An enriched environment reverses the synaptic plasticity deficit induced by chronic cerebral hypoperfusion

Abstract

Chronic cerebral hypoperfusion (CCH) leads to a long-term, inadequate blood supply in the brain, which eventually causes cognitive impairment. An enriched environment (EE) improves learning and memory by improving synaptic plasticity. The impact of an EE on cognitive impairment induced by CCH is not, however, well known. To investigate this possible effect, we permanently occluded the bilateral common carotid arteries (2-vessel occlusion) in rats to induce CCH and studied EE effects on cognitive impairment and synaptic plasticity following CCH. We found that EE treatment reversed spatial memory deficits induced by CCH. An EE also reversed the deficit in long-term potentiation following CCH, but the input–output curves and paired-pulse facilitation were not affected. CCH led to reduced expression of phosphorylated CREB in the rats, but EE reversed this reduction. In addition, CCH reduced the expression of synaptophysin and microtubule-associated protein 2, whereas EE reversed this reduced expression. Thus, EE reversed CCH-induced spatial cognitive impairment without affecting basal synaptic transmission or the release probability of presynaptic neurotransmitters. The EE effect probably resulted from the regulation of postsynaptic potentiation.