Memory loss in people can be caused due to sleep deprivation
According to an article published in the Science Daily, Ted Abel and his team have found that sleep deprivation results in increased levels of the Nucleoside Adenosine in the hippocampus, a part of brain which is associated with memory function. The increased levels of adenosine cause a number of health related problems including memory loss and attention deficits.
The study was led by Ted Abel, Professor of Biology at Penn’s School of Arts and Sciences and the Director of the University’s interdisciplinary Biological Basic of Behavior program. His partners in the study included Cedrick Florian, Postdoctoral Fellow in Biology, and Christopher Vecsey, Neuroscience graduate student, and researcher from the Massachusetts Institute of Technology and Tufts University.
To test Adenosine’s involvement in memory impairment, Abel and his team conducted two parallel experiments on sleep-deprived mice:
Experiment # 1
This experiment involved genetically engineered mice. These mice were missing a gene which is involved with the production of glial transmitters, molecules which originate from brain cells (glia) that the support function of neurons. Without these transmitters the mice were not able to produce Adenosine, which researchers believed causes the issues related to sleep-deprivation.
Experiment # 2
This experiment involved a pharmacological approach in which a pump was grafted into the brains of the mice, which were not genetically engineered. The pump delivered a drug which blocked a particular Adenosine receptor in the hippocampus. Sleep deprived mice would behave as if the additional adenosine was not present in their brains, provided the receptor is involved in memory impairment.
To check the effects of sleep deprivation on mice the researchers conducted an object recognition test.
Test Procedure and Results
- Day 1: Mice were placed in a box with two different objects. They were allowed to explore objects while being videotaped.
- The same night: Some of the mice were allowed to sleep for only half the time, instead of their normal 12-hour sleeping schedule.
- Day 2: Mice were placed back in the box where one of the objects had been moved, and were again videotaped.
The change in the reaction of the mice was studied by the researchers. Researchers expected that due to sleep deprivation, mice may not explore the moved object more than the other object. But both sets of treated mice explored the moved object as if they had received full night’s sleep. Mice didn’t realize that they were sleep deprived.
Hippocampi of the mice was also examined, using electric current to measure the synaptic plasticity (strength of memory-forming synapses).
Combined results of both experiments
- The pharmacologically and genetically protected mice showed greater synaptic plasticity after being sleep-deprived than untreated mice.
- The genetic engineering experiment showed where the Adenosine comes from, and pharmacological experiment showed where it goes.
- Mice did not show any memory impairment because of the interruption in Adenosine’s pathway.
- Researchers identified the molecule, the cellular circuit, and the sleep region by which sleep-deprivation affects memory storage.
- Loosing even half a night’s sleep can be critical for things like cognition.
Conclusion
The study by Abel and his team is a major step forward in understanding management of such impairments in humans. To be able to reverse a particular aspect of sleep deprivation, such as its effects on memory storage, the knowledge about molecular pathways and targets is very important. Such treatments would be especially enticing, given how sensitive the brain is to sleep-deprivation effects.
In addition to Ted Abel and his colleagues this study was also conducted by Michael M. Halassa, of the Department of Psychiatry at Massachusetts General Hospital and the Department of Brain and Cognitive Sciences at MIT, and Philip G. Haydon, of the Department of Neuroscience at the Tufts University School of Medicine.
The research was supported by the National Institutes of Health and published in the Journal of Neuroscience.
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