β-Amyloid peptide25–35 depresses excitatory synaptic transmission in the rat basolateral amygdala “in vitro”

The effects of β-amyloid peptide25–35 on resting membrane potential, spontaneous and evoked action potential and synaptic activity have been studied in basolateral amygdaloid complex on slices obtained from adult rats. Intracellular recordings reveal that perfusion with β-amyloid peptide25–35 at concentrations of 400 nM and less did not generate any effect on resting membrane potential. However, concentrations in the range of 800–1200 nM produced an unpredictable effect, depolarization and/or hyperpolarization, which were blocked by tetrodotoxin or 6-cyano-7-nitroquinoxaline-2,3-dione + D-(−)-2-amino-5-phosphonopentanoic acid together with bicuculline. Excitatory and inhibitory evoked responses mediated by glutamic acid or γ-aminobutyric acid decreased in amplitude after β-amyloid peptide25–35 perfusion. Additionally, results obtained using the paired-pulse protocol offer support for a presynaptic mode of action.