[Neuronal cytokine involvement in synaptic plasticity].

Abstract

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.