Corticostriatal circuit
Beta oscillations
NMDA receptors
Motor deficits
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