A role of insulin-like growth factor 1 in β amyloid-induced disinhibition of hippocampal neurons

In the present study we investigated the effects of β amyloid (Aβ) on inhibitory synaptic transmission in the cultured hippocampal neurons using whole-cell patch-clamp recordings and immunocytochemistry, and examined the role of insulin-like growth factor 1 (IGF-1). Incubation with 4 μM Aβ25-35 for 24 h significantly decreased the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), but had no effect on the mean amplitude. Pretreatment with 10 ng/ml IGF-1 for 24 h prior to Aβ25-35 exposure blocked Aβ-induced disinhibition of hippocampal neurons. The frequency and mean amplitude of miniature IPSC (mIPSCs) were not significantly affected by Aβ. The rise and decay kinetics of sIPSCs and mIPSCs were similar for the control and Aβ25-35-treated hippocampal neurons. Immunocytochemistry showed no changes in the ratio of γ-aminobutyric acid (GABA) positive cells subsequent to treatment with Aβ, or IGF-1. Together these data suggest that Aβ-induced the disinhibition in cultured hippocampal neurons, whereas IGF-1 could block this effect.