Neurobiological insights into PTSD: Impacts on spatial memory and neural circuits

Abstract

This study aimed to explore the implications of post-traumatic stress disorder (PTSD) on the action potential patterns and properties of neurons in the basolateral amygdala complex (BLA) and the ventral hippocampus (vHPC) among mice. The intent was to demystify the mechanisms driving the plasticity of neural networks within the BLA and vHPC, as well as the alterations in spatial contextual memory attributable to PTSD. A PTSD animal model was developed using the conventional foot shock (FS) paradigm. The investigation initially scrutinized spatial cognition and memory aptitudes through the Morris Water Maze (MWM) and later shed light on fluctuations in action potential encoding capacities of glutamatergic and GABAergic neurons within the BLA and vHPC, leveraging the patch clamp technique. The results unequivocally demonstrated that PTSD's core features - such as a surge in freezing percentages among mice - were both stable and enduring. PTSD discernibly extended the acquisition latency of mice, curtailed the duration required to locate the platform in the primary quadrant, and prolonged the time to identify the platform in the contralateral quadrant. The overall excitability and function of the BLA diminished, while that of the vHPC augmented. These discoveries propose that PTSD can obstruct the consolidation process of spatial contextual memory and impact the collective excitability of the BLA and vHPC. The properties of neurons within distinct brain sectors, in tandem with the disarray in the coordination mechanism between them, might be contributing to the compromised spatial contextual memory abilities seen with PTSD.