Subarachnoid hemorrhage in C57BL/6J mice increases motor stereotypies and compulsive-like behaviors. (4th March 2021)

• Record Type: Journal Article
• Authors: Nanegrungsunk, Danop; Ragozzino, Michael E.; Xu, Hao-Liang; Haselton, Kyle J.; Paisansathan, Chanannait
• Is Part Of: Neurological research. Volume 43:Number 3(2021)
• Page Start: 239
• Page End: 251
• Publication Date: 2021-03-04
• Subjects: Subarachnoid hemorrhage -- neurobehavioral tests -- stereotyped motor behavior -- compulsive-like behavior -- repetitive behavior -- mice; Neurology -- Periodicals; Neurosciences -- Periodicals; 616.8005
• DOI: 10.1080/01616412.2020.1841481
• Languages: English
• ISSNs: 0161-6412

Abstract

ABSTRACT: Objective: Long-term behavioral, mood, and cognitive deficits affect over 30% of patients with subarachnoid hemorrhage (SAH). The aim of the present study was to examine the neurobehavioral outcomes following endovascular perforation induced SAH in mice. Methods: C57BL/6 J (B6) mice were exposed to endovascular perforation induced SAH or control surgery. Three weeks later, mice received a series of behavioral tests, e.g. motor function, stereotypy, learning, memory, behavioral flexibility, depression and anxiety. The immunohistologic experiment examined neuronalloss in the cortex following SAH. Results: SAH mice exhibited increased marble burying and nestlet shredding compared to that of control mice. Although SAH did not affect memory, learning or reversal learning, mice displayed greater overall object exploration in the novel object recognition test, as well as elevated perseveration during probabilistic reversal learning.In the forced swim and open field tests, SAH mice performed comparably to that of control mice. However, SAH mice exhibited an increased frequency in 'jumping' behavior in the open field test. Histological analyses revealed reduced neuron density in the parietal-entorhinal cortices of SAH mice on the injured side compared to that of control mice. Discussion: The findings suggest that parietal-entorhinal damage from SAH increases stereotyped motor behaviors and 'compulsive-like' behaviors without affecting cognition (learning and memory) or mood (anxiety and depression). This model can be used to better understand the neuropathophysiology following SAH that contributes to behavioral impairments in survivors with no gross sensory-motor deficits.