Abstract
Much evidence indicates that fear conditioning involves potentiation of some thalamic inputs to the lateral amygdala (LA). In turn, the LA would excite more neurons in the central nucleus (CE), leading to the generation of fear responses via their brainstem and hypothalamic projections. However, the posterior thalamus not only projects to LA but also to the medial sector of CE (CEm), suggesting that CEm might also be a site of plasticity. To test whether CEm also exhibits activity-dependent synaptic plasticity, we performed whole-cell recordings of CEm neurons in amygdala slices and stimulated thalamic axons coursing through the internal capsule and, as a control, the basolateral (BL) nucleus. High-frequency stimulation of thalamic inputs led to a long-lasting potentiation of thalamic responses, whereas BL-evoked responses remained unchanged. This thalamic long-term potentiation (LTP) developed even when slices were prepared with a cut severing the connections between the LA and CEm but was greatly reduced when an NMDA receptor antagonist was added to the perfusate shortly before and during LTP induction. Yet, intracellular dialysis with the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate did not prevent induction of the thalamic LTP, suggesting that presynaptic NMDA receptors are required for its induction. Consistent with this, the thalamic LTP also developed when the cells were dialyzed with a calcium chelator or kept hyperpolarized during induction. Finally, this thalamic LTP was associated with reduced amounts of paired-pulse facilitation, suggesting that it is expressed presynaptically. These results are consistent with the idea that the CEm plays an active role in fear conditioning.