Dysregulation of Intracellular Ca2+ and Camp Signalling: Plausible Targets for Neurological Disorders
Received Date: Mar 05, 2018 / Accepted Date: Mar 07, 2018 / Published Date: Mar 12, 2018
My current field of research involves the study of the interaction between Ca2+ and cAMP signalling pathways, including its role in neurological disorders. The scientific literature now clearly accepts this interaction as a fundamental cellular process, which is also involved in synaptic transmission mainly by controlling neurotransmitter release . In several synapses, Ca2+ signalling has been considered as one of the main actors in this arena! Almost every undergraduate student knows that elevating Ca2+ within neuronal cells is crucial to start the release of neurotransmitter! Indeed, Ca2+ is an ion that participates in almost everything within the steps of neurotransmitter release. However, its dysregulation may lead to toxic effects, growing into diseases like the neurological disorders. This concept is newer and, probably, not all students know it! Indeed, dysregulations of intracellular Ca2+ signalling achieved, for example, due to an excess of Ca2+ influx through voltageactivated Ca2+ channels, and yet disturbances of Ca2+ release from ryanodine and/or IP3-sensitive intracellular Ca2+ stores have been reported in age-related animal models . Several of these alterations in Ca2+ signalling, described in normal aging, can be replicated by exposing neurons to oxidative and metabolic stress in culture or in vivo, suggesting important contributions of essential aging mechanisms to the dysregulation of neuronal Ca2+ signalling in neurological disorders, such as in Alzheimer´s disease (AD). Furthermore, reports from brain tissue samples performed through brains of AD patients, and animal models of AD, have discovered significant changes in levels of proteins and genes directly related to neuronal Ca2+ signalling . Not surprisingly, environmental factors that prevent amyloidogenesis (caloric restriction, cognitive stimulation, and antioxidants) alleviate neuronal Ca2+ signalling dysregulation, whereas factors that improve amyloidogenesis disrupt Ca2+ homeostasis.
As I stated in the beginning of this editorial, my current field of research involves the study of the interaction betweenCa2+ and cAMP signalling pathways (Ca2+/cAMP signalling interaction). Indeed, considering the dysregulation of Ca2+ signalling in neurological disorders, now became quite interesting the study of such interaction yet in neurological disorders. The cumulative knowledge in the field clearly accepts that ryanodine and/or IP3-sensitive intracellular Ca2+ stores can be modulated by cAMP, whose rise within cells achieves the release of Ca2+ from these stores. As stated above, considering the excess of intracellular Ca2+ presented in neurological disorders, the levels of cAMP within neurons may also be dysregulated due to the Ca2+/cAMP signalling interaction [3-10], thus yet affecting the release of Ca2+ from intracellular stores. Modern methodologies, which include fluorescence probes targeting Ca2+ and cAMP may provide novel insights in this arena! I am looking forward to obtaining these results!
Bergantin thanks the continued financial support from CAPES, CNPq and FAPESP (Bergantin´s Postdoctoral Fellowship FAPESP #2014/10274-3) and Prof. Afonso Caricati-Neto for the continued support.
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Citation: Bergantin LB (2018) Dysregulation of Intracellular Ca2+ and Camp Signalling:Plausible Targets for Neurological Disorders. J Neurol Disord 6: e125. DOI: 10.4172/2329-6895.1000e125
Copyright: © 2018 Bergantin LB. 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.
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