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GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation.
Cerebellum. 2020 Jul 02 [Online ahead of print]C

Abstract

G-protein-coupled inwardly rectifying potassium (GIRK) channels contribute to the resting membrane potential of many neurons and play an important role in controlling neuronal excitability. Although previous studies have revealed a high expression of GIRK subunits in the cerebellum, their functional role has never been clearly described. Using patch-clamp recordings in mice cerebellar slices, we examined the properties of the GIRK currents in Purkinje cells (PCs) and investigated the effects of a selective agonist of GIRK1-containing channels, ML297 (ML), on PC firing and synaptic plasticity. We demonstrated that GIRK channel activation decreases the PC excitability by inhibiting both sodium and calcium spikes and, in addition, modulates the complex spike response evoked by climbing fiber stimulation. Our results indicate that GIRK channels have also a marked effect on synaptic plasticity of the parallel fiber-PC synapse, as the application of ML297 increased the expression of LTP while preventing LTD. We, therefore, propose that the recruitment of GIRK channels represents a crucial mechanism by which neuromodulators can control synaptic strength and membrane conductance for proper refinement of the neural network involved in memory storage and higher cognitive functions.

Authors+Show Affiliations

Department of Pharmacy, School of Medicine, University of Naples Federico II, Naples, Italy.Department of Neuroscience, University of Turin, Turin, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Turin, Italy.Department of Neuroscience, University of Turin, Turin, Italy. filippo.tempia@unito.it. Neuroscience Institute Cavalieri Ottolenghi (NICO), Turin, Italy. filippo.tempia@unito.it. National Institute of Neuroscience (INN), Turin, Italy. filippo.tempia@unito.it.Department of Pharmacy, School of Medicine, University of Naples Federico II, Naples, Italy. maria.miniaci@unina.it.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32617840

Citation

Lippiello, Pellegrino, et al. "GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation." Cerebellum (London, England), 2020.
Lippiello P, Hoxha E, Tempia F, et al. GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation. Cerebellum. 2020.
Lippiello, P., Hoxha, E., Tempia, F., & Miniaci, M. C. (2020). GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation. Cerebellum (London, England). https://doi.org/10.1007/s12311-020-01158-y
Lippiello P, et al. GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation. Cerebellum. 2020 Jul 2; PubMed PMID: 32617840.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation. AU - Lippiello,Pellegrino, AU - Hoxha,Eriola, AU - Tempia,Filippo, AU - Miniaci,Maria Concetta, Y1 - 2020/07/02/ PY - 2020/7/4/entrez KW - Cerebellum KW - GIRK KW - Neuromodulation KW - Purkinje cell KW - Synaptic plasticity JF - Cerebellum (London, England) JO - Cerebellum N2 - G-protein-coupled inwardly rectifying potassium (GIRK) channels contribute to the resting membrane potential of many neurons and play an important role in controlling neuronal excitability. Although previous studies have revealed a high expression of GIRK subunits in the cerebellum, their functional role has never been clearly described. Using patch-clamp recordings in mice cerebellar slices, we examined the properties of the GIRK currents in Purkinje cells (PCs) and investigated the effects of a selective agonist of GIRK1-containing channels, ML297 (ML), on PC firing and synaptic plasticity. We demonstrated that GIRK channel activation decreases the PC excitability by inhibiting both sodium and calcium spikes and, in addition, modulates the complex spike response evoked by climbing fiber stimulation. Our results indicate that GIRK channels have also a marked effect on synaptic plasticity of the parallel fiber-PC synapse, as the application of ML297 increased the expression of LTP while preventing LTD. We, therefore, propose that the recruitment of GIRK channels represents a crucial mechanism by which neuromodulators can control synaptic strength and membrane conductance for proper refinement of the neural network involved in memory storage and higher cognitive functions. SN - 1473-4230 UR - https://www.unboundmedicine.com/medline/citation/32617840/GIRK1-Mediated_Inwardly_Rectifying_Potassium_Current_Is_a_Candidate_Mechanism_Behind_Purkinje_Cell_Excitability,_Plasticity,_and_Neuromodulation L2 - https://dx.doi.org/10.1007/s12311-020-01158-y DB - PRIME DP - Unbound Medicine ER -
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