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摘要Maintaining GABAergic inhibition in the amygdala within a physiological range is critical for the appropriate expression of emotions,such as fear and anxiety.The synaptic GABAA receptor(GABAAR)is generally known to mediate the primary component of amygdala inhibition and prevent inappropriate expression of fear.However,little is known about the contribution of the extrasynapticGABAAR to amygdala inhibition and fear.By using mice expressing GFP in the interneurons(INs)and lacking δ subunit-containing GABAAR(GABAA(δ)R),which is exclusively situated in extrasynaptic membrane,we systematically investigated the role of GABAA(δ)R in regulating inhibition in the lateral amygdala(LA)and fear learning by using the combined approaches of immunohistochemistry,electrophysiology and behavior.In sharp contrast to the established role of synaptic GABAAR in mediating LA inhibition,we found that either pharmacological or physiological recruitment of GABAA(δ)R resulted in the weakening of GABAergic transmission onto projection neurons in the LA while leaving the glutamatergic transmission unaltered,suggesting disinhibition by GABAA(δ)R.The disinhibition arose from INspecific expression of GABAA(δ)R,with its activation decreasing the input resistance of local INs and suppressing their activation.Genetic deletion of GABAA(δ)R attenuated its role in suppressing LA INs and disinhibiting the LA.Importantly,the GABAA(δ)R facilitated LTP in sensory afferents to the LA and permitted the expression of learned fear.Our findings suggest that GABAA(δ)R serves as a brake rather than a mediator of GABAergic inhibition in LA.The disinhibition by GABAA(δ)R may help to prevent excessive suppression of amygdala activity and thus ensure the expression of emotion.