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Sleep Med Rev. 1999 Jun;3(2):119-29.

Why we sleep: a theoretical view of sleep function.

Author information

1
Washington State University, College of Veterinary Medicine, Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, PO Box 646520, Pullman, WA 99164-6520, USA. Krueger@vetmed.wsu.edu

Abstract

We propose that sleep begins within small groups of highly interconnected neurons and is characterized by altered input --> output (i-->0) relationships for any specific neuronal group. Further, experimental findings suggest that growth factors, released locally in response to neuronal activity, and acting in paracrine and autocrine fashions, induce the altered i-->0 relationships. These growth factors also act to provide the structural basis for synapses. Thus, we envision that sleep mechanisms (neural use-dependent induction of growth factors and their subsequent effects on i-->0 relationships) cannot be separated from sleep function (growth factor-induced synaptic sculpturing). This mechanism/firnction is envisioned to take place in all areas of the brain, including sleep regulatory circuits as well as throughout the cortex. Finally, the "sleep" of neuronal groups (altered i-->o relationships) is coordinated by the known sleep regulatory circuits and activational-projection systems in the brain. The theory extends and integrates existing sleep theories to cover a broader range of phenomena.

PMID:
15310481

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