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Article ; Online: Spinal PAR2 Activation Contributes to Hypersensitivity Induced by Peripheral Inflammation in Rats.

Mrozkova, Petra / Spicarova, Diana / Palecek, Jiri

International journal of molecular sciences

2021 Volume 22, Issue 3

Abstract: The mechanisms of inflammatory pain need to be identified in order to find new superior treatments. Protease-activated receptors 2 (PAR2) and transient receptor potential vanilloid 1 (TRPV1) are highly co-expressed in dorsal root ganglion neurons and ... ...

Abstract	The mechanisms of inflammatory pain need to be identified in order to find new superior treatments. Protease-activated receptors 2 (PAR2) and transient receptor potential vanilloid 1 (TRPV1) are highly co-expressed in dorsal root ganglion neurons and implicated in pain development. Here, we examined the role of spinal PAR2 in hyperalgesia and the modulation of synaptic transmission in carrageenan-induced peripheral inflammation, using intrathecal (i.t.) treatment in the behavioral experiments and recordings of spontaneous, miniature and dorsal root stimulation-evoked excitatory postsynaptic currents (sEPSCs, mEPSCs and eEPSCs) in spinal cord slices. Intrathecal PAR2-activating peptide (AP) administration aggravated the carrageenan-induced thermal hyperalgesia, and this was prevented by a TRPV1 antagonist (SB 366791) and staurosporine i.t. pretreatment. Additionally, the frequency of the mEPSC and sEPSC and the amplitude of the eEPSC recorded from the superficial dorsal horn neurons were enhanced after acute PAR2 AP application, while prevented with SB 366791 or staurosporine pretreatment. PAR2 antagonist application reduced the thermal hyperalgesia and decreased the frequency of mEPSC and sEPSC and the amplitude of eEPSC. Our findings highlight the contribution of spinal PAR2 activation to carrageenan-induced hyperalgesia and the importance of dorsal horn PAR2 and TRPV1 receptor interactions in the modulation of nociceptive synaptic transmission.
MeSH term(s)	Anilides/pharmacology ; Animals ; Carrageenan/pharmacology ; Carrageenan/toxicity ; Cinnamates/pharmacology ; Excitatory Postsynaptic Potentials ; Hyperalgesia/etiology ; Hyperalgesia/metabolism ; Hyperalgesia/physiopathology ; Male ; Miniature Postsynaptic Potentials ; Nociception ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/metabolism ; Posterior Horn Cells/physiology ; Rats ; Rats, Wistar ; Receptor, PAR-2/metabolism ; Staurosporine/pharmacology ; TRPV Cation Channels/antagonists & inhibitors ; TRPV Cation Channels/metabolism
Chemical Substances	Anilides ; Cinnamates ; N-(3-methoxyphenyl)-4-chlorocinnamanilide ; Receptor, PAR-2 ; TRPV Cation Channels ; Trpv1 protein, rat ; Carrageenan (9000-07-1) ; Staurosporine (H88EPA0A3N)
Language	English
Publishing date	2021-01-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22030991
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Article ; Online: Chemokine CCL2 prevents opioid-induced inhibition of nociceptive synaptic transmission in spinal cord dorsal horn.

Heles, Mario / Mrozkova, Petra / Sulcova, Dominika / Adamek, Pavel / Spicarova, Diana / Palecek, Jiri

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 279

Abstract: Background: Opioid analgesics remain widely used for pain treatment despite the related serious side effects. Some of those, such as opioid tolerance and opioid-induced hyperalgesia may be at least partially due to modulation of opioid receptors (OR) ... ...

Abstract	Background: Opioid analgesics remain widely used for pain treatment despite the related serious side effects. Some of those, such as opioid tolerance and opioid-induced hyperalgesia may be at least partially due to modulation of opioid receptors (OR) function at nociceptive synapses in the spinal cord dorsal horn. It was suggested that increased release of different chemokines under pathological conditions may play a role in this process. The goal of this study was to investigate the crosstalk between the µOR, transient receptor potential vanilloid 1 (TRPV1) receptor and C-C motif ligand 2 (CCL2) chemokine and the involvement of spinal microglia in the modulation of opioid analgesia. Methods: Patch-clamp recordings of miniature excitatory postsynaptic currents (mEPSCs) and dorsal root evoked currents (eEPSC) in spinal cord slices superficial dorsal horn neurons were used to evaluate the effect of µOR agonist [D-Ala Results: Application of DAMGO induced a rapid decrease of mEPSC frequency and eEPSC amplitude, followed by a delayed increase of the eESPC amplitude, which was prevented by SB366791. Chemokine CCL2 treatment significantly diminished all the DAMGO-induced changes. Minocycline treatment prevented the CCL2 effects on the DAMGO-induced eEPSC depression, while mEPSC changes were unaffected. In behavioral experiments, i.t. injection of CCL2 completely blocked DAMGO-induced thermal hypoalgesia and intraperitoneal pre-treatment with minocycline prevented the CCL2 effect. Conclusions: Our results indicate that opioid-induced inhibition of the excitatory synaptic transmission could be severely attenuated by increased CCL2 levels most likely through a microglia activation-dependent mechanism. Delayed potentiation of neurotransmission after µOR activation is dependent on TRPV1 receptors activation. Targeting CCL2 and its receptors and TRPV1 receptors in combination with opioid therapy could significantly improve the analgesic properties of opioids, especially during pathological states.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Anilides/pharmacology ; Animals ; Chemokine CCL2/pharmacology ; Cinnamates/pharmacology ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; Excitatory Postsynaptic Potentials/drug effects ; Male ; Miniature Postsynaptic Potentials/drug effects ; Neurons/drug effects ; Nociception/drug effects ; Rats ; Rats, Wistar ; Spinal Cord/drug effects ; Spinal Cord Dorsal Horn/drug effects ; Synaptic Transmission/drug effects
Chemical Substances	Analgesics, Opioid ; Anilides ; Chemokine CCL2 ; Cinnamates ; N-(3-methoxyphenyl)-4-chlorocinnamanilide ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)- (100929-53-1)
Language	English
Publishing date	2021-12-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-021-02335-4
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Article ; Online: Hypersensitivity Induced by Activation of Spinal Cord PAR2 Receptors Is Partially Mediated by TRPV1 Receptors.

Mrozkova, Petra / Spicarova, Diana / Palecek, Jiri

PloS one

2016 Volume 11, Issue 10, Page(s) e0163991

Abstract: Protease-activated receptors 2 (PAR2) and transient receptor potential vanilloid 1 (TRPV1) receptors in the peripheral nerve endings are implicated in the development of increased sensitivity to mechanical and thermal stimuli, especially during ... ...

Abstract	Protease-activated receptors 2 (PAR2) and transient receptor potential vanilloid 1 (TRPV1) receptors in the peripheral nerve endings are implicated in the development of increased sensitivity to mechanical and thermal stimuli, especially during inflammatory states. Both PAR2 and TRPV1 receptors are co-expressed in nociceptive dorsal root ganglion (DRG) neurons on their peripheral endings and also on presynaptic endings in the spinal cord dorsal horn. However, the modulation of nociceptive synaptic transmission in the superficial dorsal horn after activation of PAR2 and their functional coupling with TRPV1 is not clear. To investigate the role of spinal PAR2 activation on nociceptive modulation, intrathecal drug application was used in behavioural experiments and patch-clamp recordings of spontaneous, miniature and dorsal root stimulation-evoked excitatory postsynaptic currents (sEPSCs, mEPSCs, eEPSCs) were performed on superficial dorsal horn neurons in acute rat spinal cord slices. Intrathecal application of PAR2 activating peptide SLIGKV-NH2 induced thermal hyperalgesia, which was prevented by pretreatment with TRPV1 antagonist SB 366791 and was reduced by protein kinases inhibitor staurosporine. Patch-clamp experiments revealed robust decrease of mEPSC frequency (62.8 ± 4.9%), increase of sEPSC frequency (127.0 ± 5.9%) and eEPSC amplitude (126.9 ± 12.0%) in dorsal horn neurons after acute SLIGKV-NH2 application. All these EPSC changes, induced by PAR2 activation, were prevented by SB 366791 and staurosporine pretreatment. Our results demonstrate an important role of spinal PAR2 receptors in modulation of nociceptive transmission in the spinal cord dorsal horn at least partially mediated by activation of presynaptic TRPV1 receptors. The functional coupling between the PAR2 and TRPV1 receptors on the central branches of DRG neurons may be important especially during different pathological states when it may enhance pain perception.
MeSH term(s)	Anilides/pharmacology ; Animals ; Behavior, Animal/drug effects ; Cinnamates/pharmacology ; Excitatory Postsynaptic Potentials/drug effects ; Hyperalgesia/etiology ; Hyperalgesia/prevention & control ; Hypersensitivity/metabolism ; Hypersensitivity/pathology ; In Vitro Techniques ; Male ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/physiology ; Protein Kinase Inhibitors/pharmacology ; Rats ; Rats, Wistar ; Receptor, PAR-2/agonists ; Receptor, PAR-2/metabolism ; Spinal Cord/metabolism ; Staurosporine/pharmacology ; Synaptic Transmission/physiology ; TRPV Cation Channels/antagonists & inhibitors ; TRPV Cation Channels/metabolism
Chemical Substances	Anilides ; Cinnamates ; N-(3-methoxyphenyl)-4-chlorocinnamanilide ; Oligopeptides ; Protein Kinase Inhibitors ; Receptor, PAR-2 ; TRPV Cation Channels ; TRPV1 receptor ; seryl-leucyl-isoleucyl-glycyl-lysyl-valinamide ; Staurosporine (H88EPA0A3N)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0163991
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Article ; Online: Peripheral inflammation affects modulation of nociceptive synaptic transmission in the spinal cord induced by N-arachidonoylphosphatidylethanolamine.

Nerandzic, Vladimir / Mrozkova, Petra / Adamek, Pavel / Spicarova, Diana / Nagy, Istvan / Palecek, Jiri

British journal of pharmacology

2017 Volume 175, Issue 12, Page(s) 2322–2336

Abstract: Background and purpose: Endocannabinoids play an important role in modulating spinal nociceptive signalling, crucial for the development of pain. The cannabinoid CB: Experimental approach: Spontaneous (sEPSCs) and dorsal root stimulation-evoked ( ... ...

Abstract	Background and purpose: Endocannabinoids play an important role in modulating spinal nociceptive signalling, crucial for the development of pain. The cannabinoid CB Experimental approach: Spontaneous (sEPSCs) and dorsal root stimulation-evoked (eEPSCs) excitatory postsynaptic currents from superficial dorsal horn neurons in rat spinal cord slices were assessed. Peripheral inflammation was induced by carrageenan. Anandamide concentration was assessed by mass spectrometry. Key results: Application of 20:4-NAPE increased anandamide concentration in vitro. 20:4-NAPE (20 μM) decreased sEPSCs frequency and eEPSCs amplitude in control and inflammatory conditions. The inhibitory effect of 20:4-NAPE was sensitive to CB Conclusions and implications: While 20:4-NAPE treatment inhibited the excitatory synaptic transmission in both naive and inflammatory conditions, peripheral inflammation altered the underlying mechanisms. Our data indicate that 20:4-NAPE application induced mainly CB Linked articles: This article is part of a themed section on Recent Advances in Targeting Ion Channels to Treat Chronic Pain. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc.
MeSH term(s)	Animals ; Carrageenan ; Dose-Response Relationship, Drug ; Inflammation/chemically induced ; Inflammation/metabolism ; Male ; Mass Spectrometry ; Phosphatidylethanolamines/chemical synthesis ; Phosphatidylethanolamines/chemistry ; Phosphatidylethanolamines/pharmacology ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/metabolism ; Rats ; Rats, Wistar ; Spinal Cord/drug effects ; Spinal Cord/metabolism ; Structure-Activity Relationship ; Synaptic Transmission/drug effects
Chemical Substances	Phosphatidylethanolamines ; Carrageenan (9000-07-1)
Language	English
Publishing date	2017-06-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.13849
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Article ; Online: TRPV1 receptor inhibition decreases CCL2-induced hyperalgesia.

Spicarova, Diana / Adamek, Pavel / Kalynovska, Nataliia / Mrozkova, Petra / Palecek, Jiri

Neuropharmacology

2014 Volume 81, Page(s) 75–84

Abstract: Modulation of nociceptive synaptic transmission in the spinal cord is implicated in the development and maintenance of several pathological pain states. The chemokine CCL2 (C-C motif ligand 2) was shown to be an important factor in the development of ... ...

Abstract	Modulation of nociceptive synaptic transmission in the spinal cord is implicated in the development and maintenance of several pathological pain states. The chemokine CCL2 (C-C motif ligand 2) was shown to be an important factor in the development of neuropathic pain after peripheral nerve injury. In our experiments we have studied the effect of CCL2 application and TRPV1 (transient receptor potential vanilloid 1) receptor activation on nociceptive signaling and the modulation of synaptic transmission. Intrathecal drug application in behavioral experiments and patch-clamp recordings of spontaneous, miniature and dorsal root stimulation-evoked excitatory postsynaptic currents (sEPSCs, mEPSCs, eEPSCs) from superficial dorsal horn neurons in acute rat spinal cord slices were used. The intrathecal application of CCL2 induced thermal hyperalgesia and mechanical allodynia, while pretreatment with the TRPV1 receptor antagonist SB366791 diminished the thermal but not the mechanical hypersensitivity. Patch-clamp experiments showed an increase of sEPSC and mEPSC (124.5 ± 12.8% and 161.2 ± 17.3%, respectively) frequency in dorsal horn neurons after acute CCL2 application. This CCL2-induced increase was prevented by SB366791 pretreatment (89.4 ± 6.0%, 107.5 ± 14.2%). CCL2 application increased the amplitude of eEPSCs (188.1 ± 32.1%); this increase was significantly lower in experiments with SB366791 pretreatment (120.8 ± 17.2%). Our results demonstrate that the activation of spinal TRPV1 receptors plays an important role in the modulation of nociceptive signaling induced by CCL2 application. The mechanisms of cooperation between the CCL2 activated receptors and TRPV1 receptors on the central branches of primary afferent fibers may be especially important during different pathological pain states and need to be further investigated.
MeSH term(s)	Anilides/therapeutic use ; Animals ; Animals, Newborn ; Capsaicin/pharmacology ; Chemokine CCL2/toxicity ; Cinnamates/therapeutic use ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Excitatory Postsynaptic Potentials/drug effects ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy ; Hyperalgesia/metabolism ; In Vitro Techniques ; MAP Kinase Kinase Kinase 3/metabolism ; Male ; Pain Threshold/drug effects ; Patch-Clamp Techniques ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/physiology ; Rats ; Rats, Wistar ; Sensory System Agents/pharmacology ; Spinal Cord/cytology ; Spinal Cord/drug effects ; Spinal Cord/metabolism ; TRPV Cation Channels/antagonists & inhibitors ; TRPV Cation Channels/metabolism ; Time Factors
Chemical Substances	Anilides ; Chemokine CCL2 ; Cinnamates ; N-(3-methoxyphenyl)-4-chlorocinnamanilide ; Sensory System Agents ; TRPV Cation Channels ; Trpv1 protein, rat ; MAP Kinase Kinase Kinase 3 (EC 2.7.11.25) ; Capsaicin (S07O44R1ZM)
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2014.01.041
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Article ; Online: The Cancer Chemotherapeutic Paclitaxel Increases Human and Rodent Sensory Neuron Responses to TRPV1 by Activation of TLR4.

Li, Yan / Adamek, Pavel / Zhang, Haijun / Tatsui, Claudio Esteves / Rhines, Laurence D / Mrozkova, Petra / Li, Qin / Kosturakis, Alyssa K / Cassidy, Ryan M / Harrison, Daniel S / Cata, Juan P / Sapire, Kenneth / Zhang, Hongmei / Kennamer-Chapman, Ross M / Jawad, Abdul Basit / Ghetti, Andre / Yan, Jiusheng / Palecek, Jiri / Dougherty, Patrick M

The Journal of neuroscience : the official journal of the Society for Neuroscience

2015 Volume 35, Issue 39, Page(s) 13487–13500

Abstract: Peripheral neuropathy is dose limiting in paclitaxel cancer chemotherapy and can result in both acute pain during treatment and chronic persistent pain in cancer survivors. The hypothesis tested was that paclitaxel produces these adverse effects at least ...

Abstract	Peripheral neuropathy is dose limiting in paclitaxel cancer chemotherapy and can result in both acute pain during treatment and chronic persistent pain in cancer survivors. The hypothesis tested was that paclitaxel produces these adverse effects at least in part by sensitizing transient receptor potential vanilloid subtype 1 (TRPV1) through Toll-like receptor 4 (TLR4) signaling. The data show that paclitaxel-induced behavioral hypersensitivity is prevented and reversed by spinal administration of a TRPV1 antagonist. The number of TRPV1(+) neurons is increased in the dorsal root ganglia (DRG) in paclitaxel-treated rats and is colocalized with TLR4 in rat and human DRG neurons. Cotreatment of rats with lipopolysaccharide from the photosynthetic bacterium Rhodobacter sphaeroides (LPS-RS), a TLR4 inhibitor, prevents the increase in numbers of TRPV1(+) neurons by paclitaxel treatment. Perfusion of paclitaxel or the archetypal TLR4 agonist LPS activated both rat DRG and spinal neurons directly and produced acute sensitization of TRPV1 in both groups of cells via a TLR4-mediated mechanism. Paclitaxel and LPS sensitize TRPV1 in HEK293 cells stably expressing human TLR4 and transiently expressing human TRPV1. These physiological effects also are prevented by LPS-RS. Finally, paclitaxel activates and sensitizes TRPV1 responses directly in dissociated human DRG neurons. In summary, TLR4 was activated by paclitaxel and led to sensitization of TRPV1. This mechanism could contribute to paclitaxel-induced acute pain and chronic painful neuropathy. Significance statement: In this original work, it is shown for the first time that paclitaxel activates peripheral sensory and spinal neurons directly and sensitizes these cells to transient receptor potential vanilloid subtype 1 (TRPV1)-mediated capsaicin responses via Toll-like receptor 4 (TLR4) in multiple species. A direct functional interaction between TLR4 and TRPV1 is shown in rat and human dorsal root ganglion neurons, TLR4/TRPV1-coexpressing HEK293 cells, and in both rat and mouse spinal cord slices. Moreover, this is the first study to show that this interaction plays an important role in the generation of behavioral hypersensitivity in paclitaxel-related neuropathy. The key translational implications are that TLR4 and TRPV1 antagonists may be useful in the prevention and treatment of chemotherapy-induced peripheral neuropathy in humans.
MeSH term(s)	Animals ; Antineoplastic Agents, Phytogenic/antagonists & inhibitors ; Antineoplastic Agents, Phytogenic/pharmacology ; Calcium/metabolism ; Excitatory Postsynaptic Potentials/drug effects ; Ganglia, Spinal/cytology ; Ganglia, Spinal/drug effects ; HEK293 Cells ; Humans ; Hyperalgesia/chemically induced ; Hyperalgesia/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Paclitaxel/antagonists & inhibitors ; Paclitaxel/pharmacology ; Pain Measurement/drug effects ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Sensory Receptor Cells/drug effects ; Signal Transduction/drug effects ; Spinal Cord/drug effects ; TRPV Cation Channels/antagonists & inhibitors ; Toll-Like Receptor 4/antagonists & inhibitors ; Toll-Like Receptor 4/drug effects
Chemical Substances	Antineoplastic Agents, Phytogenic ; TRPV Cation Channels ; TRPV1 receptor ; Toll-Like Receptor 4 ; Paclitaxel (P88XT4IS4D) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2015-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1956-15.2015
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Article ; Online: Spinal PAR2 Activation Contributes to Hypersensitivity Induced by Peripheral Inflammation in Rats.

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Article ; Online: Chemokine CCL2 prevents opioid-induced inhibition of nociceptive synaptic transmission in spinal cord dorsal horn.

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Article ; Online: Hypersensitivity Induced by Activation of Spinal Cord PAR2 Receptors Is Partially Mediated by TRPV1 Receptors.

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Article ; Online: Peripheral inflammation affects modulation of nociceptive synaptic transmission in the spinal cord induced by N-arachidonoylphosphatidylethanolamine.

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Article ; Online: TRPV1 receptor inhibition decreases CCL2-induced hyperalgesia.

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Article ; Online: The Cancer Chemotherapeutic Paclitaxel Increases Human and Rodent Sensory Neuron Responses to TRPV1 by Activation of TLR4.

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