Caffeine prevents sleep loss-induced deficits in long-term potentiation and related signaling molecules in the dentate gyrus

• Published in: The European journal of neuroscience 2010-04, Vol.31 (8), p.1368-1376
• Main Authors: Alhaider, Ibrahim A., Aleisa, Abdulaziz M., Tran, Trinh T., Alkadhi, Karim A.
• Format: Article
• Language: English
• Subjects: Administration, Oral; Animals; Brain-Derived Neurotrophic Factor - metabolism; caffeine; Caffeine - administration & dosage; Caffeine - pharmacology; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism; Central Nervous System Stimulants - administration & dosage; Central Nervous System Stimulants - pharmacology; Dentate Gyrus - drug effects; Dentate Gyrus - physiopathology; DG area; In Vitro Techniques; long-term potentiation; Long-Term Potentiation - drug effects; Male; P-CaMKII; Phosphorylation; Random Allocation; Rats; Rats, Wistar; sleep deprivation; Sleep Deprivation - drug therapy; Sleep Deprivation - physiopathology; Synapses - drug effects; Synapses - physiology; Time Factors
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/j.1460-9568.2010.07175.x

We have previously reported that caffeine prevented sleep deprivation‐induced impairment of long‐term potentiation (LTP) of area CA1 as well as hippocampus‐dependent learning and memory performance in the radial arm water maze. In this report we examined the impact of long‐term (4‐week) caffeine consumption (0.3 g/L in drinking water) on synaptic plasticity (Alhaider et al., 2010) deficit in the dentate gyrus (DG) area of acutely sleep‐deprived rats. The sleep deprivation and caffeine/sleep deprivation groups were sleep‐deprived for 24 h by using the columns‐in‐water technique. We tested the effect of caffeine and/or sleep deprivation on LTP and measured the basal levels as well as stimulated levels of LTP‐related molecules in the DG. The results showed that chronic caffeine administration prevented the impairment of early‐phase LTP (E‐LTP) in the DG of sleep‐deprived rats. Additionally, chronic caffeine treatment prevented the sleep deprivation‐associated decreases in the basal levels of the phosphorylated calcium/calmodulin‐dependent protein kinase II (P‐CaMKII) and brain derived neurotrophic factor (BDNF) as well as in the stimulated levels of P‐CaMKII in the DG area. The results suggest that chronic use of caffeine prevented anomalous changes in the basal levels of P‐CaMKII and BDNF associated with sleep deprivation and as a result contributes to the revival of LTP in the DG region.