Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity
GABAergic inhibition plays a critical role in the regulation of neuron excitability; thus, it is subject to modulations by many factors. Recent evidence suggests the elevation of intracellular calcium ([Ca2+]i) and calcium-dependent signaling molecules underlie the modulations. Caffeine induces a re...
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Wiley
2016-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2016/1239629 |
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| author | Masako Isokawa |
| author_facet | Masako Isokawa |
| author_sort | Masako Isokawa |
| collection | DOAJ |
| description | GABAergic inhibition plays a critical role in the regulation of neuron excitability; thus, it is subject to modulations by many factors. Recent evidence suggests the elevation of intracellular calcium ([Ca2+]i) and calcium-dependent signaling molecules underlie the modulations. Caffeine induces a release of calcium from intracellular stores. We tested whether caffeine modulated GABAergic transmission by increasing [Ca2+]i. A brief local puff-application of caffeine to hippocampal CA1 pyramidal cells transiently suppressed GABAergic inhibitory postsynaptic currents (IPSCs) by 73.2 ± 6.98%. Time course of suppression and the subsequent recovery of IPSCs resembled DSI (depolarization-induced suppression of inhibition), mediated by endogenous cannabinoids that require a [Ca2+]i rise. However, unlike DSI, caffeine-induced suppression of IPSCs (CSI) persisted in the absence of a [Ca2+]i rise. Intracellular applications of BAPTA and ryanodine (which blocks caffeine-induced calcium release from intracellular stores) failed to prevent the generation of CSI. Surprisingly, ruthenium red, an inhibitor of multiple calcium permeable/release channels including those of stores, induced metaplasticity by amplifying the magnitude of CSI independently of calcium. This metaplasticity was accompanied with the generation of a large inward current. Although ionic basis of this inward current is undetermined, the present result demonstrates that caffeine has a robust Ca2+-independent inhibitory action on GABAergic inhibition and causes metaplasticity by opening plasma membrane channels. |
| format | Article |
| id | doaj-art-2b6c7621d005462dadc66f7ed7512128 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-2b6c7621d005462dadc66f7ed75121282025-02-03T01:12:13ZengWileyNeural Plasticity2090-59041687-54432016-01-01201610.1155/2016/12396291239629Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent MetaplasticityMasako Isokawa0Department of Health and Biomedical Sciences, The University of Texas Rio Grande Valley, One West University Boulevard, Brownsville, TX 78520, USAGABAergic inhibition plays a critical role in the regulation of neuron excitability; thus, it is subject to modulations by many factors. Recent evidence suggests the elevation of intracellular calcium ([Ca2+]i) and calcium-dependent signaling molecules underlie the modulations. Caffeine induces a release of calcium from intracellular stores. We tested whether caffeine modulated GABAergic transmission by increasing [Ca2+]i. A brief local puff-application of caffeine to hippocampal CA1 pyramidal cells transiently suppressed GABAergic inhibitory postsynaptic currents (IPSCs) by 73.2 ± 6.98%. Time course of suppression and the subsequent recovery of IPSCs resembled DSI (depolarization-induced suppression of inhibition), mediated by endogenous cannabinoids that require a [Ca2+]i rise. However, unlike DSI, caffeine-induced suppression of IPSCs (CSI) persisted in the absence of a [Ca2+]i rise. Intracellular applications of BAPTA and ryanodine (which blocks caffeine-induced calcium release from intracellular stores) failed to prevent the generation of CSI. Surprisingly, ruthenium red, an inhibitor of multiple calcium permeable/release channels including those of stores, induced metaplasticity by amplifying the magnitude of CSI independently of calcium. This metaplasticity was accompanied with the generation of a large inward current. Although ionic basis of this inward current is undetermined, the present result demonstrates that caffeine has a robust Ca2+-independent inhibitory action on GABAergic inhibition and causes metaplasticity by opening plasma membrane channels.http://dx.doi.org/10.1155/2016/1239629 |
| spellingShingle | Masako Isokawa Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity Neural Plasticity |
| title | Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity |
| title_full | Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity |
| title_fullStr | Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity |
| title_full_unstemmed | Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity |
| title_short | Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity |
| title_sort | caffeine induced suppression of gabaergic inhibition and calcium independent metaplasticity |
| url | http://dx.doi.org/10.1155/2016/1239629 |
| work_keys_str_mv | AT masakoisokawa caffeineinducedsuppressionofgabaergicinhibitionandcalciumindependentmetaplasticity |