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Figure 16.3
Caffeine treatment prevents the sleep deprivation-induced decrease in
the levels of calcium calmodulin kinase-II. Effect of chronic caffeine
treatment and-or sleep deprivation (SD) on the basal expression of total
CaMKII, measured in the DG area and expressed as a ratio to the
GAPDH. Note that chronic caffeine increased CaMKII level in normal
rats (caffeine group) and prevented SD-induced decrease in CaMKII
(Caf-SD group). Each point is the mean ยก SEM of 4-6 rats. *Indicates
significant difference from all other groups (p,0.05). (Modified from
Alhaider et al 2010a, with permission).
suppressing natural inhibitor-1, which leads to stimulation of protein
phosphatase 1 (PP1) (Mulkey et al 1994). The activated PP1 dephosphorylates
P-CaMKII, which results in reduction of memory retention (Wang and Kelly
1997). It has been reported that the activity, but not the basal protein levels, of
calcineurin is increased after 72 h of SD (Wang et al 2009). We have recently
showed that the protein levels of calcineurin in the hippocampal CA1 and DG
areas are not affected by 24 h of SD or by caffeine administration (Alhaider et
al 2010a). Furthermore, it has been proposed that SD does not influence the
level of PP1, which is activated by calcineurin (Guan et al 2004).
The protein family of neurotrophins, including BDNF, is well known to
regulate the survival of neurons and encourage growth and differentiation of
new neurons and synapses (Huang and Reichardt 2001). In the last decades,
accumulated evidence suggests that BDNF plays a pivotal role in hippocampal
synaptic plasticity and spatial learning (Kesslak et al 1998). BDNF influences
synaptic plasticity by raising the efficiency of synaptic transmission through
activation of CaMKII and CREB in the hippocampus (Boulanger and Poo
1999). Acute SD for 8 or 48 h periods decrease the gene expression and protein
levels of BDNF in the hippocampus (Guzman-Marin et al 2006). In parallel, it
has been shown that 24 h SD reduces the basal levels of BDNF in the CA1 and
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