Meeting Abstract
Predators are traditionally thought to affect prey solely through direct killing, with the consequences of an attack dissipating shortly after a predator encounter. It is becoming clear that the ‘fear’ (the prospect of imminent, violent death i.e. perceived predation risk) of predators shapes prey ecology, in that the mere presence of a predator leaves lasting effects on physiology and reproduction. It is unknown whether or how predation risk alters avian neurobiology and whether there is a ‘fear network’ in the brain that processes predator cues. To investigate these changes, black-capped chickadees (Poecile atricapillus) were exposed to short-term auditory cues simulating levels of predation risk. We found that the expression of the immediate-early gene (IEG) ZENK was significantly greater in the nucleus taeniae of the amygdala (TnA), a brain region thought to be homologous to the mammalian medial amygdala, in response to playbacks simulating high predation risk (owl calls and chickadee high zee calls) compared to calls representing moderate risk (chickadee mobbing calls) and non-threatening controls (nuthatch calls) In the hippocampus (Hp), on the other hand, expression of ZENK was significantly greater for both conspecific alarm calls. This suggests that cues of predation risk may be processed in both of these areas, but that the TnA is more sensitive to level of risk, while the Hp is sensitive to social cues of threat. The expression of the short-term IEG c-fos will be investigated in the same brain regions in order to examine any differences in the expression of these two IEGs. On-going experiments are examining lasting changes in brain activation due to chronic predator stimuli using FosB, an IEG commonly used in small lab mammals, but never before used in birds.
