Tissue plasminogen activator is required for striatal post-ischemic synaptic potentiation

Diego Centonze, Emilia Saulle, Antonio Pisani, Paola Bonsi, Domenicantonio Tropepi, Giorgio Bernardi, Paolo Calabresi

Research output: Contribution to journalArticlepeer-review

Abstract

Recent experimental observations indicate that tPA plays a key role in the development of neuronal damage that follows cerebral ischemia and excitotoxicity. In an attempt to clarify how tPA favors ischemia-induced neuronal damage, we performed in vitro electrophysiological experiments in striatal slices by using mice selectively lacking this serine protease. We found that tPA ablation did not affect the membrane depolarization of striatal neurons exposed to combined oxygen and glucose deprivation but fully prevented the induction of NMDA-dependent post-ischemic long-term synaptic potentiation. The absence of striatal post-ischemic potentiation observed in tPA-lacking mice may account for the significant neuroprotection observed in these animals after the occlusion of middle cerebral artery.

Original languageEnglish
Pages (from-to)115-118
Number of pages4
JournalNeuroReport
Volume13
Issue number1
Publication statusPublished - Jan 21 2002

Keywords

  • Electrophysiology
  • Excitotoxicity
  • Neuroprotection
  • Plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

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