Hippocampal function following trauma

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Post-traumatic stress disorder (PTSD) is a debilitating disorder that can manifest after a traumatic experience. Of the people that experience a trauma, around 20% develops PTSD, while the remainder recovers adequately. Little is known about the underlying mechanisms of this differential susceptibility. Aberrant hippocampal function is an often-replicated observation in PTSD patients and has been suggested to underlie trauma memory overgeneralization. Human patient studies lack spatial specificity to determine the contribution of hippocampal subregions – known for distinct memory functions – in this, let alone specific neuronal subpopulations. It is currently unclear how abnormal activity and morphology of the hippocampus relate to the trauma memory itself; are specifically neurons affected that represent the trauma memory engram? We investigated this using an animal model for PTSD (implementing severe foot shocks), distinguishing resilient and susceptible animals. To assess ongoing hippocampal neuronal activity, targeted recombination in active population transgenic mice were injected with tamoxifen post-trauma (under basal conditions). To assess the trauma memory engram, animals were re-exposed to the trauma context before perfusion and recall-induced neuronal activity was assessed by c-Fos immunohistochemistry. A neuronal marker for somatostatin was added to determine contribution of this inhibitory interneuron population. Tonic hippocampal activity was compared between resilient, susceptible and control animals. Trauma-exposed animals showed higher activity under basal conditions in the dorsal CA1. Additionally, neuronal morphology was assessed using a Golgi-staining. Our data indicate more excitatory input from the entorhinal cortex, amygdala and prefrontal cortex into the stratum lacunosum-moleculare in both dorsal and ventral (trend) CA1 of PTSD-susceptible animals.
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