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AdenosineâÂÂs Autacoid Function in the Central Nervous System and the Behavioral State of Conservation-Withdrawal
| Brandy A. Briones1, Traci N. Plumb2 and Thomas R. Minor2,3,4* | ||
| 1Department of Psychology, Princeton University, | ||
| 2Department of Psychology, University of California, Los Angeles | ||
| 3Brain Research Institute, UCLA | ||
| 4Integrative Center for Learning and Memory, UCLA | ||
| Corresponding Author : | Thomas R. Minor, Ph. D Department of Psychology Campus Box: 156304, UCLA Los Angeles, CA 90095-1563 Tel: (310) 625-3611 Email: minor@psych.ucla.edu |
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| Received August 04, 2014; Accepted October 16, 2014; Published October 18, 2014 | ||
| Citation: Briones BA, Plumb TN, Minor TR (2014) Adenosine’s Autacoid Function in the Central Nervous System and the Behavioral State of Conservation- Withdrawal. Autacoids 3:106. doi: 10.4172/2161-0479.1000106 | ||
| Copyright: © 2014 Briones BA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | ||
Related article at Pubmed Scholar Google |
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Abstract
The purine nucleoside adenosine has the critical autacoid function of directly linking cellular excitability to energy availability. The mechanism is activated whenever the rate of adenosine triphosphate (ATP) utilization exceeds the rate of synthesis. In CNS neurons, adenosine is produced by the rapid intracellular hydrolysis of purine nucleotides during neural excitation and then is extruded into extracellular space. The nucleoside is also produced by the extracellular hydrolysis of ATP by ectonucleotidases. Extracellular adenosine interacts with G-protein linked stereospecific receptors to reestablish metabolic homeostasis by exerting extraordinarily potent inhibition of neural excitation via a number of mechanisms. This autacoid mechanism is directly linked to the production of a depression like behavioral state termed conservation-withdrawal during times of physical stress or severe emotional distress. We review evidence here that adenosine produces a transition to conservation-withdrawal by activation of A2A receptors in the ventral-medial striatum.
