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

To determine which type of receptors and/or channels are involved in the presynaptic mechanism of action, a specific blocker of alpha-7 nicotinic receptors (methyllycaconitine citrate) or L-type calcium channel blockers (calcicludine or nifedipine) were used. β-amyloid petide25-35 decreased excitatory postsynaptic potentials amplitude in control conditions and also in slices permanently perfused with methyllycaconitine citrate. However, this effect was blocked in slices perfused with calcicludine or nifedipine suggesting the involvement of the L-type calcium channels. On the whole, these experiments provide evidence that β-amyloid peptide25-35 affects neurotransmission in basolateral amygdala and its action is mediated through L-type calcium channels.