Activity-dependent long-term potentiation (LTP) of excitatory neurotransmission underlies specific forms of associative learning and memory. A brief period of energy deprivation induces LTP in specific subsets of neurons; this synaptic plasticity might contribute to the delayed effects of brain ischaemia. In this review, we discuss the similarities and differences between LTP induced by energy deprivation and "physiological" LTP. On the basis of recent studies, we propose that pathological plasticity induced by energy deprivation can play a part in delayed neuronal death in the hippocampus and the striatum after global ischaemia and in the conversion of ischaemic penumbra to infarct core after focal ischaemia. We discuss evidence that ischaemia could also induce protective and reparative forms of neuronal plasticity that may play a part in ischaemic tolerance and poststroke recovery.
Synaptic plasticity in the ischaemic brain
PISANI, ANTONIO;
2003-01-01
Abstract
Activity-dependent long-term potentiation (LTP) of excitatory neurotransmission underlies specific forms of associative learning and memory. A brief period of energy deprivation induces LTP in specific subsets of neurons; this synaptic plasticity might contribute to the delayed effects of brain ischaemia. In this review, we discuss the similarities and differences between LTP induced by energy deprivation and "physiological" LTP. On the basis of recent studies, we propose that pathological plasticity induced by energy deprivation can play a part in delayed neuronal death in the hippocampus and the striatum after global ischaemia and in the conversion of ischaemic penumbra to infarct core after focal ischaemia. We discuss evidence that ischaemia could also induce protective and reparative forms of neuronal plasticity that may play a part in ischaemic tolerance and poststroke recovery.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
