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. Author manuscript; available in PMC: 2008 Jan 1.
Published in final edited form as: J Neurophysiol. 2006 Nov 8;97(1):837–848. doi: 10.1152/jn.00873.2006

Fig.6.

Fig.6

A2 adenosine receptors are not responsible for the effect of adenosine in hypocretin/orexin neurons. Whole-cell recordings were performed in hypocretin/orexin neurons held at −60 mV under voltage clamp. Bicuculline (30 μM) was present in all solutions. Selective A2 receptor antagonists, MRS 1706 and SCH 58261, were applied to the recorded neurons. After a stable recording of sEPSCs were obtained, in the presence of MRS 1706 and SCH 58261, adenosine (100 μM) was applied and its effect on the frequency of sEPSCs was monitored. Sample traces are presented in A and the time course of a typical experiment is shown in B. In the presence of MRS 1706 and SCH 58261, the frequency of sEPSCs declined in the presence of adenosine (100 μM) and recovered after its withdrawal. Application of adenosine is indicated by the filled bar. C, pooled data from all neurons examined in our experiments show that the inhibitory effect of adenosine was intact in the presence of selective A2 receptor antagonists (**, P<0.01, ANOVA).