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The role of Ca 2+ ‐dependent K + ‐ channels at the rat corticostriatal synapses revealed by paired pulse stimulation
Author(s) -
Robles Gómez Angel A.,
Vega Ana V.,
GónzalezSandoval Carolina,
Barral Jaime
Publication year - 2018
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.22017
Subject(s) - stimulation , pulse (music) , synapse , neuroscience , chemistry , physics , biophysics , biology , voltage , quantum mechanics
Potassium channels play an important role in modulating synaptic activity both at presynaptic and postsynaptic levels. We have shown before that presynaptically located K V and K IR channels modulate the strength of corticostriatal synapses in rat brain, but the role of other types of potassium channels at these synapses remains largely unknown. Here, we show that calcium‐dependent potassium channels BK‐type but not SK‐type channels are located presynaptically in corticostriatal synapses. We stimulated cortical neurons in rat brain slices and recorded postsynaptic excitatory potentials (EPSP) in medium spiny neurons (MSN) in dorsal neostriatum. By using a paired pulse protocol, we induced synaptic facilitation before applying either BK‐ or SK‐specific toxins. Thus, we found that blockage of BK Ca with iberiotoxin (10 nM) reduces synaptic facilitation and increases the amplitude of the EPSP, while exposure to SK‐blocker apamin (100 nM) has no effect. Additionally, we induced train action potentials on striatal MSN by current injection before and after the exposure to K Ca toxins. We found that the action potential becomes broader when the MSN is exposed to iberiotoxin, although it has no impact on frequency. In contrast, exposure to apamin results in loss of afterhyperpolarization phase and an increase of spike frequency. Therefore, we concluded that postsynaptic SK channels are involved in afterhyperpolarization and modulation of spike frequency while the BK channels are involved on the late repolarization phase of the action potential. Altogether, our results show that calcium‐dependent potassium channels modulate both input towards and output from the striatum.

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