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Published on: March 31, 2015
mPFC hemorrhage induces hippocampal CA1 dendritic spine plasticity and attentional deficits in mice
Zahra Akhoond-Ali1,2, Hamed Ghazavi1,2, Mahmoud Hosseini3
1Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, I.R. Iran.
Background And Purpose:
Damage to a specific brain region, in addition to its local effects, can influence brain function by inducing neuroplasticity in remote areas. This study hypothesized that hemorrhage of the medial prefrontal cortex (mPFC) is associated with deficits in shifting attention through structural alterations in the hippocampal CA1 region, an area with known functional connections to the mPFC.
Experimental Approach:
C57BL/6 mice were subjected to intracerebral hemorrhage (ICH) or sham surgery. Neurological function was assessed using the neurological deficit score (NDS) on different days after injury, and cognitive flexibility was evaluated using the attentional set shifting task (AST) over a 17-day protocol. Structural changes were examined by assessing white matter and dendritic spine density using Luxol fast blue (LFB) and Golgi staining techniques on brain tissue. Statistical analysis was performed with SPSS-26.
Findings/Results:
No significant difference was observed in NDS between the groups. Mice with ICH demonstrated a lower task completion rate, along with an increased number of trials and set-loss errors in the AST. Dendritic spine density in the CA1 region was higher in the ICH group compared to the sham group, particularly in the right hemisphere, but no significant changes were noted in the white matter.
Conclusion And Implications:
The observed results following mPFC injury indicated an association between cortical damage, hippocampal plasticity, and cognitive dysfunction, consequently identifying hippocampal plasticity as a potential target for future therapeutic strategies aimed at improving post-stroke cognitive recovery.
Insights
Medial prefrontal cortex (mPFC) hemorrhage in mice impaired cognitive flexibility and increased hippocampal CA1 dendritic spine density. This suggests hippocampal plasticity changes may underlie attention deficits after brain injury.
Area of Science:
- Neuroscience
- Cognitive Neuroscience
- Neuroplasticity
Background:
- Brain damage can induce neuroplasticity in remote areas, affecting overall brain function.
- The medial prefrontal cortex (mPFC) plays a crucial role in attention and cognitive control.
Purpose of the Study:
- To investigate the association between medial prefrontal cortex (mPFC) hemorrhage and cognitive flexibility deficits.
- To examine structural alterations in the hippocampal CA1 region following mPFC injury.
Main Methods:
- C57BL/6 mice underwent intracerebral hemorrhage (ICH) or sham surgery.
- Cognitive flexibility was assessed using the attentional set shifting task (AST).
- Structural changes in white matter and dendritic spine density were analyzed.
Main Results:
- ICH mice showed impaired performance on the AST, with more trials and errors.
- Increased dendritic spine density was observed in the hippocampal CA1 region of ICH mice, particularly in the right hemisphere.
- No significant changes in white matter were detected.
Conclusions:
- mPFC injury is linked to hippocampal plasticity changes and cognitive dysfunction.
- Hippocampal plasticity alterations may contribute to attention deficits after stroke.
- Targeting hippocampal plasticity could be a therapeutic strategy for post-stroke cognitive recovery.
