Abstract
The basolateral amygdala (BLA) plays a key role in fear-related learning and memory, in the modulation of cognitive functions, and in the overall regulation of emotional behavior. Pathophysiological alterations involving hyperexcitability in this brain region underlie anxiety and other emotional disorders as well as some forms of epilepsy. GABAergic interneurons exert a tight inhibitory control over the BLA network; understanding the mechanisms that regulate their activity is necessary for understanding physiological and disordered BLA functions. The BLA receives dense cholinergic input from the basal forebrain, affecting both normal functions and dysfunctions of the amygdala, but the mechanisms involved in the cholinergic regulation of inhibitory activity in the BLA are unclear. Using whole cell recordings in rat amygdala slices, here we demonstrate that the α(7)-containing nicotinic acetylcholine receptors (α(7)-nAChRs) are present on somatic or somatodendritic regions of BLA interneurons. These receptors are active in the basal state enhancing GABAergic inhibition, and their further, exogenous activation produces a transient but dramatic increase of spontaneous inhibitory postsynaptic currents in principal BLA neurons. In the absence of AMPA/kainate receptor antagonists, activation of α(7)-nAChRs in the BLA network increases both GABAergic and glutamatergic spontaneous currents in BLA principal cells, but the inhibitory currents are enhanced significantly more than the excitatory currents, reducing overall excitability. The anxiolytic effects of nicotine as well as the role of the α(7)-nAChRs in seizure activity involving the amygdala and in mental illnesses, such as schizophrenia and Alzheimer's disease, may be better understood in light of the present findings.