Scholarlink

<p>Clinical studies suggest that Parkinson’s disease (PD) patients exhibit sensorimotor gating impairment, as manifested by deficits in prepulse inhibition (PPI). However, the underlying neural mechanisms remain elusive. Using the MPTP-induced PD mouse model, we demonstrated that substantia nigra pars compacta dopaminergic (SNc<sup>DA</sup>) neurons damage directly induces a reduction in PPI, whereas activation of these neurons reverses MPTP-induced PPI deficits. Viral tracing revealed an inferior colliculus (IC)-SNc<sup>DA</sup> circuit, whose bidirectional modulation mimics or rescues PPI impairment in MPTP male mice. Furthermore, the SNc<sup>DA</sup> neurons outputs from pedunculopontine nucleus (PPN) to reticulotegmental nucleus (RtTg) also involved in regulating MPTP-induced PPI deficits. This study identifies SNc<sup>DA</sup> neurons inputs and outputs as key modulators of PPI deficits in MPTP-treated male mice, thereby providing the circuit-level mechanism of sensorimotor gating impairment in early-stage PD.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The IC-SNc neural circuit mediates prepulse inhibition deficits in MPTP-induced Parkinson’s disease male mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月14日

查看全文
  • Xiang Peng,
  • Chi Cui,
  • Yulong Shi,
  • Tongxia Li,
  • Ming Li,
  • Xueke Yang,
  • Jie Lei,
  • Jian Yang,
  • Yibo Yao,
  • Gangan Luo,
  • Junsong Du,
  • Sitong Chen,
  • Huijuan Wang,
  • Hongchu Zha,
  • Shiqi Xu,
  • Pei Zhang,
  • Bo Tian

摘要

Clinical studies suggest that Parkinson’s disease (PD) patients exhibit sensorimotor gating impairment, as manifested by deficits in prepulse inhibition (PPI). However, the underlying neural mechanisms remain elusive. Using the MPTP-induced PD mouse model, we demonstrated that substantia nigra pars compacta dopaminergic (SNcDA) neurons damage directly induces a reduction in PPI, whereas activation of these neurons reverses MPTP-induced PPI deficits. Viral tracing revealed an inferior colliculus (IC)-SNcDA circuit, whose bidirectional modulation mimics or rescues PPI impairment in MPTP male mice. Furthermore, the SNcDA neurons outputs from pedunculopontine nucleus (PPN) to reticulotegmental nucleus (RtTg) also involved in regulating MPTP-induced PPI deficits. This study identifies SNcDA neurons inputs and outputs as key modulators of PPI deficits in MPTP-treated male mice, thereby providing the circuit-level mechanism of sensorimotor gating impairment in early-stage PD.