In MPTP mice, transcranial magneto-acoustic stimulation (TMAS) reduced presynaptic glutamate release, improved NMDAR- and D1 receptor–dependent corticostriatal synaptic transmission and plasticity, normalized spine subtype distribution, decreased α-synuclein and dopaminergic neuron loss, and…

The study links a noninvasive neuromodulation method to mechanistic readouts (glutamatergic signaling, NMDAR/D1 function, synaptic structure, and transcriptional programs) and shows neuroprotective effects in a PD model, supporting translation toward device-based therapies and pathway-focused…

Transcranial magneto-acoustic stimulation (TMAS) is a noninvasive neuromodulation technique that has demonstrated benefits for neuroplasticity in Parkinson's disease (PD), yet its underlying mechanisms remain inadequately understood. This study aimed to investigate how TMAS affects dysfunction and synaptic-plasticity impairments in the corticostriatal pathway in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. The results indicated that TMAS was associated with reduced presynaptic glutamate release and with improved N-methyl-D-aspartate receptor (NMDAR)-mediated responses. It also enhanced D1 dopamine receptor-dependent basal synaptic transmission and partially restored bidirectional corticostriatal synaptic plasticity. Furthermore, TMAS tended to normalize the distribution of spine subtypes, improve motor deficits, reduce dopaminergic neuron loss, and decrease aberrant α-synuclein expression. Transcriptomic and enrichment analyses further suggested a coordinated modulation of gene programs related to synaptic organization, ion homeostasis, and immune responses. These findings support TMAS as a promising noninvasive neuromodulation approach in the MPTP mouse model. TMAS attenuated excessive glutamatergic transmission and improved corticostriatal synaptic plasticity, providing a testable mechanistic framework for future studies.