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Synaptic plasticity in the ischaemic brain
Paolo Calabresi1, Diego Centonze, Antonio Pisani
1Clinica Neurologica, Dipartimento di Neuroscienze, Università Tor Vergata and the IRCCS Fondazione Santa Lucia, Rome, Italy. calabre@uniroma2.it
The Lancet. Neurology
|September 25, 2003
Summary
Energy deprivation can induce long-term potentiation (LTP), a form of synaptic plasticity, which may contribute to brain damage after ischaemia. This review explores pathological and protective plasticity following brain energy loss.
Area of Science:
- Neuroscience
- Cellular and Molecular Biology
- Pathophysiology
Background:
- Activity-dependent long-term potentiation (LTP) is crucial for learning and memory.
- Energy deprivation in the brain can induce LTP, potentially linking synaptic plasticity to delayed ischaemic effects.
Purpose of the Study:
- To review and compare LTP induced by energy deprivation with physiological LTP.
- To explore the role of pathological and protective neuronal plasticity in brain ischaemia and recovery.
Main Methods:
- Literature review of recent studies on LTP and brain ischaemia.
- Analysis of similarities and differences between physiological and deprivation-induced LTP.
- Examination of evidence for plasticity's role in neuronal death and recovery.
Main Results:
- Energy deprivation can induce pathological LTP, contributing to neuronal death in the hippocampus and striatum after global ischaemia.
- Pathological plasticity may drive the conversion of the ischaemic penumbra to infarct core in focal ischaemia.
- Ischaemia can also trigger protective and reparative neuronal plasticity, potentially conferring ischaemic tolerance and aiding post-stroke recovery.
Conclusions:
- Pathological plasticity induced by energy deprivation is implicated in delayed neuronal death and infarct expansion after ischaemia.
- Protective and reparative plasticity mechanisms offer potential targets for enhancing ischaemic tolerance and post-stroke recovery.