Circadian rhythm in adenosine A1 receptor of mouse cerebral cortex

Florio, Chiara; Rosati, Anna; Traversa, U.; Vertua, R.

doi:10.1016/0024-3205(91)90476-r

Cited by 10 publications

(4 citation statements)

References 20 publications

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“…Caffeine is an antagonist of the adenosine A 1 and A 2A receptors, the two major adenosine receptors in the central nervous system (Fredholm et al ., ). The density of adenosine receptors in the central nervous system is under circadian control (Florio et al ., ). From the present results, we cannot determine where between the retina and the SCN caffeine influences the light sensitivity of the circadian system.…”

Section: Discussionmentioning

confidence: 97%

Caffeine increases light responsiveness of the mouse circadian pacemaker

Diepen

Lucassen

Yasenkov

et al. 2014

Eur J of Neuroscience

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Caffeine is the most commonly used psychoactive stimulant worldwide. It reduces sleep and sleepiness by blocking access to the adenosine receptor. The level of adenosine increases during sleep deprivation, and is thought to induce sleepiness and initiate sleep. Light-induced phase shifts of the rest-activity circadian rhythms are mediated by light-responsive neurons of the suprachiasmatic nucleus (SCN) of the hypothalamus, where the circadian clock of mammals resides. Previous studies have shown that sleep deprivation reduces circadian clock phase-shifting capacity and decreases SCN neuronal activity. In addition, application of adenosine agonists and antagonists mimics and blocks, respectively, the effect of sleep deprivation on light-induced phase shifts in behaviour, suggesting a role for adenosine. In the present study, we examined the role of sleep deprivation in and the effect of caffeine on light responsiveness of the SCN. We performed in vivo electrical activity recordings of the SCN in freely moving mice, and showed that the sustained response to light of SCN neuronal activity was attenuated after 6 h of sleep deprivation prior to light exposure. Subsequent intraperitoneal application of caffeine was able to restore the response to light. Finally, we performed behavioural recordings in constant conditions, and found enhanced period lengthening during chronic treatment with caffeine in drinking water in constant light conditions. The data suggest that increased homeostatic sleep pressure changes circadian pacemaker functioning by reducing SCN neuronal responsiveness to light. The electrophysiological and behavioural data together provide evidence that caffeine enhances clock sensitivity to light.

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Section: Discussionmentioning

confidence: 97%

Caffeine increases light responsiveness of the mouse circadian pacemaker

Diepen

Lucassen

Yasenkov

et al. 2014

Eur J of Neuroscience

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“…Circadian temporal variations have been reported in extracellular adenosine levels of the basal forebrain (Murillo-Rodriguez et al, 2004) and blood (Chagoya de Sánchez et al, 1983) and density of brain adenosine receptors (Florio et al, 1991). The involvement of adenosine receptors in regulating the response of the biological clock to light (Elliott et al, 2001) and temporal expression of Per1 gene (von Gall et al, 2002) also have been demonstrated.…”

Section: Discussionmentioning

confidence: 97%

24-HOUR TEMPORAL PATTERN OF NTPDase AND 5′-NUCLEOTIDASE ENZYMES IN RAT BLOOD SERUM

Detanico¹,

Souza²,

Medeiros³

et al. 2010

Chronobiology International

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Circadian rhythms represent an important mechanism to prepare the organism for environmental variations. ATP, ADP, AMP, and adenosine can act as extracellular messengers in a range of biological processes and are metabolized by a number of enzymes, including NTPDases and 5'-nucleotidase. In the present study the authors report that ATPase and ADPase activities present 24-h temporal variations that peak during dark (activity) span. These findings suggest that this enzymatic temporal pattern in blood serum might be important for the normal physiology and function of the organism through the maintenance of extracellular nucleotides at physiological levels.

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“…ATP-induced activation of P2X receptors in the hypothalamus regulates both hormone secretion and body temperature while adenosine is associated with sleep need (Porkka-Heiskanen et al, 1997; Blanco-Centurion et al, 2006). Adenosine content in basal ganglia shows daily variations that were proposed to be related to changes in sleep-wake cycles during aging while A1 receptors and 5′-ectonucleotidase activity are rhythmic in cortex presumably playing a role in sleep (Virus et al, 1984; Florio et al, 1991; Rosati et al, 1993; Mackiewicz et al, 2003; Murillo-Rodriguez et al, 2004). Sleep deprivation can shift circadian rhythms (Antle and Mistlberger, 2000; Antle et al, 2001), possibly through adenosine that accumulates with sleep need, a mechanism supported by the findings that light induced phase shifts can be blocked by both, A1 agonists and IP3 blockers (Watanabe et al, 1996; Marpegan et al, 2005; Leone et al, 2006; Krueger, 2008).…”

Section: Discussionmentioning

confidence: 99%

Circadian Regulation of ATP Release in Astrocytes

Marpegan

Swanstrom²,

Chung³

et al. 2011

Journal of Neuroscience

161

136

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Circadian clocks sustain daily oscillations in gene expression, physiology and behavior, relying on transcription-translation feedback loops of clock genes for rhythm generation. Cultured astrocytes display daily oscillations of extracellular ATP, suggesting that ATP release is a circadian output. We hypothesized that the circadian clock modulates ATP release via mechanisms that regulate acute ATP release from glia. To test the molecular basis for circadian ATP release, we developed methods to measure in real-time ATP release and Bmal1::dLuc circadian reporter expression in cortical astrocyte cultures from mice of different genotypes. Daily rhythms of gene expression required functional Clock and Bmal1, both Per1 and Per2, and both Cry1 and Cry2 genes. Similarly, high level, circadian ATP release also required a functional clock mechanism. Whereas blocking IP3 signaling significantly disrupted ATP rhythms with no effect on Bmal1::dLuc cycling, blocking vesicular release did not alter circadian ATP release or gene expression. We conclude that astrocytes depend on circadian clock genes and IP3 signaling to express daily rhythms in ATP release.

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Circadian rhythm in adenosine A1 receptor of mouse cerebral cortex

Cited by 10 publications

References 20 publications

Caffeine increases light responsiveness of the mouse circadian pacemaker

Caffeine increases light responsiveness of the mouse circadian pacemaker

24-HOUR TEMPORAL PATTERN OF NTPDase AND 5′-NUCLEOTIDASE ENZYMES IN RAT BLOOD SERUM

Circadian Regulation of ATP Release in Astrocytes

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