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 beta amyloid (A beta) 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 mu M A beta 25-35 for 24 It 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 A beta 25-35 exposure blocked A beta-induced disinhibition of hippocampal neurons. The frequency and mean amplitude of miniature IPSC (mIPSCs) were not significantly affected by A beta. The rise and decay kinetics of sIPSCs and mIPSCs were similar for the control and A beta 25-35-treated hippocampal neurons. Immunocytochemistry showed no changes in the ratio of gamma-aminobutyric acid (GABA) positive cells subsequent to treatment with A beta, or IGF-1. Together these data suggest that A beta-induced the disinhibition in cultured hippocampal neurons, whereas IGF-1 could block this effect. (c) 2005 Elsevier Ireland Ltd. All rights reserved.