Physiological Consequences of Sleep Loss in the Rat

In this thesis, I examined the homeostatic and physiological consequences of acute total sleep deprivation (TSD) and chronic sleep restriction (CSR) in the rat. I first developed a rat model of CSR using a walking wheel to confine sleep opportunities to designated times. I used this model to investigate the response of the sleep homeostat to a sleep deficit accumulated at different rates. I then compared the effects of CSR to the well-established acute ‘sleep deprivation syndrome’. Further, I considered a role for TSD in the production of reversible neuron damage. Finally, I investigated the impact of TSD and CSR on the integrity of neurons using an adapted model of mild traumatic brain injury (TBI). My research program led to the following conclusions: 1. CSR results in selective attenuation of the non-rapid eye movement (NREM) sleep homeostat, while leaving the rapid eye movement (REM) sleep homeostat intact. 2. CSR induces weight loss, body temperature and metabolic alterations that are qualitatively similar but quantitatively diminished compared to those of TSD. 3. TSD does not result in neuron damage in the rat sensorimotor cortex as measured by classical dark neurons (DNs). 4. Developing a sleep deficit from TSD or CSR prior to mild TBI does not cause exacerbation of neuron damage as measured by classical DN production. 5. There may be two under-represented demonstrations of neuron damage in the rat cortex: non-compacted DNs and light compacted neurons. When these neuron types are accounted for, a sleep deficit developed from TSD reduces the significant neuron damage produced by mild TBI. A sleep deficit developed by CSR does not afford the same neuroprotection as TSD.Ph.D