Dialysis delivery of an adenosine A2A agonist into the pontine reticular formation of C57BL/6J mouse increases pontine acetylcholine release and sleep

Christal G. Coleman, Helen Baghdoyan, Ralph Lydic

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Abstract

In vivo microdialysis in C57BL/6J (B6) mouse was used to test the hypothesis that activating adenosine A2A receptors in the pontine reticular formation (PRF) increases acetylcholine (ACh) release and rapid eye movement (REM) sleep. Eight concentrations of the adenosine A2A receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5′-N- ethylcarboxamidoadenosine hydrochloride (CGS 21680; CGS) were delivered to the PRF and ACh in the PRF was quantified. ACh release was significantly increased by dialysis with 3 μM CGS and significantly decreased by dialysis with 10 and 100 μM CGS. Co-administration of the adenosine A2A receptor antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5- ylamino]ethyl)phenol (ZM 241385; 30 nm) blocked the CGS-induced increase in ACh release. In a second series of experiments, CGS (3 μM) was delivered by dialysis to the PRF for 2 h while recording sleep and wakefulness. CGS significantly decreased time in wakefulness (-51% in h 1; -54% in h 2), increased time in non-rapid eye movement (NREM) sleep (90% in h 1; 151% in h 2), and increased both time in REM sleep (331% in h 2) and the number of REM sleep episodes (488% in h 2). The enhancement of REM sleep is consistent with the interpretation that adenosine A2A receptors in the PRF of the B6 mouse contribute to REM sleep regulation, in part, by increasing ACh release in the PRF. A2A receptor activation may promote NREM sleep via GABAergic inhibition of arousal promoting neurons in the PRF.

Original languageEnglish (US)
Pages (from-to)1750-1759
Number of pages10
JournalJournal of Neurochemistry
Volume96
Issue number6
DOIs
StatePublished - Mar 1 2006
Externally publishedYes

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Dialysis
Eye movements
Inbred C57BL Mouse
Adenosine
Acetylcholine
Sleep
REM Sleep
Adenosine A2A Receptors
Wakefulness
Eye Movements
Adenosine A2 Receptor Agonists
Adenosine A2 Receptor Antagonists
Pontine Tegmentum
Microdialysis
Phenol
Arousal
Neurons
Chemical activation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

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title = "Dialysis delivery of an adenosine A2A agonist into the pontine reticular formation of C57BL/6J mouse increases pontine acetylcholine release and sleep",
abstract = "In vivo microdialysis in C57BL/6J (B6) mouse was used to test the hypothesis that activating adenosine A2A receptors in the pontine reticular formation (PRF) increases acetylcholine (ACh) release and rapid eye movement (REM) sleep. Eight concentrations of the adenosine A2A receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5′-N- ethylcarboxamidoadenosine hydrochloride (CGS 21680; CGS) were delivered to the PRF and ACh in the PRF was quantified. ACh release was significantly increased by dialysis with 3 μM CGS and significantly decreased by dialysis with 10 and 100 μM CGS. Co-administration of the adenosine A2A receptor antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5- ylamino]ethyl)phenol (ZM 241385; 30 nm) blocked the CGS-induced increase in ACh release. In a second series of experiments, CGS (3 μM) was delivered by dialysis to the PRF for 2 h while recording sleep and wakefulness. CGS significantly decreased time in wakefulness (-51{\%} in h 1; -54{\%} in h 2), increased time in non-rapid eye movement (NREM) sleep (90{\%} in h 1; 151{\%} in h 2), and increased both time in REM sleep (331{\%} in h 2) and the number of REM sleep episodes (488{\%} in h 2). The enhancement of REM sleep is consistent with the interpretation that adenosine A2A receptors in the PRF of the B6 mouse contribute to REM sleep regulation, in part, by increasing ACh release in the PRF. A2A receptor activation may promote NREM sleep via GABAergic inhibition of arousal promoting neurons in the PRF.",
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T1 - Dialysis delivery of an adenosine A2A agonist into the pontine reticular formation of C57BL/6J mouse increases pontine acetylcholine release and sleep

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AU - Lydic, Ralph

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N2 - In vivo microdialysis in C57BL/6J (B6) mouse was used to test the hypothesis that activating adenosine A2A receptors in the pontine reticular formation (PRF) increases acetylcholine (ACh) release and rapid eye movement (REM) sleep. Eight concentrations of the adenosine A2A receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5′-N- ethylcarboxamidoadenosine hydrochloride (CGS 21680; CGS) were delivered to the PRF and ACh in the PRF was quantified. ACh release was significantly increased by dialysis with 3 μM CGS and significantly decreased by dialysis with 10 and 100 μM CGS. Co-administration of the adenosine A2A receptor antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5- ylamino]ethyl)phenol (ZM 241385; 30 nm) blocked the CGS-induced increase in ACh release. In a second series of experiments, CGS (3 μM) was delivered by dialysis to the PRF for 2 h while recording sleep and wakefulness. CGS significantly decreased time in wakefulness (-51% in h 1; -54% in h 2), increased time in non-rapid eye movement (NREM) sleep (90% in h 1; 151% in h 2), and increased both time in REM sleep (331% in h 2) and the number of REM sleep episodes (488% in h 2). The enhancement of REM sleep is consistent with the interpretation that adenosine A2A receptors in the PRF of the B6 mouse contribute to REM sleep regulation, in part, by increasing ACh release in the PRF. A2A receptor activation may promote NREM sleep via GABAergic inhibition of arousal promoting neurons in the PRF.

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