Results: 4

1.
Figure 2

Figure 2. From: Adenosine Signalling and Function in Glial Cells.

Adenosine receptors, their coupling to G-proteins and some of the down-stream consequences of receptor activation.

Detlev Boison, et al. Cell Death Differ. ;17(7):1071-1082.
2.
Figure 4

Figure 4. From: Adenosine Signalling and Function in Glial Cells.

The dual functions of A2A receptor antagonists in Parkinson’s disease models: A2AR antagonists act at the A2AR in striatal neurons to stimulate motor activity. Furthermore, it is postulated that A2AR antagonists may modulate microglial activation in substantia nigra to exert a possible neuroprotective effect in an animal model of Parkinson’s disease.

Detlev Boison, et al. Cell Death Differ. ;17(7):1071-1082.
3.
Figure 1

Figure 1. From: Adenosine Signalling and Function in Glial Cells.

Extracellular adenosine levels are thought to be regulated by an astrocyte-based adenosine-cycle. Astrocytes can release ATP via vesicular release and/or by direct release through hemichannels (h-ch). Extracellular ATP is rapidly degraded into adenosine (ADO) by a series of ectonucleotidases. Adenosine can also be released directly via equilibrative nucleoside transporters (nt). Intracellularly adenosine levels are largely controlled by adenosine kinase, which is part of a substrate cycle between adenosine and AMP. Small changes in adenosine kinase activity rapidly translate into major changes in adenosine. Intracellular adenosine kinase is considered to be a metabolic reuptake system for adenosine. Only selected mechanisms and pathways are shown; for details please refer to main text.

Detlev Boison, et al. Cell Death Differ. ;17(7):1071-1082.
4.
Figure 3

Figure 3. From: Adenosine Signalling and Function in Glial Cells.

Role of the adenosine (ADO) / adenosine kinase (ADK) system in regulating acute and chronic responses to injury. Left: Within hours after brain injury (e.g. stroke, trauma, prolonged seizures) a surge in micromolar levels of ADO results that protects the brain from further injury and from seizures. Hypoxia and trauma can directly lead to a rise in extracellular ATP that is rapidly degraded into adenosine. High levels of adenosine are known to inhibit ADK, further amplifying the adenosine surge. Right: The acute adenosine surge contributes to trigger astrogliosis via a variety of mechanisms that include modulation of astrocytic adenosine receptors (ARs), modulation of inflammatory processes and the release of cytokines. Astrogliosis leads to overexpression of ADK resulting in adenosine-deficiency, which contributes to seizure generation.

Detlev Boison, et al. Cell Death Differ. ;17(7):1071-1082.

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