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Neuroprotective effects of enriched environment housing after transient global cerebral ischaemia are associated with the upregulation of insulin‐like growth factor‐1 signalling
Author(s) -
Wadowska Magdalena,
Woods Julie,
Rogozinska Magdalena,
Briones Teresita L.
Publication year - 2015
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12146
Subject(s) - neuroprotection , ischemia , medicine , hippocampus , protein kinase b , environmental enrichment , insulin like growth factor , neurodegeneration , endocrinology , downregulation and upregulation , anesthesia , growth factor , apoptosis , biology , receptor , disease , biochemistry , gene
Aims Use of enriched environment ( EE ) housing has been shown to promote recovery from cerebral ischaemic injury but the underlying mechanisms of their beneficial effects remains unclear. Here we examined whether the beneficial effects of EE housing on ischaemia‐induced neurodegeneration and cognitive impairment are associated with increased insulin‐like growth factor‐1 ( IGF ‐1) signalling in the hippocampus. Methods Forty‐two adult male W istar rats were included in the study and received either ischaemia or sham surgery. Rats in each group were further randomized to either: EE or standard laboratory cage housing (control). Rats were placed in their assigned housing condition immediately after recovery from anaesthesia. Behavioural testing in the cued learning and discrimination learning tasks were conducted 2 weeks after ischaemia. Rats were euthanized after behavioural testing and the hippocampus was analysed for IGF ‐1 level, IGF ‐1 receptor ( IGF ‐1 R ) activation, protein kinase B ( Akt ) pathway activation, neurone loss and caspase 3 expression. Results Our data showed that EE housing: (1) mitigated ischaemia‐induced neuronal loss; (2) attenuated ischaemia‐induced increase in caspase 3 immunoreactivity in the hippocampus; (3) ameliorated ischaemia‐induced cognitive impairments; and (4) increased IGF ‐1 R activation and signalling through the Akt pathway after ischaemic injury. Conclusion Ultimately, these findings suggest the possibility that IGF ‐1 signalling may be one of the underlying mechanisms involved in the beneficial effects of EE in optimizing recovery following cerebral ischaemic injury.