G protein-gated inwardly rectifying potassium channel subunits 1 and 2 are down-regulated in rat dorsal root ganglion neurons and spinal cord after peripheral axotomy.

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Abstract

Increased nociceptive neuronal excitability underlies chronic pain conditions. Various ion channels, including sodium, calcium and potassium channels have pivotal roles in the control of neuronal excitability. The members of the family of G protein-gated inwardly rectifying potassium (GIRK) channels, GIRK1-4, have been implicated in modulating excitability. Here, we investigated the expression and distribution of GIRK1 and GIRK2 in normal and injured dorsal root ganglia (DRGs) and spinal cord of rats.

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Emerging roles for G protein-gated inwardly rectifying potassium (GIRK) channels in health and disease.

Christian Lüscher, Paul A. Slesinger (2010)

G protein-gated inwardly rectifying potassium (GIRK) channels hyperpolarize neurons in response to activation of many different G protein-coupled receptors and thus control the excitability of neurons through GIRK-mediated self-inhibition, slow synaptic potentials and volume transmission. GIRK channel function and trafficking are highly dependent on the channel subunit composition. Pharmacological investigations of GIRK channels and studies in animal models suggest that GIRK activity has an important role in physiological responses, including pain perception and memory modulation. Moreover, abnormal GIRK function has been implicated in altering neuronal excitability and cell death, which may be important in the pathophysiology of diseases such as epilepsy, Down's syndrome, Parkinson's disease and drug addiction. GIRK channels may therefore prove to be a valuable new therapeutic target.

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Regulating excitability of peripheral afferents: emerging ion channel targets.

Stephen G. Waxman, Gerald Zamponi (2014)

The transmission and processing of pain signals relies critically on the activities of ion channels that are expressed in afferent pain fibers. This includes voltage-gated channels, as well as background (or leak) channels that collectively regulate resting membrane potential and action potential firing properties. Dysregulated ion channel expression in response to nerve injury and inflammation results in enhanced neuronal excitability that underlies chronic neuropathic and inflammatory pain. Pharmacological modulators of ion channels, particularly those that target channels on peripheral neurons, are being pursued as possible analgesics. Over the past few years, a number of different types of ion channels have been implicated in afferent pain signaling. Here we give an overview of recent advances on sodium, calcium, potassium and chloride channels that are emerging as especially attractive targets for the treatment of pain.

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Physiology, signaling, and pharmacology of galanin peptides and receptors: three decades of emerging diversity.

Roland Lang, Andrew L. Gundlach, Fiona E Holmes … (2015)

Galanin was first identified 30 years ago as a "classic neuropeptide," with actions primarily as a modulator of neurotransmission in the brain and peripheral nervous system. Other structurally-related peptides-galanin-like peptide and alarin-with diverse biologic actions in brain and other tissues have since been identified, although, unlike galanin, their cognate receptors are currently unknown. Over the last two decades, in addition to many neuronal actions, a number of nonneuronal actions of galanin and other galanin family peptides have been described. These include actions associated with neural stem cells, nonneuronal cells in the brain such as glia, endocrine functions, effects on metabolism, energy homeostasis, and paracrine effects in bone. Substantial new data also indicate an emerging role for galanin in innate immunity, inflammation, and cancer. Galanin has been shown to regulate its numerous physiologic and pathophysiological processes through interactions with three G protein-coupled receptors, GAL1, GAL2, and GAL3, and signaling via multiple transduction pathways, including inhibition of cAMP/PKA (GAL1, GAL3) and stimulation of phospholipase C (GAL2). In this review, we emphasize the importance of novel galanin receptor-specific agonists and antagonists. Also, other approaches, including new transgenic mouse lines (such as a recently characterized GAL3 knockout mouse) represent, in combination with viral-based techniques, critical tools required to better evaluate galanin system physiology. These in turn will help identify potential targets of the galanin/galanin-receptor systems in a diverse range of human diseases, including pain, mood disorders, epilepsy, neurodegenerative conditions, diabetes, and cancer. Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics.

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Author and article information

Journal

Journal ID (iso-abbrev): Mol Pain

Title: Molecular pain

Publisher: Springer Science and Business Media LLC

ISSN (Electronic): 1744-8069

ISSN (Print): 1744-8069

Publication date (Electronic): Jul 22 2015

Volume: 11

Affiliations

[1 ] School of Life Science and Technology, Harbin Institute of Technology, 150001, Harbin, China. htylv123@126.com.

[2 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. htylv123@126.com.

[3 ] Department of Neuroscience, Science for Life Laboratory, Karolinska Institutet, 171 77, Stockholm, Sweden. Jan.Mulder@ki.se.

[4 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Swapnali.Barde@ki.se.

[5 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Kristoffer.Sahlholm@ki.se.

[6 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Hugo.Zeberg@ki.se.

[7 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Johanna.Nilsson@ki.se.

[8 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Peter.Arhem@ki.se.

[9 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Tomas.Hokfelt@ki.se.

[10 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. Kaj.Fried@ki.se.

[11 ] School of Life Science and Technology, Harbin Institute of Technology, 150001, Harbin, China. tjstenshi@gmail.com.

[12 ] Department of Neuroscience, Karolinska Institutet, 171 77, Stockholm, Sweden. tjstenshi@gmail.com.

Article

Publisher Item ID: 10.1186/s12990-015-0044-z

DOI: 10.1186/s12990-015-0044-z

PMC ID: 4511542

PubMed ID: 26199148

SO-VID: 3920dc4b-ab64-498d-bff3-de6368fea5e2

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G protein-gated inwardly rectifying potassium channel subunits 1 and 2 are down-regulated in rat dorsal root ganglion neurons and spinal cord after peripheral axotomy.

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Abstract

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Most cited references 108

Emerging roles for G protein-gated inwardly rectifying potassium (GIRK) channels in health and disease.

Regulating excitability of peripheral afferents: emerging ion channel targets.

Physiology, signaling, and pharmacology of galanin peptides and receptors: three decades of emerging diversity.

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Cited by 8

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