[Neuronal cytokine involvement in synaptic plasticity].
Hippocampal long-term potentiation (LTP) is one of the best-studied models of learning and memory at the molecular level. In the hippocampal CA1 region, at least three different LTPs were reported: early phase LTP (E-LTP), late phase LTP (L-LTP) and anoxic LTP (A-LTP). E-LTP is induced by the activation of postsynaptically silent synapses. Unlike the E-LTP, L-LTP is dependent on protein synthesis and may be due to an increase in the number of sites of synapse. Unlike the E- and L-LTP, A-LTP is induced by presynaptic K+ channel modulations and is a crucial trigger for neuronal cell death. Interleukin-1 beta (IL-1 beta), which is produced under the anoxic conditions, plays an important role in A-LTP induction, and brain-derived neurotrophic factor (BDNF) plays a crucial role in L-LTP induction. IL-1 beta antagonist and or BDNF improve the cerebral anoxia-induced inhibition of E-LTP. These results suggested that the new synaptic sites, products of the BDNF induced L-LTP, will play an important role in synaptic plasticity (ex. E-LTP) instead of the synaptic sites of death neurons (induced by A-LTP). The neuronal cytokine system regulates these LTP expressions co-operatively and may play a crucial role to keep the brain system in the steady-state condition.
Takagi
H
H
Department of Neuroplasticity, Shinshu University School of Medicine, Nagano, Japan.
D000818:Animals; D016923:Cell Death; D016207:Cytokines / Q000502:physiology*; D006624:Hippocampus / Q000502:physiology; D006801:Humans; D017774:Long-Term Potentiation; D008568:Memory / Q000502:physiology*; D008960:Models, Psychological; D009473:Neuronal Plasticity; D013569:Synapses / Q000502:physiology*
D016207:Cytokines