Auditory fear conditioning is likely mediated by plastic changes in two inputs entering the lateral amygdala (LA), one from the auditory thalamus and the other from auditory cortex.These inputs enter LA via internal and external capsule respectively.However, the specific roles of these inputs are still debated.Attempts have been made using anatomic lesions to disclose their roles in fear conditioning, which, unexpectedly, leads to contradictory conclusions.As an alternative and novel strategy to anatomic lesions, we here employed conditional mutation of Rapl, a small GTPase, which has been recently shown to be involved in AMPA receptor trafficking and long-term potentiation (LTP) of synaptic transmission in hippocampus as well as spatial learning by genetically ablating rap 1 a/1 b genes in mice using a Cre-recombinase under the control of CaMKⅡα promoter.We found that conditional inactivation of rap 1 genes selectively altered synaptic transmission in the cortical but not thalamic inputs by increasing the number of quanta released by a single presynaptic action potential by about three folds, raising presynaptic glutamate release probability and disrupting presynaptically expressed long-term potentiation (LTP).These alterations were accompanied by impaired fear learning and reduced anxiety-like behaviors, suggesting that modulation of synaptic transmission from cortex to LA only is sufficient to affect innate and leamed fear.