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248 EFFECTS OF STRESScortex will affect amygdala output, particularly after chronic stress, as outlinedbelow.Modulation of the AmygdalaBasal/Lateral Complex. The amygdala is under the regulatory control ofseveral systems that appear to exert a modulatory influence over this region andits response to stressors. In particular, the prefrontal cortex and the dopamine systemhave potent regulatory influences over the amygdala. Moreover, these afferentsystems also show complex interactions with each other. We have shown thatstimulation of sensory afferents, such as the auditory association cortex, will causea depolarization and activation of neurons in the basal/lateral amygdala nucleus(Rosenkranz & Grace, 1999; Rosenkranz & Grace, 2001). However, stimulationof the prefrontal cortex evokes a very different response. Thus, when the prefrontalcortex is stimulated electrically, we observe an inhibitory postsynaptic potential(IPSP). When the membrane potential of the pyramidal (output) neuron ishyperpolarized by current injection, the IPSP exhibits a reversal potential of approximately–68 mV; this is consistent with a reversal potential for a chloride ionmediatedconductance, such as those activated by GABA A -mediated synapses.Because the prefrontal cortical afferents to the amygdala are known to be glutamatergicand not GABAergic in nature, this response appears to be mediated byan interneuron within the amygdala that is activated by prefrontal cortical afferents.Indeed, we have shown that stimulation of the prefrontal cortical input tothe amygdala will preferentially activate interneurons within this structure, whereassensory cortical input will preferentially activate the pyramidal neurons (Rosenkranz& Grace, 2001; Rosenkranz & Grace, 2002a). Moreover, it is clear fromthe analysis of latencies that the evoked IPSP is due to prefrontal cortical excitationof interneurons (Rosenkranz & Grace, 2002a), and not antidromic activationof amygdalofugal neurons and activation of interneurons by local collaterals, asproposed by others (Likhtik et al., 2005).The ability of the prefrontal cortex to activate interneurons has important functionalconsequences. Thus, stimulation of the auditory association cortex is capableof evoking action potentials within the lateral amygdala nucleus. However,if the prefrontal cortex is stimulated first, the resultant IPSP will block activationproduced by auditory association cortex stimulation. This blockade will take placeonly if the interval after prefrontal cortical stimulation is brief (i.e., about 50 msor less). Therefore, this is a type of event-related attenuation. We have proposedthat this type of attenuation has important implications for prefrontal regulationof emotional responses. We believe that, via activation of interneurons, the prefrontalcortex has the capacity to attenuate responses to inappropriate stimuli. Forexample, a higher-level sensory input (e.g., the sound of a dog barking) may typicallyevoke a fear response via activation of the amygdala. However, if the bark-