Postsynaptic zinc potentiation elicited by KCl depolarization at hippocampal mossy fiber synapses

The hippocampal mossy fibers contain a substantial quantity of loosely-bound zinc in their glutamatergic presynaptic vesicles, which is released in synaptic transmission processes. Despite the large number of studies about this issue, the zinc changes related to short and long-term forms of potentia...

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Bibliographic Details
Published in:General physiology and biophysics 2017-07, Vol.36 (3), p.289-296
Main Authors: Bastos, Fatima Mc, Lopes, Sandra A, Corceiro, Vanessa N, Matias, Carlos M, Dionísio, Jose C, Sampaio Dos Aidos, Fernando Ds, Mendes, Paulo J, Santos, Rosa M, Quinta-Ferreira, Rosa M, Quinta-Ferreira, M Emilia
Format: Article
Language:English
Subjects:
Animals
Cells, Cultured
Female
Long-Term Potentiation - drug effects
Long-Term Potentiation - physiology
Membrane Potentials - drug effects
Membrane Potentials - physiology
Mossy Fibers, Hippocampal - drug effects
Mossy Fibers, Hippocampal - physiology
Neuronal Plasticity - drug effects
Neuronal Plasticity - physiology
Potassium Chloride - administration & dosage
Rats
Rats, Wistar
Synapses - drug effects
Synapses - physiology
Synaptic Transmission - drug effects
Synaptic Transmission - physiology
Zinc - metabolism
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Summary:The hippocampal mossy fibers contain a substantial quantity of loosely-bound zinc in their glutamatergic presynaptic vesicles, which is released in synaptic transmission processes. Despite the large number of studies about this issue, the zinc changes related to short and long-term forms of potentiation are not totally understood. This work focus on zinc signals associated with chemically-induced mossy fiber synaptic plasticity, in particular on postsynaptic zinc signals evoked by KCl depolarization. The signals were detected using the medium affinity fluorescent zinc indicator Newport Green. The application of large concentrations of KCl, 20 mM and 60 mM, in the extracellular medium evoked zinc potentiations that decreased and remained stable after washout of the first and the second media, respectively. These short and long-lasting enhancements are considered to be due to zinc entry into postsynaptic neurons. We have also observed that following established zinc potentiation, another application of 60 mM KCl only elicited further enhancement when combined with external zinc. These facts support the idea that the KCl-evoked presynaptic depolarization causes higher zinc release leading to zinc influx into the postsynaptic region.
ISSN:0231-5882
DOI:10.4149/gpb_2017001