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Study Of Adenosine-induced Calcium Dynamics In DRG Neurons By Optical Detection And Microscopy

Posted on:2015-06-11Degree:MasterType:Thesis
Country:ChinaCandidate:J X ChenFull Text:PDF
GTID:2180330467961628Subject:Optical Engineering
Abstract/Summary:PDF Full Text Request
Pain influences many aspects of human life. Acupuncture has significant effects especially on pain though the mechanism of it is not yet clear. Adenosine is an important signal molecules involving the process of acupuncture analgesia. Moreover, many neural physiological processes are closely concerned with cellular Ca2+level. Above all, investigation of effects of adenosine on Ca2+dynamics in neuron is useful to learn more about the mechanism of acupuncture analgesia in the cellular and molecular level. This paper investigates the relationship between pain signal molecular adenosine and second messenger Ca2+based on optical detection and microscope imaging technology, which aiming at revealing molecular mechanism of acupuncture analgesia. First, we identify expression level of adenosine receptors in DRG neurons by single photon imaging technology and immunofluorescence antibody technique, results showed that four types of ARs are all expressed in DRG neurons. Secondly, Ca2+dynamics induced by different concentrations of adenosine and possible ways causing this dynamics was studied by optical detection and imaging technology combined with specific Ca2+fluorescent probe Fluo4/AM, results showed that adenosine induced elevation of cellular Ca2+level, and it was dose dependent with adenosine concentration. Moreover, Ca2+release from intracellular Ca2+stores was the main cause of Ca2+elevation. Finally, mechanism of adenosine effects on intracellular Ca2+release was studied by specific agonist and antagonist of adenosine receptors, results showed that the adenosine A1and A3receptors may involve Ca2+release in DRG neurons induced by adenosine.
Keywords/Search Tags:optical detection and imaging, adenosine, Ca2+, laser confocal microscopy
PDF Full Text Request
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