Sleep deprivation adenosine

Porkka-Heiskanen, T., Strecker, R. E. McCarley, R. W. (2000). Brain site-specificity of extracellular adenosine concentration changes during sleep deprivation and spontaneous sleep an in vivo microdialysis study. Neuroscience 99, 507-17. 

Figure 12.1 Extracellular adenosine concentrations in different brain areas, measured with in vivo microdialysis from cats during sleep deprivation (6 h gentle handling) and recovery sleep. Concentrations are given as a percentage of pre-deprivation values. BF, basal forebrain CX, cingulate cortex TH, VA/VL nucleus of thalamus POA, preoptic hypothalamic area DRN, dorsal raphe nucleus PPT, pedunculopontine nucleus. In BF and CX adenosine rises during sleep deprivation, but starts to decline during deprivation in CX, whereas the decline occurs during recovery in the BF. In other areas there is no accumulation during sleep deprivation. Modified from Porkka-Heiskanen et al. (2000).

Sleep deprivation and adenosine source of the increased adenosine... 

Basheer, R., Halldner, L., Alanko, L. et al. (2001a). Opposite changes in adenosine A1 and A2A receptor mRNA in the rat following sleep deprivation. Neuroreport 12 (8), 1577-80. 

Benington JH, Kodali SK, Heller HC. Stimulation of A1 adenosine receptors mimics the electroencephalographic effects of sleep deprivation. Brain Res 1995 692 79-85. 

There is also support for a role of PGD2 in sleep control and homeostasis (Hayaishi, 2002). PGD2 is synthesized in the subarachnoid space ventral to the POA. Administration of PGD2 in the subarachnoid space induces normal sleep, and inhibition of synthesis or receptors suppresses sleep. Sleep rebound after deprivation is reduced in mice in which the synthetic enzyme is knocked out. Administration of PGD2 to the subarachnoid space also induces c-Fos in the VLPO as well as dorsal POA neurons (Scammel et a ., 1998). The hypnogenic actions of PGD2 seem to be mediated by an adenosine A2a pathway (Satoh et al, 1966). 

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