Long-term depression of excitatory synaptic transmission in the rat amygdala

In view of the fact that both kindling and fear-potentiated startle are expressed by long-term enhancement of synaptic transmission in the amygdala, synaptic plasticity in this area of the brain is of particular importance. Here, we show for the first time that low-frequency stimulation of the lateral nucleus at 1 Hz for 15 min elicited a long-term depression (LTD) in the basolateral amygdala (BLA) neurons. LTD is expressed specifically at the lateral-BLA synapses but not at ventral endopyriform nucleus-BLA synapses. The induction of LTD requires activation of both NMDA and metabotropic glutamate receptors. Loading cells with a Ca2+ chelator BAPTA or extracellular superfusion with protein phosphatase inhibitors prevents LTD, suggesting that LTD may result from dephosphorylation of AMPA receptors. The same stimulating protocol could not elicit LTD in neurons from kindled animals, whereas neurons from sham-operated or age-matched control rats were able to exhibit LTD. Together, this study characterizes the properties of LTD in the naive amygdala slices for the first time and demonstrates that epileptogenesis in vivo induces disruption of LTD in the in vitro preparation.