By Hiroshi Kase
This e-book is the 1st definitive assessment on adenosine receptor antagonists and their program to the remedy of Parkinson's affliction. The influence of those novel non-dopamine medications on vitro and in vivo structures sincerely indicates their power for the remedy of this debilitating affliction. This booklet covers how the Parkinson's affliction antagonist drug, A2A, has been researched, constructed, and validated. it's an important e-book for researchers drawn to the basal ganglia, purine biology, and Parkinson's affliction. Key positive aspects* Discusses the invention and improvement of a singular non-dopaminomimetic agent for Parkinson's disorder* offers the 1st definitive assessment of adenosine antagonists and their function within the therapy of Parkinson's sickness* provides a brand new mechanism of motion of adenosine A2A receptor antagonists in motor functionProposes a speculation of adenosine A2A receptor functionality within the striatum* entire evaluation of adenosine, its receptor subtypes, their antagonists/agonists from biochemistry, molecular biology, medicinal chemistry, body structure, pharmacology, and neurochemistry viewpoints
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Extra info for Adenosine Receptors and Parkinson's Disease
Membranes from rat striatum, otherwise noted. from rhesus monkey cortex. from rhesus monkey striatum. from HEK-293 cells stably transfected with recombinant The most intensively investigated class of adenosine A 1 antagonists besides the xanthines are adenine derivatives. These compounds are derived from the physiological agonist adenosine, but they lack the ribose moiety that is necessary for receptor activation. , 1987). , 1996), which is a potent Al-selective adenosine receptor antagonist. The chemical structures and adenosine receptor binding affinity of representative adenosine A 1 antagonists are shown in Figure 1 and Table I, respectively.
1994). , 1995). 2. Central Nervous System receptors in hippocampus are densely concentrated in the CA1 and CA3 regions (Onodera and Kogure, 1988). In general, the presynaptic A 1 receptors cause an inhibition of the release of neurotransmitters and the postsynaptic A 1 receptors cause a decrease in excitability (Dunwiddie and Fredholm, 1989). , 1990). LTP is one of the most striking examples of synaptic plasticity, which is postulated to underly learning and memory. From these results, A1 antagonists might be expected to enhance the release of various neurotransmitters, such as acetylcholine to depolarize postsynaptic neurons and to increase LTP (Suzuki, 1992).
40. , Adenosine A2B-receptor-mediated cyclic AMP accumulation in primary rat astrocytes. BrJ Pharmacol, 111 (1994) 191-198. 41. Peterfreund, R. , and Fink, J. , Characterization and expression of the human A2Aadenosine receptor gene. J Neurochem, 66 (1996) 362-368. 42. , Molecular cloning and expression of an adenosine A2B receptor from human brain. Biochem Biophys Res Commun, 187 (1992) 86-93. 43. , Production and characterization of multiple antigenic peptide antibodies to the adenosine A2Breceptor.
Adenosine Receptors and Parkinson's Disease by Hiroshi Kase