Prevention by Regular Exercise of Acute Sleep Deprivation-Induced Impairment of Late Phase LTP and Related Signaling Molecules in the Dentate Gyrus

Abstract

The dentate gyrus (DG) and CA1 regions of the hippocampus are intimately related physically and functionally, yet they react differently to insults. The purpose of this study was to determine the protective effects of regular treadmill exercise on late phase long-term potentiation (L-LTP) and its signaling cascade in the DG region of the hippocampus of rapid eye movement (REM) sleep-deprived rats. Adult Wistar rats ran on treadmills for 4 weeks then were acutely sleep deprived for 24 h using the modified multiple platform method. After sleep deprivation, the rats were anesthetized and L-LTP was induced in the DG region. Extracellular field potentials from the DG were recorded in vivo, and levels of L-LTP-related signaling proteins were assessed both before and after L-LTP expression using immunoblot analysis. Sleep deprivation reduced the basal levels of phosphorylated cAMP response element-binding protein (P-CREB) as well as other upstream modulators including calcium/calmodulin kinase IV (CaMKIV) and brain-derived neurotrophic factor (BDNF) in the DG of the hippocampus. Regular exercise prevented impairment of the basal levels of P-CREB and total CREB as well as those of CaMKIV in sleep-deprived animals. Furthermore, regular exercise prevented sleep deprivation-induced inhibition of L-LTP and post-L-LTP downregulation of P-CREB and BDNF levels in the DG. The current findings show that our exercise regimen prevents sleep deprivation-induced deficits in L-LTP as well as the basal and poststimulation levels of key signaling molecules.

Dietary polyphenols promote resilience against sleep deprivation‐induced cognitive impairment by activating protein translation

“…It has been reported that, of the various forms of synaptic plasticity, SD inhibits the induction of hippocampal long-term potentiation, a neural substrate of learning and memory (22). In particular, SD has been identified to impair late-phase long-term potentiation (23,24), which correlates with long-term memory and requires the de novo synthesis of proteins (25)(26)(27).…”

Acute sleep deprivation induces cardioprotection against ischemia/ reperfusion injury through reducing inflammatory responses: the role of central GABA-A receptors

“…24-h sleep deprivation was induced by putting the animals in an 8 circular small platforms aquarium (125 × 44 × 44 cm and 6.5 cm in diameter) has been explained before (Parsa et al 2016;Zagaar et al 2016). The EEG recording confirmed the induction of sleep deprivation by multiple plate forms model (Arthaud et al 2015).…”

Changes of Cerebral and/or Peripheral Adenosine A1 Receptor and IGF-I Concentrations under Extended Sleep Duration in Rats

“…The non-significant effect of extended sleep on hippocampal IGF-I levels supported previous results showing that sleep quality and sleep quantity in non-stressed animals showed predictive changes in translational factor activity in cortical but not hippocampal regions [ 39 ]. The absence of effect may also be due to IGF-I measurement in whole hippocampal tissue—not specific areas dedicated to learning and short-term memory—and synaptic plasticity such as CA1 or dentate gyrus [ 40 ]. In our study, additional sleep time induced higher circulating and muscle IGF-I levels, and higher weight gain was positively correlated with them, and these results shed light on the anabolic properties of sleep [ 33 ].…”