L-type voltage-gated calcium channels mediate NMDA-independent associativelong-term potentiation at thalamic input synapses to the amygdala

Long-term potentiation (LTP) in the amygdala is a leading candidate mechani sm to explain fear conditioning, a prominent model of emotional memory. LTP occurs in the pathway from the auditory thalamus to the lateral amygdala, and during fear conditioning LTP-like changes occur in the synapses of this pathway. Nevertheless, LTP has not been investigated in the thalamoamygdal a pathway using in vitro recordings; hence little is known about the underl ying mechanisms. We therefore examined thalamoamygdala LTP in vitro using v isualized whole-cell patch recording. LTP at these synapses was dependent o n postsynaptic calcium entry, similar to synaptic plasticity in other regio ns of the brain. However, unlike many forms of synaptic plasticity, thalamo amygdala LTP was independent of NMDA receptors, despite their presence at t hese synapses, and instead was dependent on L-type voltage-gated calcium ch annels. This was true when LTP was induced by pairing presynaptic activity with either action potentials or constant depolarization in the postsynapti c cell. In addition, the LTP was associative, in that it required concurren t pre- and postsynaptic activity, and it was synapse specific. Thus, althou gh this LTP is different from that described at other synapses in the brain , it is nonetheless well suited to mediate classical fear conditioning.