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Adenosine is a key factor in regulating the body's sleep-wake cycle. [40] Adenosine levels rise during periods of wakefulness and lowers during sleep. Higher adenosine levels correlate with a stronger feeling of sleepiness, also known as sleep drive or sleep pressure. [41]
Adenosine is a neuromodulator that is responsible for motor function, mood, memory, and learning. Its main purpose is the coordination of responses to different neurotransmitters. [5] Adenosine plays many important roles in biological systems, for example in the central nervous-, cardiovascular-, hepatic-, renal- and respiratory system.
Caffeine keeps you awake by blocking adenosine receptors. Each type of adenosine receptor has different functions, although with some overlap. [3] For instance, both A 1 receptors and A 2A play roles in the heart, regulating myocardial oxygen consumption and coronary blood flow, while the A 2A receptor also has broader anti-inflammatory effects throughout the body. [4]
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The adenosine A2A receptor has also been shown to play a regulatory role in the adaptive immune system. In this role, it functions similarly to programmed cell death-1 (PD-1) and cytotoxic t-lymphocyte associated protein-4 ( CTLA-4 ) receptors, namely to suppress immunologic response and prevent associated tissue damage.
Since in quiet waking the brain is responsible for 20% of the body's energy use, this reduction has an independently noticeable impact on overall energy consumption.) [11] During slow-wave sleep, humans secrete bursts of growth hormone. All sleep, even during the day, is associated with the secretion of prolactin. [12]
Thus, damage to the basal forebrain can reduce the amount of acetylcholine in the brain and impair learning. This may be one reason why basal forebrain damage can result in memory impairments such as amnesia and confabulation. One common cause of basal forebrain damage is an aneurysm of the anterior communicating artery. [6]
The P2RY1 receptor is responsible for shape change in platelets, increased intracellular calcium levels and transient platelet aggregation, while the P2Y12 receptor is responsible for sustained platelet aggregation through the inhibition of adenylate cyclase and a corresponding decrease in cyclic adenosine monophosphate (cAMP) levels.