Clinical conditions altering IL-1 or TNF activity are associated with changes in sleep, for example, infectious disease and sleep apnea. Endogenous substances moderating the effects of IL-1 and TNF include anti-inflammatory cytokines such as IL-4, IL-10, and IL-13. Downstream events include nitric oxide, growth hormone releasing hormone, nerve growth factor, nuclear factor kappa B, and possibly adenosine and prostaglandins. ![]() ![]() IL-1 and TNF are part of a complex biochemical cascade regulating sleep. Brain levels of IL-1 and TNF correlate with sleep propensity for example, after sleep deprivation, their levels increase. Stimulation of the endogenous production of IL-1 and TNF enhances NREMS. Inhibition of either IL-1 or TNF inhibits spontaneous sleep and the sleep rebound that occurs after sleep deprivation. Injection of IL-1 or TNF enhances non-rapid eye movement sleep (NREMS). Among these substances, the most extensively studied for their role in sleep regulation are interleukin-1beta (IL-1) and tumor necrosis factor alpha (TNF). ![]() All the GFs currently identified as sleep regulatory substances are also implicated in synaptic plasticity. ![]() These GFs also influence synaptic efficacy. It is posited that these GFs are produced in response to neural activity and affect input-output relationships within the neural circuits where they are produced, thereby inducing a local state shift. Several growth factors (GFs) are implicated in sleep regulation.
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