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Research progress on circulating tumor cell detection in brain gliomas
Xiaodong Wang, Gang Yang
Journal of Translational Neuroscience. 2021, 6 (1): 1-6.
https://doi.org/10.3868/j.issn.2096-0689.2021.01.001
Glioma, the most common primary intracranial tumor, has high morbidity and mortality. The detection of circulating tumor cells (CTCs) is an important part of the liquid biopsy of gliomas. CTCs, carrying the genetic and biological information of tumor tissue, provide a new perspective and dimension for the study of tumor metastasis, progression, chemotherapy sensitivity and drug resistance. Cerebrospinal fluid (CSF) circulates through the ventricle and spinal cord cistern, which can better maintain the original information of tumor cells compared with the complicated environments of tissues and plasma. Study on the dynamic changes of CTCs in the CSF of the central nervous system (CNS) is relatively rare. However, the analysis of CTCs in CSF can be used to guide the treatment of gliomas and reveal the pathophysiological and genetic mechanisms of tumor cell metastasis to the CSF. This paper reviews the progress in the research on CTC detection in gliomas.
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Two mathematical frameworks for vesicle release from a ribbon synapse of a retinal bipolar cell
Hassan Bassereh, Frank Rattay
Journal of Translational Neuroscience. 2021, 6 (1): 7-28.
https://doi.org/10.3868/j.issn.2096-0689.2021.01.002
Objective: bipolar cells (BCs) communicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses. Reconstructing the published quantitative release data from electrical soma stimulation (voltage clamp experiments) of rat rod BCs were used to develop two simple models to predict the number of released vesicles as time series. In the experiment, the currents coming to the AII amacrine cell originating from releasing vesicles from the rod BC were recorded using paired-recordings in whole-cell voltage-clamp method. Method: one of the models is based directly on terminal transmembrane voltage, so-called ‘modelV’, whereas the temporally exacter modelCa includes changes of intracellular calcium concentrations at terminals. Result: the intracellular calcium concentration method replicates a 0.43 ms signal delay for the transient release to pulsatile stimulation as a consequence of calcium channel dynamics in the presynaptic membrane, while the modelV has no signal delay. Both models produce the quite similar results in low stimuli amplitudes. However, for large stimulation intensities that may be done during extracellular stimulations in retinal implants, the modelCa predicts that the reversal potential of calcium limits the number of transiently released vesicles. Adding sodium and potassium ion channels to the axon of the cell enable to study the impact of spikes on the transient release in BC ribbons. Conclusion: a spike elicited by somatic stimulation causes the rapid release of all vesicles that are available for transient release, while a non-spiking BC with a similar morphometry needs stronger stimuli for any transient vesicle release. During extracellular stimulation, there was almost no difference in transient release between the active and passive cells because in both cases the terminal membrane of the cell senses the same potentials originating from the microelectrode. An exception was found for long pulses when the spike has the possibility to generate a higher terminal voltage than the passive cell. Simulated periodic 5 Hz stimulation showed a reduced transient release of 3 vesicles per stimulus, which is a recovery effect.
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