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Figure 16.4
Decline of levels of brain derived neurotrophic factor (BDNF) in dentate
gyrus of sleep-deprived rats and prevention by chronic caffeine
treatment. Effect of chronic caffeine treatment and-or sleep deprivation
(SD) on the protein levels of BDNF measured in the DG area and
expressed as a ratio to the GAPDH. Note that SD caused a marked
decrease in BDNF level (SD group) whereas chronic caffeine treatment
(Caf-SD group) prevented SD-induced effect. 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).
DG areas (Alhaider et al 2010a; Figure 16.4). Caffeine treatment prevents
reduction of BDNF protein levels in sleep-deprived rats (Alhaider et al 2010a).
This decrease in the basal levels of BDNF in sleep-deprived rats may be
considered a factor involved in the reduction of both P-CaMKII and P-CREB
basal levels. It appears that by preventing the reduction in the basal levels of
BDNF, caffeine prevents the SD-induced reduction of P-CaMKII and P-
CREB protein levels and the subsequent impairment of E-LTP and L-LTP in
brain hippocampal regions (Alhaider et al 2010a).
The activity dependent BDNF can be increased by HFS of the hippocampus
(Gartner and Staiger 2002). Five hours after stimulation, the protein levels of
BDNF are not increased in area CA1 of untreated sleep-deprived rats, but are
markedly enhanced in sleep-deprived caffeine treated rats. Thus, chronic
caffeine treatment prevents the SD-induced decrease in BDNF protein levels
(Alhaider et al 2011). It has been revealed that BDNF activates CREB-
dependent protein synthesis, and that the BDNF gene is considered to be one
of the CREB targets (Tao et al 1998). As a consequence, BDNF synthesis can
be stimulated upon CREB activation. We have recently shown a normal
activation of CREB in caffeine and caffeine-treated sleep-deprived rats
(Alhaider et al 2011). It appeared that the levels of BDNF during the
expression of L-LTP follow those of P-CREB (Alhaider et al 2011). Applying
BDNF after stimulation seems adequate to express L-LTP in slices treated
with a protein synthesis inhibitor (Pang et al 2004). Therefore, the inability of
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