Abstract
The hippocampus has been implicated in anxiety disorders and post-traumatic stress disorder (PTSD); human studies suggest that a dysfunctional hippocampus may be a vulnerability factor for the development of PTSD. In the current study, we examined the effect of hippocampal damage in avoidance learning, as avoidance is a core symptom of all anxiety disorders. First, the effect of hippocampal damage on avoidance learning was investigated in outbred Sprague Dawley (SD) rats. Second, the function of the hippocampus in Wistar-Kyoto (WKY) rats was compared to SD rats. The WKY rat is an animal model of behavioral inhibition, a risk factor for anxiety, and demonstrates abnormal avoidance learning, marked by facilitated avoidance acquisition and resistance to extinction. The results of the current study indicate that hippocampal damage in SD rats leads to impaired extinction of avoidance learning similar to WKY rats. Furthermore, WKY rats have reduced hippocampal volume and impaired hippocampal synaptic plasticity as compared to SD rats. These results suggest that hippocampal dysfunction enhances the development of persistent avoidance responding and, thus, may confer vulnerability to the development of anxiety disorders and PTSD.
Highlights
The development of post-traumatic stress disorder (PTSD) and anxiety disorders is a function of an individual’s experience and inherent vulnerability
Acquisition of avoidance in WKY rats did not differ from Sprague Dawley (SD) rats (Figure 2B)
Comparisons made between sham and lesions and between unoperated SD and WKY rats for first minute intertrial interval (ITI) responses revealed that hippocampal but not entorhinal lesions facilitated responding [main effect, F (1,13) = 8.32, p = 0.013], and strain differences trended toward significance with WKY tending to make more ITI responses than SD rats [session × strain interaction, F (11,154) = 2.42, corrected p = 0.051]
Summary
The development of post-traumatic stress disorder (PTSD) and anxiety disorders is a function of an individual’s experience and inherent vulnerability. Comparisons made between sham and lesions and between unoperated SD and WKY rats for first minute ITI responses revealed that hippocampal but not entorhinal lesions facilitated responding [main effect, F (1,13) = 8.32, p = 0.013], and strain differences trended toward significance with WKY tending to make more ITI responses than SD rats [session × strain interaction, F (11,154) = 2.42, corrected p = 0.051]. Hippocampal lesion and WKY rats were impaired in extinction of avoidance responding (Figures 2A,B).
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