Glutamate-induced excitotoxicity in Parkinson's disease: The role of glial cells

L. Iovino, M. E. Tremblay, L. Civiero

Research output: Contribution to journalReview articlepeer-review


Glutamate is the major excitatory neurotransmitter in the central nervous system. Glutamate transmission efficiency depends on the correct functionality and expression of a plethora of receptors and transporters, located both on neurons and glial cells. Of note, glutamate reuptake by dedicated transporters prevents its accumulation at the synapse as well as non-physiological spillover. Indeed, extracellular glutamate increase causes aberrant synaptic signaling leading to neuronal excitotoxicity and death. Moreover, extrasynaptic glutamate diffusion is strongly associated with glia reaction and neuroinflammation. Glutamate-induced excitotoxicity is mainly linked to an impaired ability of glial cells to reuptake and respond to glutamate, then this is considered a common hallmark in many neurodegenerative diseases, including Parkinson's disease (PD). In this review, we discuss the function of astrocytes and microglia in glutamate homeostasis, focusing on how glial dysfunction causes glutamate-induced excitotoxicity leading to neurodegeneration in PD.

Original languageEnglish
Pages (from-to)151-164
Number of pages14
JournalJournal of Pharmacological Sciences
Issue number3
Publication statusPublished - Nov 2020


  • Astrocytes
  • Glutamate-induced excitotoxicity
  • Inflammation
  • Microglia
  • Parkinson's disease

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology


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