Neuronal responsiveness
Prolonged wakefulness alters neuronal responsiveness to local electrical stimulation of the neocortex in awake rats
Article first published online: 21 NOV 2012
DOI: 10.1111/jsr.12009
© 2012 European Sleep Research Society
Additional Information
How to Cite
Vyazovskiy, V. V., Olcese, U., Cirelli, C. and Tononi, G. (2013), Prolonged wakefulness alters neuronal responsiveness to local electrical stimulation of the neocortex in awake rats. Journal of Sleep Research, 22: 239–250. doi: 10.1111/jsr.12009
Publication History
- Issue published online: 13 MAY 2013
- Article first published online: 21 NOV 2012
- Manuscript Accepted: 4 OCT 2012
- Manuscript Received: 28 MAY 2012
Funded by
- NIMH. Grant Number: P20 MH077967 C. C.
- NIH Director's Pioneer award (G. T.)
- AFOSR. Grant Number: FA9550-08-1-0244 G. T.
- Abstract
- Article
- References
- Cited By
Keywords:
- cerebral cortex;
- evoked responses;
- local field potential;
- multi-unit recording;
- prolonged wakefulness;
- sleep
Summary
Prolonged wakefulness or a lack of sleep lead to cognitive deficits, but little is known about the underlying cellular mechanisms. We recently found that sleep deprivation affects spontaneous neuronal activity in the neocortex of sleeping and awake rats. While it is well known that synaptic responses are modulated by ongoing cortical activity, it remains unclear whether prolonged waking affects responsiveness of cortical neurons to incoming stimuli. By applying local electrical microstimulation to the frontal area of the neocortex, we found that after a 4 h period of waking the initial neuronal response in the contralateral frontal cortex was stronger and more synchronous, and was followed by a more profound inhibition of neuronal spiking as compared with the control condition. These changes in evoked activity suggest increased neuronal excitability and indicate that, after staying awake, cortical neurons become transiently bistable. We propose that some of the detrimental effects of sleep deprivation may be a result of altered neuronal responsiveness to incoming intrinsic and extrinsic inputs.

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