This information suggests that specific intracellular signaling pathways required for LTP are affected during sleep deprivation. These pathways were examined in a study that used in vitro electrophysiological recordings to observe the effects of sleep deprivation on LTP in the hippocampus (Vescey, 2009). Ten mice were contained in individual chambers but only half of the mice were sleep-deprived of 5 hours of sleep. After, the mice were tested for contextual memory 24 hours after within the same chambers. After 48 hours, the mice were tested again for contextual memory but instead moved to different chambers before testing. Hippocampal slices were then taken from all mice and results found that sleep deprivation for 5 hours impaired spaced four-train LTP, theta-burst LTP, and forskolin-induced potentiation (Vescey, 2009). The functioning of all these forms of LTP are dependent of the operation of the cAMP-PKA pathway. This pathway is a receptor-triggered signaling mechanism that is used for cell communication during memory consolidation (Havekes et al., 2012). The experiment (Vescey, 2009) found that the cAMP activity was reduced in forskolin-induced potentiation after 5 hours of sleep deprivation. However, in four-train LTP the levels of the cAMP-PKA signaling pathways does not have an effect on the production of LTP. These forms of LTP are translation-dependent, and are differently unimpaired by the 5-hour sleep deprivation time period. The fact that four-train LTP was unaffected by sleep deprivation suggests that sleep deprivation has no effect on translation in the hippocampus. Researchers suggest that while translation processes are not affected, molecular mechanisms such as cAMP-PKA signaling pathways can be altered (Vescey, 2009). Because one of PKA’s nuclear targets include
This information suggests that specific intracellular signaling pathways required for LTP are affected during sleep deprivation. These pathways were examined in a study that used in vitro electrophysiological recordings to observe the effects of sleep deprivation on LTP in the hippocampus (Vescey, 2009). Ten mice were contained in individual chambers but only half of the mice were sleep-deprived of 5 hours of sleep. After, the mice were tested for contextual memory 24 hours after within the same chambers. After 48 hours, the mice were tested again for contextual memory but instead moved to different chambers before testing. Hippocampal slices were then taken from all mice and results found that sleep deprivation for 5 hours impaired spaced four-train LTP, theta-burst LTP, and forskolin-induced potentiation (Vescey, 2009). The functioning of all these forms of LTP are dependent of the operation of the cAMP-PKA pathway. This pathway is a receptor-triggered signaling mechanism that is used for cell communication during memory consolidation (Havekes et al., 2012). The experiment (Vescey, 2009) found that the cAMP activity was reduced in forskolin-induced potentiation after 5 hours of sleep deprivation. However, in four-train LTP the levels of the cAMP-PKA signaling pathways does not have an effect on the production of LTP. These forms of LTP are translation-dependent, and are differently unimpaired by the 5-hour sleep deprivation time period. The fact that four-train LTP was unaffected by sleep deprivation suggests that sleep deprivation has no effect on translation in the hippocampus. Researchers suggest that while translation processes are not affected, molecular mechanisms such as cAMP-PKA signaling pathways can be altered (Vescey, 2009). Because one of PKA’s nuclear targets include