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Related Experiment Videos

Tissue plasminogen activator controls multiple forms of synaptic plasticity and memory.

P Calabresi1, M Napolitano, D Centonze

  • 1Clinica Neurologica, Dip. Neuroscienze, Università di Tor Vergata, Via di Tor Vergata 135, Rome 00133, Italy. calabre@uniroma2.it

The European Journal of Neuroscience
|April 13, 2000
PubMed
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Tissue-plasminogen activator (t-PA) is crucial for synaptic plasticity and memory. Mice lacking t-PA show deficits in long-term depression, long-term potentiation, and learning behaviors.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Synaptic plasticity, the ability of synapses to strengthen or weaken over time, is crucial for learning and memory.
  • Tissue-plasminogen activator (t-PA) is an enzyme involved in the breakdown of blood clots, but its role in synaptic plasticity is less understood.

Purpose of the Study:

  • To investigate the role of t-PA in synaptic plasticity, specifically long-term depression (LTD) in the striatum.
  • To examine the impact of t-PA gene disruption on synaptic plasticity in the hippocampus and striatum.
  • To assess the behavioral consequences of t-PA deficiency on learning and memory.

Main Methods:

  • Used mRNA differential display to detect changes in gene expression during LTD induction.
  • Recorded electrophysiological activity from striatal and hippocampal slices of wild-type (WT) and t-PA knockout (t-PA-KO) mice.

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  • Assessed learning and memory using behavioral tests including context conditioning, two-way active avoidance, and object exploration.

    • Main Results:

    • LTD induction in WT mice was associated with increased t-PA mRNA expression.
    • t-PA-KO mice exhibited absent LTD in a significant proportion of striatal neurons.
    • t-PA-KO mice showed reduced late-phase long-term potentiation (LTP) in the hippocampus.
    • t-PA-KO mice displayed deficits in hippocampus-dependent and striatum-dependent learning and memory tasks.
    • Behavioral abnormalities in t-PA-KO mice suggest altered hippocampal and striatal function.

    Conclusions:

    • t-PA plays a critical role in the formation of synaptic plasticity, including LTD and LTP.
    • t-PA is essential for normal learning and memory processes.
    • Disruption of the t-PA gene leads to widespread deficits in cognitive functions mediated by both the hippocampus and striatum.