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252 EFFECTS OF STRESS2000). It is also likely that the amygdala plays a role in how an organism respondsto maintained, chronic stressors. We examined this effect using chronic cold exposure(Zigmond et al., 1995), a well-characterized stress paradigm that has beenemployed at the University of Pittsburgh for over 25 years. In this paradigm, ratsare exposed to a cold environment for a prolonged period of time (i.e., 5°C for 14days) and then are subjected to study 24 hours following removal from the cold.Overall, this is a rather mild stressor, in that indices of stress return to baselinelevels within 24–72 hours after initiation of cold exposure and do not produce asmany external signs of a stress as those elicited by other procedures such as inescapableshock (see Moore et al., 2001b). Nonetheless, the rats show a sensitizedresponse to acute stressors when tested a day or more following the cold exposure(Zigmond et al., 1995). We examined the effects of this chronic stress exposureparadigm on neuronal activity and response to acute noxious stimuli withinthe amygdala complex.Recordings performed from the basolateral amygdala reveal that followingchronic stress exposure, there is a small but nonsignificant increase in baselinespike discharge rate. Nonetheless, if a count is made regarding the proportion ofneurons showing spontaneous activity (i.e., cells/track, as first defined by Bunney& Grace, 1978), an increase in the number of spontaneously active basolateralamygdala neurons is observed. However, the most significant change is the responseof basolateral amygdala neurons to acute noxious stimuli. Thus, a footshocktypically causes a small activation of neuronal firing within this brain region incontrol rats. However, following chronic stress exposure, the same amplitude offootshock evokes a powerful excitatory response in these neurons. Therefore,chronic cold stress causes an increase in baseline population activity and responsivityof neurons in the basolateral amygdala complex.The basolateral amygdala also exerts modulatory control over the centralamygdala, as described above. Given that the central amygdala, and the medialportion of the central amygdala in particular, is considered to be the output regionof this nucleus with respect to the regulation of autonomic structures (Veeninget al., 1984), we examined how neurons in the central medial amygdala are affectedby chronic stress. We found that chronic stress alters the baseline activityand responsivity of the neurons in the central medial amygdala as well. Followingchronic stress, there was a significant decrease in both the baseline firing rate(by 56%) and the population activity of neurons within the medial central nucleus(Correll et al., 2005). This was opposite of what was observed in the basolateralarea, but consistent with our observed reciprocal relationship between these structures.This was not the case with the response to footshock, however. In controlrats, a footshock causes only a minimal change in central amygdala neuron firingrate; moreover, this response accommodates after only a few exposures. However,following chronic stress, the same amplitude of footshock produces a dramaticactivation of the central medial nucleus. Moreover, there is an absence of