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Article: Chloride regulation in the pain pathway.

Price, Theodore J / Cervero, Fernando / Gold, Michael S / Hammond, Donna L / Prescott, Steven A

2008 Volume 60, Issue 1, Page(s) 149–170

Abstract: ... inhibition is dynamically regulated, mechanisms underlying the regulation of inhibition have turned out to be ... that an exquisitely sensitive form of regulation involves changes in anion equilibrium potential (E(anion ... NKCC1 and KCC2) have emerged as proteins that play a critical role in the dynamic regulation of E(anion ...

Abstract	Melzack and Wall's Gate Control Theory of Pain laid the theoretical groundwork for a role of spinal inhibition in endogenous pain control. While the Gate Control Theory was based on the notion that spinal inhibition is dynamically regulated, mechanisms underlying the regulation of inhibition have turned out to be far more complex than Melzack and Wall could have ever imagined. Recent evidence indicates that an exquisitely sensitive form of regulation involves changes in anion equilibrium potential (E(anion)), which subsequently impacts fast synaptic inhibition mediated by GABA(A), and to a lesser extent, glycine receptor activation, the prototypic ligand gated anion channels. The cation-chloride co-transporters (in particular NKCC1 and KCC2) have emerged as proteins that play a critical role in the dynamic regulation of E(anion) which in turn appears to play a critical role in hyperalgesia and allodynia following peripheral inflammation or nerve injury. This review summarizes the current state of knowledge in this area with particular attention to how such findings relate to endogenous mechanisms of hyperalgesia and allodynia and potential applications for therapeutics based on modulation of intracellular Cl(-) gradients or pharmacological interventions targeting GABA(A) receptors.
MeSH term(s)	Animals ; Chloride Channels/metabolism ; Chlorides/metabolism ; Humans ; Hyperalgesia/metabolism ; Hyperalgesia/physiopathology ; Ion Channel Gating/physiology ; Nervous System/metabolism ; Nervous System/physiopathology ; Neural Inhibition/physiology ; Nociceptors/metabolism ; Pain/metabolism ; Pain/physiopathology ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Symporters/metabolism ; K Cl- Cotransporters
Chemical Substances	Chloride Channels ; Chlorides ; SLC12A2 protein, human ; Sodium-Potassium-Chloride Symporters ; Solute Carrier Family 12, Member 2 ; Symporters
Language	English
Publishing date	2008-12-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	423722-5
ISSN	1872-6321 ; 0165-0173
ISSN (online)	1872-6321
ISSN	0165-0173
DOI	10.1016/j.brainresrev.2008.12.015
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Article ; Online: Neurodegeneration Upon Dysfunction of Endosomal/Lysosomal CLC Chloride Transporters

Shroddha Bose / Hailan He / Tobias Stauber

Frontiers in Cell and Developmental Biology, Vol

2021 Volume 9

Abstract: The regulation of luminal ion concentrations is critical for the function of, and transport between ... of ion transporters and channels is involved in the regulation of the organelles' complex ion homeostasis ... regulation, has been associated with lysosomal storage diseases in general. This review discusses ...

Abstract	The regulation of luminal ion concentrations is critical for the function of, and transport between intracellular organelles. The importance of the acidic pH in the compartments of the endosomal-lysosomal pathway has been well-known for decades. Besides the V-ATPase, which pumps protons into their lumen, a variety of ion transporters and channels is involved in the regulation of the organelles' complex ion homeostasis. Amongst these are the intracellular members of the CLC family, ClC-3 through ClC-7. They localize to distinct but overlapping compartments of the endosomal-lysosomal pathway, partially with tissue-specific expression. Functioning as 2Cl−/H+ exchangers, they can support the vesicular acidification and accumulate luminal Cl−. Mutations in the encoding genes in patients and mouse models underlie severe phenotypes including kidney stones with CLCN5 and osteopetrosis or hypopigmentation with CLCN7. Dysfunction of those intracellular CLCs that are expressed in neurons lead to neuronal defects. Loss of endosomal ClC-3, which heteromerizes with ClC-4, results in neurodegeneration. Mutations in ClC-4 are associated with epileptic encephalopathy and intellectual disability. Mice lacking the late endosomal ClC-6 develop a lysosomal storage disease with reduced pain sensitivity. Human gene variants have been associated with epilepsy, and a gain-of-function mutation causes early-onset neurodegeneration. Dysfunction of the lysosomal ClC-7 leads to a lysosomal storage disease and neurodegeneration in mice and humans. Reduced luminal chloride, as well as altered calcium regulation, has been associated with lysosomal storage diseases in general. This review discusses the properties of endosomal and lysosomal Cl−/H+ exchange by CLCs and how various alterations of ion transport by CLCs impact organellar ion homeostasis and function in neurodegenerative disorders.
Keywords	autophagy ; chloride transport ; endosome ; ion homeostasis ; lysosome ; neurodegeneration ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Combined Changes in Chloride Regulation and Neuronal Excitability Enable Primary Afferent Depolarization to Elicit Spiking without Compromising its Inhibitory Effects.

Takkala, Petri / Zhu, Yi / Prescott, Steven A

PLoS computational biology

2016 Volume 12, Issue 11, Page(s) e1005215

Abstract: ... could contribute to pain in the case of nociceptive fibers. PAD-induced spiking is assumed to override presynaptic ... receptors (GABAAR) because their intracellular chloride concentration is maintained above electrochemical ...

Abstract	The central terminals of primary afferent fibers experience depolarization upon activation of GABAA receptors (GABAAR) because their intracellular chloride concentration is maintained above electrochemical equilibrium. Primary afferent depolarization (PAD) normally mediates inhibition via sodium channel inactivation and shunting but can evoke spikes under certain conditions. Antidromic (centrifugal) conduction of these spikes may contribute to neurogenic inflammation while orthodromic (centripetal) conduction could contribute to pain in the case of nociceptive fibers. PAD-induced spiking is assumed to override presynaptic inhibition. Using computer simulations and dynamic clamp experiments, we sought to identify which biophysical changes are required to enable PAD-induced spiking and whether those changes necessarily compromise PAD-mediated inhibition. According to computational modeling, a depolarizing shift in GABA reversal potential (EGABA) and increased intrinsic excitability (manifest as altered spike initiation properties) were necessary for PAD-induced spiking, whereas increased GABAAR conductance density (ḡGABA) had mixed effects. We tested our predictions experimentally by using dynamic clamp to insert virtual GABAAR conductances with different EGABA and kinetics into acutely dissociated dorsal root ganglion (DRG) neuron somata. Comparable experiments in central axon terminals are prohibitively difficult but the biophysical requirements for PAD-induced spiking are arguably similar in soma and axon. Neurons from naïve (i.e. uninjured) rats were compared before and after pharmacological manipulation of intrinsic excitability, and against neurons from nerve-injured rats. Experimental data confirmed that, in most neurons, both predicted changes were necessary to yield PAD-induced spiking. Importantly, such changes did not prevent PAD from inhibiting other spiking or from blocking spike propagation. In fact, since the high value of ḡGABA required for PAD-induced spiking still mediates strong inhibition, we conclude that PAD-induced spiking does not represent failure of presynaptic inhibition. Instead, diminished PAD caused by reduction of ḡGABA poses a greater risk to presynaptic inhibition and the sensory processing that relies upon it.
MeSH term(s)	Action Potentials/physiology ; Afferent Pathways/physiology ; Animals ; Cells, Cultured ; Chlorine/metabolism ; Computer Simulation ; Male ; Membrane Potentials/physiology ; Models, Neurological ; Neural Inhibition/physiology ; Neurons, Afferent/physiology ; Presynaptic Terminals/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA/metabolism
Chemical Substances	Receptors, GABA ; Chlorine (4R7X1O2820)
Language	English
Publishing date	2016-11-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2193340-6
ISSN	1553-7358 ; 1553-734X
ISSN (online)	1553-7358
ISSN	1553-734X
DOI	10.1371/journal.pcbi.1005215
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Article: Analgesic effect of intrathecal bumetanide is accompanied by changes in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain.

He, Yanbing / Xu, Shiyuan / Huang, Junjie / Gong, Qingjuan

Neural regeneration research

2014 Volume 9, Issue 10, Page(s) 1055–1062

Abstract: ... through chloride regulation in the pain pathway and by effecting neuronal excitability and pain sensitization ... potassium-chloride co-transporter 2 have a role in the modulation of pain transmission at the spinal level ... potassium-chloride co-transporter 2 expression in a rat model of incisional pain. Results showed that intrathecal ...

Abstract	Accumulating evidence has demonstrated that the sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 have a role in the modulation of pain transmission at the spinal level through chloride regulation in the pain pathway and by effecting neuronal excitability and pain sensitization. The present study aimed to investigate the analgesic effect of the specific sodium-potassium-chloride co-transporter 1 inhibitor bumetanide, and the change in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain. Results showed that intrathecal bumetanide could decrease cumulative pain scores, and could increase thermal and mechanical pain thresholds in a rat model of incisional pain. Sodium-potassium-chloride co-transporter 1 expression increased in neurons from dorsal root ganglion and the deep laminae of the ipsilateral dorsal horn following incision. By contrast, potassium-chloride co-transporter 2 expression decreased in neurons of the deep laminae from the ipsilateral dorsal horn. These findings suggest that spinal sodium-potassium-chloride co-transporter 1 expression was up-regulated and spinal potassium-chloride co-transporter 2 expression was down-regulated following incision. Intrathecal bumetanide has analgesic effects on incisional pain through inhibition of sodium-potassium-chloride co-transporter 1.
Language	English
Publishing date	2014-08-26
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.133170
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Article: On the mechanism of antidepressant-like action of berberine chloride.

Kulkarni, Shrinivas K / Dhir, Ashish

European journal of pharmacology

2008 Volume 589, Issue 1-3, Page(s) 163–172

Abstract: ... serotonin and dopamine). Further, nitric oxide pathway and/or sigma receptors are involved in mediating ... chloride in different behavioural paradigms of despair. Berberine (5, 10, 20 mg/kg, i.p.) inhibited ...

Abstract	Berberine, an alkaloid isolated from Berberis aristata Linn. has been used in the Indian system of medicines as a stomachic, bitter tonic, antiamoebic and also in the treatment of oriental sores. Evidences have demonstrated that berberine possesses central nervous system activities, particularly the ability to inhibit monoamine oxidase-A, an enzyme involved in the degradation of norepinephrine and serotonin (5-HT). With this background, the present study was carried out to elucidate the antidepressant-like effect of berberine chloride in different behavioural paradigms of despair. Berberine (5, 10, 20 mg/kg, i.p.) inhibited the immobility period in mice in both forced swim and tail-suspension test, however, the effect was not dose-dependent. Berberine (5 and 10 mg/kg, i.p.) also reversed the reserpine-induced behavioral despair. Berberine (5 mg/kg, i.p.) enhanced the anti-immobility effect of subeffective doses of various typical but not atypical antidepressant drugs in forced swim test. Berberine (5 mg/kg, i.p.) following its acute administration in mice resulted in increased levels of norepinephrine (31%), serotonin (47%) and dopamine (31%) in the whole brain. Chronic administration of berberine (5 mg/kg, i.p.) for 15 days significantly increased the levels of norepinephrine (29%), serotonin (19%) as well as dopamine (52%) but at higher dose (10 mg/kg, i.p.), there was no change in the norepinephrine (12%) levels but a significant increase in the serotonin (53%) and dopamine (31%) levels was found. The antidepressant-like effect of berberine (5 mg/kg, i.p.) in forced swim test was prevented by pretreatment with l-arginine (750 mg/kg, i.p.) or sildenafil (5 mg/kg, i.p.). On the contrary, pretreatment of mice with 7-nitroindazole (7-NI) (25 mg/kg, i.p.) or methylene blue (10 mg/kg, i.p.) potentiated the effect of berberine (2 mg/kg, i.p.) in the forced swim test. Pretreatment of mice with (+)-pentazocine (2.5 mg/kg, i.p.), a high-affinity sigma1 receptor agonist, produced synergism with subeffective dose of berberine (2 mg/kg, i.p.). Pretreatment with various sigma receptor antagonists viz. progesterone (10 mg/kg, s.c.), rimcazole (5 mg/kg, i.p.) and N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(dimethylamino)ethylamine (BD1047; 1 mg/kg, i.p.) reversed the anti-immobility effects of berberine (5 mg/kg, i.p.). Berberine at lower dose did not affect the locomotor activity and barbiturate-induced sleep time. It produced mild hypothermic action in rats and displayed analgesic effect in mice. Taken together, theses findings demonstrate that berberine exerted antidepressant-like effect in various behavioural paradigms of despair possibly by modulating brain biogenic amines (norepinephrine, serotonin and dopamine). Further, nitric oxide pathway and/or sigma receptors are involved in mediating its antidepressant-like activity in mouse forced swim test.
MeSH term(s)	Analgesics/pharmacology ; Animals ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Berberine/analogs & derivatives ; Berberine/pharmacology ; Body Temperature/drug effects ; Brain/drug effects ; Brain/metabolism ; Depression/chemically induced ; Depression/drug therapy ; Depression/psychology ; Disease Models, Animal ; Dopamine/metabolism ; Dose-Response Relationship, Drug ; Drug Interactions ; Drug Therapy, Combination ; Hot Temperature ; Male ; Mice ; Motor Activity/drug effects ; Nitric Oxide/metabolism ; Norepinephrine/metabolism ; Pain/etiology ; Pain/physiopathology ; Pain/prevention & control ; Pain Measurement ; Pain Threshold/drug effects ; Rats ; Rats, Wistar ; Receptors, sigma/drug effects ; Receptors, sigma/metabolism ; Reserpine ; Serotonin/metabolism ; Sleep/drug effects ; Swimming ; Time Factors ; Up-Regulation ; Sigma-1 Receptor
Chemical Substances	Analgesics ; Antidepressive Agents ; Receptors, sigma ; Berberine (0I8Y3P32UF) ; Nitric Oxide (31C4KY9ESH) ; Serotonin (333DO1RDJY) ; Reserpine (8B1QWR724A) ; Dopamine (VTD58H1Z2X) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2008-06-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2008.05.043
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Article ; Online: MicroRNA-mediated downregulation of potassium-chloride-cotransporter and vesicular γ-aminobutyric acid transporter expression in spinal cord contributes to neonatal cystitis-induced visceral pain in rats.

Zhang, Jian / Yu, James / Kannampalli, Pradeep / Nie, Linghui / Meng, Hui / Medda, Bidyut K / Shaker, Reza / Sengupta, Jyoti N / Banerjee, Banani

Pain

2017 Volume 158, Issue 12, Page(s) 2461–2474

Abstract: Loss of GABAergic inhibition in pain pathways has been considered to be a key component ... regulation of spinal GABAergic system plays an important role in sensory pathophysiology of zymosan-induced ... in the development of chronic pain. In the present study, we intended to examine whether miR-92b-mediated ...

Abstract	Loss of GABAergic inhibition in pain pathways has been considered to be a key component in the development of chronic pain. In the present study, we intended to examine whether miR-92b-mediated posttranscriptional dysregulation of spinal potassium chloride cotransporter (KCC2) and vesicular γ-aminobutyric acid transporter (VGAT) plays a major role in the development and maintenance of long-term visceral hyperalgesia in neonatal zymosan-treated rats. Neonatal cystitis was induced by transurethral zymosan administration from postnatal (P) days 14 to 16 (protocol 1). Two other zymosan protocols were also used: adult rechallenge on P57 to 59 following neonatal P14 to 16 exposures (protocol 2), and adult zymosan exposures on P57 to 59 (protocol 3). Both neonatal and adult bladder inflammation protocols demonstrated an increase in spinal miR-92b-3p expression and subsequent decrease in KCC2 and VGAT expression in spinal dorsal horn neurons. In situ hybridization demonstrated a significant upregulation of miR-92b-3p in the spinal dorsal horn neurons of neonatal cystitis rats compared with saline-treated controls. In dual in situ hybridization and immunohistochemistry studies, we further demonstrated coexpression of miR-92b-3p with targets KCC2 and VGAT in spinal dorsal horn neurons, emphasizing a possible regulatory role both at pre- and post-synaptic levels. Intrathecal administration of lentiviral pLSyn-miR-92b-3p sponge (miR-92b-3p inhibitor) upregulated KCC2 and VGAT expression in spinal dorsal horn neurons. In behavioral studies, intrathecal administration of lentiviral miR-92b-3p sponge attenuated an increase in visceromotor responses and referred viscerosomatic hypersensitivity following the induction of cystitis. These findings indicate that miR-92b-3p-mediated posttranscriptional regulation of spinal GABAergic system plays an important role in sensory pathophysiology of zymosan-induced cystitis.
MeSH term(s)	Animals ; Chronic Pain/metabolism ; Chronic Pain/physiopathology ; Down-Regulation ; Female ; Hyperalgesia/physiopathology ; MicroRNAs/metabolism ; Posterior Horn Cells/metabolism ; Rats, Sprague-Dawley ; Spinal Cord/metabolism ; Visceral Pain/metabolism ; Visceral Pain/physiopathology
Chemical Substances	MicroRNAs
Language	English
Publishing date	2017-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1097/j.pain.0000000000001057
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Article: Reduced potassium-chloride co-transporter expression in spinal cord dorsal horn neurons contributes to inflammatory pain hypersensitivity in rats.

Zhang, W / Liu, L-Y / Xu, T-L

Neuroscience

2008 Volume 152, Issue 2, Page(s) 502–510

Abstract: ... to chronic inflammatory pain. We investigated the expression of potassium-chloride co-transporter 2 (KCC2 ... that blockade of endogenous brain-derived neurotrophic factor-tyrosine receptor kinase B pathway inhibited ... which may in turn facilitate the development and/or maintenance of chronic inflammatory pain. The data also support ...

Abstract	Cation chloride co-transporters are important determinants for the efficacy of inhibitory neurotransmission in the spinal cord and alterations in their expression levels contribute to allodynia and hyperalgesia associated with neuropathy. However, it remains unknown whether these co-transporters contribute to chronic inflammatory pain. We investigated the expression of potassium-chloride co-transporter 2 (KCC2) and sodium-potassium-chloride co-transporter 1 (NKCC1) in the rat spinal cord after peripheral inflammation induced by complete Freund's adjuvant (CFA) injection. Our results suggest that the expression of KCC2, but not that of NKCC1, was significantly reduced in CFA-injected rats. We also found that blockade of endogenous brain-derived neurotrophic factor-tyrosine receptor kinase B pathway inhibited the inflammation-induced KCC2 downregulation. Moreover, intrathecal injection of KCC2 antisense oligodeoxynucleotides into naïve rats reduced KCC2 expression in the spinal cord, leading to behavioral hypersensitivity similar to the hyperalgesia induced by peripheral inflammation. Taken together, these results indicate that peripheral inflammation induces downregulation of KCC2 in the dorsal horn of the spinal cord, which may in turn facilitate the development and/or maintenance of chronic inflammatory pain. The data also support the notion that disinhibition in the spinal cord is a general feature of inflammatory and neuropathic pain conditions, and suggest new therapeutic intervention.
MeSH term(s)	Analysis of Variance ; Animals ; Behavior, Animal ; Carbazoles/pharmacology ; Enzyme Inhibitors/pharmacology ; Freund's Adjuvant ; Functional Laterality ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Hyperalgesia/etiology ; Hyperalgesia/pathology ; Indole Alkaloids/pharmacology ; Inflammation/chemically induced ; Inflammation/complications ; Inflammation/pathology ; Male ; Oligodeoxyribonucleotides, Antisense/administration & dosage ; Pain Measurement/methods ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/metabolism ; Rats ; Rats, Sprague-Dawley ; Reaction Time/drug effects ; Spinal Cord/pathology ; Symporters/genetics ; Symporters/metabolism ; Time Factors ; K Cl- Cotransporters
Chemical Substances	Carbazoles ; Enzyme Inhibitors ; Indole Alkaloids ; Oligodeoxyribonucleotides, Antisense ; Symporters ; Freund's Adjuvant (9007-81-2) ; staurosporine aglycone (97161-97-2)
Language	English
Publishing date	2008-01-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2007.12.037
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Article: Chloride regulation in the pain pathway.

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Article ; Online: Neurodegeneration Upon Dysfunction of Endosomal/Lysosomal CLC Chloride Transporters

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Article ; Online: Combined Changes in Chloride Regulation and Neuronal Excitability Enable Primary Afferent Depolarization to Elicit Spiking without Compromising its Inhibitory Effects.

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Article: Analgesic effect of intrathecal bumetanide is accompanied by changes in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain.

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Article: On the mechanism of antidepressant-like action of berberine chloride.

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Article ; Online: MicroRNA-mediated downregulation of potassium-chloride-cotransporter and vesicular γ-aminobutyric acid transporter expression in spinal cord contributes to neonatal cystitis-induced visceral pain in rats.

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Article: Reduced potassium-chloride co-transporter expression in spinal cord dorsal horn neurons contributes to inflammatory pain hypersensitivity in rats.

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