Effect of postnatal intermittent hypoxia on locomotor activity and neuronal development in rats tested in early adulthood.

Abstract

The present study evaluated the effects of postnatal intermittent hypoxia on locomotor activity and neuronal cell survival in early adulthood rats. During a critical period of brain development on postnatal day (PD) 7-11, male rat pups were exposed to intermittent hypoxia and randomly assigned to three experimental groups: (1) intermittent hypoxia, (2) normoxia, and (3) control (unhandled). One and a half months later on PD56, a behavioral test was conducted, and cell survival was estimated in the hilus, dental gyrus, and CA1 and CA3 subfields of the hippocampus, nucleus accumbens shell and core, dorsal and ventral striatum, and prefrontal cortex. Our results showed that intermittent hypoxia produced hyperactivity that correlated well with psychomotor agitation observed in patients with schizophrenia. Moreover, post-hypoxic rats exhibited a reduction of the number of neurons in the hilar region of the hippocampusanddorsalstriatum,structuresthathavebeenneuropathologicallyassociatedwithschizophrenia.Thesefindingssuggest that intermittent hypoxia can modify the pattern of locomotor activity and selectively affect neurons in rats tested in early adulthood.

Lasting mesothalamic dopamine imbalance and altered exploratory behavior in rats after a mild neonatal hypoxic event

“…Perinatal exposure to hypoxia has been frequently reported to affect locomotor activity and exploratory tendency, as the aspects of novel space exploration, without affecting anxiety. Increased ambulation in an open field was observed in juvenile rats exposed to intermittent hypoxia at P7-11 ( Decker et al, 2005 ; Yamada et al, 2014 ), chronic NH at P0-21 ( Mikati et al, 2005 ), as well as anoxia at P2 ( Rogalska et al, 2004 ) and P4 ( Shimomura and Ohta, 1988 ). A significant increase in both ambulation and rearing was reported in pre-pubertal rats after P2 NH ( Ordyan et al, 2017 ) and juvenile rats after P0 anoxia ( Speiser et al, 1983 ; Dell'Anna et al, 1991 ; Iuvone et al, 1996 ).…”

Does Perinatal Intermittent Hypoxia Affect Cerebrovascular Network Development?

“…However, the behavior observed in adolescence and adulthood after perinatal CIH deviates from the norm, such as altered locomotor activity [[94]] and language and cognitive delays [[95]]. Many of these alterations have been attributed to neuronal loss [[96]], synaptogenesis alterations [[97]], or neuronal development [[13]] as well as glial response [[98]]. Our hypothesis is that CIH induces a positive feedback loop to perpetuate metabolic insufficiency through derailment of normal cerebrovascular development and that this leads to long-term deficiency in cerebrovascular function.…”