ABSTRACT
Past experiments investigating the effects of total sleep deprivation (TSD) on the functioning of the central nervous system have been disappointing. Prolonged sleep deprivation has not revealed changes in: (a) brain histology at the light microscopic level, (b) brain histology using electron microscopy, (c) level and/or turnover of brain monoamines, (d) cholinergic receptor density and affinity, (e) adrenergic receptor binding and affinity, (f) incorporation of 2-deoxyglucose, and (g) the expression of the immediate early gene epidermal growth factor-1 (EGR1) (see 1 and 2 for review). Although recent studies have begun to reveal more clues using molecular-genetic strategies (see Ref. 3 for review), the nature of the underlying pathological process remains a mystery. These results are somewhat surprising when one considers that long-term TSD is invariably fatal (4,5). Nonetheless, the inability to detect major pathological modifications in the brains of sleep-deprived animals suggest that the deficits produced by TSD result not from a general impairment of the CNS but rather from modifications in specific functional systems (6).
