Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia

<div>Effect of common carotid artery occlusion on the immunoreactivity against CCR2. Representative micrographs of CCR2 immunofluorescence ((a) to (o)) using a rabbit antibody against CCR2 and a goat antibody anti-rabbit IgG conjugated with fluorescein isothiocyanate (green color). The cerebral region was identified by propidium iodide (red color) counterstaining. CA, Cornu Ammonis, and DG, dentate gyrus, of the hippocampus. LV, layer V of the cerebral cortex. Plexus, choroid plexus. Values are the mean ± SEM from 3 rats in each experimental condition.</div>

Neural Plasticity

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Figure 3: Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia 

Figure 3 | Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia 