@article {2130,
	title = {Sleep deprivation-induced alterations in excitatory synaptic transmission in the CA1 region of the rat hippocampus.},
	journal = {The Journal of Physiology},
	volume = {570},
	year = {2006},
	month = {2006 Feb 1},
	pages = {553-65},
	abstract = {<p>Although the function of sleep remains elusive, there is compelling evidence to suggest that sleep plays an important role in learning and memory. A number of studies have now shown that sleep deprivation (SD) results in significant impairment of long-term potentiation (LTP) in the hippocampus. In this study, we have attempted to determine the mechanisms responsible for this impairment. After 72 h SD using the multiple-platform technique, we observed a reduction in the whole-cell recorded NMDA/AMPA ratio of CA1 pyramidal cells in response to Schaffer collateral stimulation. This impairment was specific to sleep deprivation as rats placed over a single large platform, which allowed sleep, had a normal NMDA/AMPA ratio. mEPSCs evoked by local application of a high osmolarity solution revealed no differences in the AMPA receptor function. NMDA currents recorded from outside-out patches excised from the distal dendrites of CA1 cells displayed a reduction in amplitude after SD. While there were no alterations in the glutamate sensitivity, channel open probability or the single channel conductance of the receptor, a crosslinking assay demonstrated that the NR1 and NR2A subunits of NMDA receptors were preferentially retained in the cytoplasm after SD, indicating that SD alters NMDAR surface expression. In summary, we have identified a potential mechanism underlying SD-induced LTP impairment. This synaptic alteration may underlie the cognitive deficits seen following sleep deprivation and could represent a target for future intervention studies.</p>
},
	keywords = {AMPA, Animals, Electric Stimulation, Excitatory Postsynaptic Potentials, Glutamic Acid, Glycine, Hippocampus, Ion Channel Gating, Kinetics, Long-Term Potentiation, Male, N-Methyl-D-Aspartate, Patch-Clamp Techniques, Rats, Receptors, Sleep Deprivation, Sprague-Dawley, Synaptic Transmission},
	issn = {0022-3751},
	doi = {10.1002/cbic.201000254},
	author = {McDermott, Carmel M and Hardy, Mattie N and Bazan, Nicolas G and Magee, Jeffrey C}
}
@article {2136,
	title = {Sleep deprivation causes behavioral, synaptic, and membrane excitability alterations in hippocampal neurons.},
	journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience},
	volume = {23},
	year = {2003},
	month = {2003 Oct 22},
	pages = {9687-95},
	abstract = {<p>Although the function of sleep remains elusive, several lines of evidence suggest that sleep has an important role in learning and memory. In light of the available data and with the prevalence of sleep deprivation (SD), we sought to determine the effect of SD on neuronal functioning. We found that the exposure of rats to 72 hr of primarily rapid eye movement SD impaired their subsequent performance on a hippocampus-dependent spatial learning task but had no effect on an amygdala-dependent learning task. To determine the underlying cellular level mechanisms of this hippocampal deficit, we examined the impact of SD on several fundamental aspects of membrane excitability and synaptic physiology in hippocampal CA1 pyramidal neurons and dentate gyrus granule cells. We found that neuronal excitability was severely reduced in CA1 neurons but not in granule cells and that the production of long-term potentiation of synaptic strength was inhibited in both areas. Using multiple SD methods we further attempted to differentiate the effects of sleep deprivation from those associated with the nonspecific stress induced by the sleep deprivation methods. Together these data suggest that failure to acquire adequate sleep produces several molecular and cellular level alterations that profoundly inhibit hippocampal functioning.</p>
},
	keywords = {Amygdala, Animal, Animals, Behavior, Cell Membrane, Cues, Electroencephalography, Excitatory Postsynaptic Potentials, Hippocampus, Long-Term Potentiation, Long-Term Synaptic Depression, Male, Memory, Neuronal Plasticity, Neurons, Physiological, Pyramidal Cells, Rats, Sleep Deprivation, Sprague-Dawley, Stress, Synapses},
	issn = {1529-2401},
	doi = {10.1002/cbic.201000254},
	author = {McDermott, Carmel M and LaHoste, Gerald J and Chen, Chu and Musto, Alberto and Bazan, Nicolas G and Magee, Jeffrey C}
}
