Abstract
Ischemic strokes cause devastating brain damage and functional deficits with few treatments available. Previous studies have shown that the ischemia-hypoxia rapidly induces clinically similar thrombosis and neuronal loss, but any resulting behavioral changes are largely unknown. The goal of this study was to evaluate motor and cognitive deficits in adult HI mice. Following a previously established procedure, HI mouse models were induced by first ligating the right common carotid artery and followed by hypoxia. Histological data showed significant long-term neuronal losses and reactive glial cells in the ipsilateral striatum and hippocampus of the HI mice. Whereas the open field test and the rotarod test could not reliably distinguish between the sham and HI mice, in the tapered beam and wire-hanging tests, the HI mice showed short-term and long-term deficits, as evidenced by the increased number of foot faults and decreased hanging time respectively. In cognitive tests, the HI mice swam longer distances and needed more time to find the platform in the Morris water maze test and showed shorter freezing time in fear contextual tests after fear training. In conclusion, this study demonstrates that adult HI mice have motor and cognitive deficits and could be useful models for preclinical stroke research.
Highlights
Ischemic strokes cause devastating brain damage and functional deficits with few treatments available
(12- to 14-weeks old) were subjected to permanent ligation of the right common carotid arteries (RCCA) and underwent 40-min hypoxia as previously r eported8. 36 mice survived the procedure with a 60.0% survival rate consistent with a previous report8. 25 mice were used as sham control
We found obvious Fluoro‐Jade B (FJB)+ cells scattered in the ipsilateral striatum, CA1 and CA3 pyramidal layers, and DG hilus area (Fig. 2F), showing neuronal degeneration at an early stage after ischemia and hypoxia, which is similar to the previous report[8]
Summary
Ischemic strokes cause devastating brain damage and functional deficits with few treatments available. Previous studies have shown that the ischemia-hypoxia rapidly induces clinically similar thrombosis and neuronal loss, but any resulting behavioral changes are largely unknown. Most recent studies of the adult HI model are limited to the short-term neuropathology and molecular m echanisms[8], but long-term pathology and behavioral deficits remain largely unknown. To answer these questions, we first used FJB staining[16,21] to confirm the early stage of neuron degeneration, and used immunostaining to examine the long-term neuronal loss (NeuN+), dendrite damage ( MAP2+)[17] and reactive glial cells (GFAP+ or IBA1+)[15] in the adult HI mice. We performed a series of behavioral tests to demonstrate that the adult HI mice have short-term and long-term motor and cognitive deficits
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