Bidirectional modulation of synaptic transmission by insulin-like growth factor-I.

ABSTRACT: Insulin-like growth factor-I (IGF-I) plays a key role in the modulation of synaptic plasticity and is an essential factor in learning and memory processes. However, during aging, IGF-I levels are decreased, and the effect of this decrease in the induction of synaptic plasticity remains unknown. Here we show that the induction of N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) at layer 2/3 pyramidal neurons (PNs) of the mouse barrel cortex is favored or prevented by IGF-I (10 nM) or IGF-I (7 nM), respectively, when IGF-I is applied 1 h before the induction of Hebbian LTP. Analyzing the cellular basis of this bidirectional control of synaptic plasticity, we observed that while 10 nM IGF-I generates LTP (LTP_IGF-I) of the post-synaptic potentials (PSPs)

SUBMITTER: Noriega-Prieto JA 

PROVIDER: S-EPMC11193368 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature