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1 Research Service (151A3), Veteran Affairs Greater Los Angeles Healthcare System, Sepulveda, CA, USA; Psychology, University of California, Los Angeles, CA, USA
2 Research Service (151A3), Veteran Affairs Greater Los Angeles Healthcare System, Sepulveda, CA, USA; Medicine, University of California, Los Angeles, CA, USA; Zoology, Patna University, Patna, Bihar, India
3 Research Service (151A3), Veteran Affairs Greater Los Angeles Healthcare System, Sepulveda, CA, USA; Medicine, University of California, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: dmcginty{at}ucla.edu.
Evidence suggests that adenosine (AD) is an endogenous sleep factor. The hypnogenic action of AD is mediated through its inhibitory A1 and excitatory A2A receptors. Although AD is thought to have a predominant action in the wake active region of the basal forebrain (BF), hypnogenic action of AD has been demonstrated in several other brain areas including the preoptic area (POA). We hypothesized that in lateral preoptic area (lPOA), a region with an abundance of sleep active neurons, AD acting via A1 receptors would induce waking by inhibition of sleep-active neurons, and that AD acting via A2A receptors would promote sleep by stimulating the sleep-active neurons. To this end, we studied the effects on sleep of an AD transport inhibitor, nitrobenzyl-thio -inosine (NBTI), and A1 and A2A receptor agonists/antagonists by microdialysing them into the lPOA. The results showed that, in the sleep promoting area of lPOA: (1) A1 receptor stimulation or inhibition of AD transport by NBTI induced waking and (2) A2A receptor stimulation induced sleep. We also confirmed that NBTI administration in the wake promoting area of the BF increased sleep. The effects of AD could be mediated either directly or indirectly via interaction with other neurotransmitter systems. These observations support a hypothesis that AD mediated effects on sleep-wake are site and receptor dependent.
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