Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.

Hongseong Shin; Yoon Ji Kwon; Hyunjung Hwang; Taewoo Ko; Eun Bi Choi; Yang Tae Kim; Yu Mi Han; Jae Geun Kim; Qiang Zhou; Sungchil Yang; Sunggu Yang

doi:10.3390/ijms27177564

PubMed · 42737467

Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.

Hongseong Shin·Yoon Ji Kwon·Hyunjung Hwang·Taewoo Ko·Eun Bi Choi·Yang Tae Kim·Yu Mi Han·Jae Geun Kim·Qiang Zhou·Sungchil Yang·Sunggu Yang

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Abstract

Parkinson's disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory-inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input-output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR1/5)-dependent long-term depression (LTD) was abolished in the ipsilateral PD hemisphere, whereas NMDAR-dependent LTD remained intact. In summary, dopamine depletion appears to enhance network excitation and disrupt mGluR1/5-mediated control of M1 surface circuitry. Our findings identify altered cortical surface mGluR-dependent plasticity in the hemi-parkinsonian model; however, the relationship between these electrophysiological alterations and individual motor outcomes remains to be determined.

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Animals Receptors, Metabotropic Glutamate Motor Cortex Rats Neuronal Plasticity Parkinson Disease Disease Models, Animal Receptor, Metabotropic Glutamate 5 Oxidopamine Excitatory Postsynaptic Potentials Male Receptors, AMPA Rats, Sprague-Dawley Parkinson’s disease metabotropic glutamate receptor motor cortex sensorimotor deficits synaptic plasticity Journal Article

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Hongseong Shin, Yoon Ji Kwon, Hyunjung Hwang, Taewoo Ko, Eun Bi Choi, Yang Tae Kim, Yu Mi Han, Jae Geun Kim, Qiang Zhou, Sungchil Yang, Sunggu Yang. 2026-08-24. Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.. https://doi.org/10.3390/ijms27177564

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