KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat
In the last years it has been increasingly clear that KV-channel activity modulates neurotransmitter release. The subcellular localization and composition of potassium channels are crucial to understanding its influence on neurotransmitter release. To investigate the role of KV in corticostriatal sy...
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Wiley
2016-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2016/8782518 |
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| author | David Meneses Ana V. Vega Francisco Miguel Torres-Cruz Jaime Barral |
| author_facet | David Meneses Ana V. Vega Francisco Miguel Torres-Cruz Jaime Barral |
| author_sort | David Meneses |
| collection | DOAJ |
| description | In the last years it has been increasingly clear that KV-channel activity modulates neurotransmitter release. The subcellular localization and composition of potassium channels are crucial to understanding its influence on neurotransmitter release. To investigate the role of KV in corticostriatal synapses modulation, we combined extracellular recording of population-spike and pharmacological blockage with specific and nonspecific blockers to identify several families of KV channels. We induced paired-pulse facilitation (PPF) and studied the changes in paired-pulse ratio (PPR) before and after the addition of specific KV blockers to determine whether particular KV subtypes were located pre- or postsynaptically. Initially, the presence of KV channels was tested by exposing brain slices to tetraethylammonium or 4-aminopyridine; in both cases we observed a decrease in PPR that was dose dependent. Further experiments with tityustoxin, margatoxin, hongotoxin, agitoxin, dendrotoxin, and BDS-I toxins all rendered a reduction in PPR. In contrast heteropodatoxin and phrixotoxin had no effect. Our results reveal that corticostriatal presynaptic KV channels have a complex stoichiometry, including heterologous combinations KV1.1, KV1.2, KV1.3, and KV1.6 isoforms, as well as KV3.4, but not KV4 channels. The variety of KV channels offers a wide spectrum of possibilities to regulate neurotransmitter release, providing fine-tuning mechanisms to modulate synaptic strength. |
| format | Article |
| id | doaj-art-a8fc3e3ae957419fa20f28d8e923f08a |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
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| series | Neural Plasticity |
| spelling | doaj-art-a8fc3e3ae957419fa20f28d8e923f08a2025-02-03T05:51:28ZengWileyNeural Plasticity2090-59041687-54432016-01-01201610.1155/2016/87825188782518KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in RatDavid Meneses0Ana V. Vega1Francisco Miguel Torres-Cruz2Jaime Barral3Neurociencias (UIICSE), FES Iztacala, Universidad Nacional Autónoma de México (UNAM), 54090 Tlalnepantla, MEX, MexicoCarrera de Médico Cirujano (UBIMED), FES Iztacala, Universidad Nacional Autónoma de México (UNAM), 54090 Tlalnepantla, MEX, MexicoNeurociencias (UIICSE), FES Iztacala, Universidad Nacional Autónoma de México (UNAM), 54090 Tlalnepantla, MEX, MexicoNeurociencias (UIICSE), FES Iztacala, Universidad Nacional Autónoma de México (UNAM), 54090 Tlalnepantla, MEX, MexicoIn the last years it has been increasingly clear that KV-channel activity modulates neurotransmitter release. The subcellular localization and composition of potassium channels are crucial to understanding its influence on neurotransmitter release. To investigate the role of KV in corticostriatal synapses modulation, we combined extracellular recording of population-spike and pharmacological blockage with specific and nonspecific blockers to identify several families of KV channels. We induced paired-pulse facilitation (PPF) and studied the changes in paired-pulse ratio (PPR) before and after the addition of specific KV blockers to determine whether particular KV subtypes were located pre- or postsynaptically. Initially, the presence of KV channels was tested by exposing brain slices to tetraethylammonium or 4-aminopyridine; in both cases we observed a decrease in PPR that was dose dependent. Further experiments with tityustoxin, margatoxin, hongotoxin, agitoxin, dendrotoxin, and BDS-I toxins all rendered a reduction in PPR. In contrast heteropodatoxin and phrixotoxin had no effect. Our results reveal that corticostriatal presynaptic KV channels have a complex stoichiometry, including heterologous combinations KV1.1, KV1.2, KV1.3, and KV1.6 isoforms, as well as KV3.4, but not KV4 channels. The variety of KV channels offers a wide spectrum of possibilities to regulate neurotransmitter release, providing fine-tuning mechanisms to modulate synaptic strength.http://dx.doi.org/10.1155/2016/8782518 |
| spellingShingle | David Meneses Ana V. Vega Francisco Miguel Torres-Cruz Jaime Barral KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat Neural Plasticity |
| title | KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat |
| title_full | KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat |
| title_fullStr | KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat |
| title_full_unstemmed | KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat |
| title_short | KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat |
| title_sort | kv1 and kv3 potassium channels identified at presynaptic terminals of the corticostriatal synapses in rat |
| url | http://dx.doi.org/10.1155/2016/8782518 |
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