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Article ; Online: Astrocytes express functional TRPV2 ion channels.

Shibasaki, Koji / Ishizaki, Yasuki / Mandadi, Sravan

Biochemical and biophysical research communications

2013 Volume 441, Issue 2, Page(s) 327–332

Abstract: Thermosensitive transient receptor potential (thermo TRP) channels are important for sensory transduction. Among them, TRPV2 has an interesting characteristic of being activated by very high temperature (>52 °C). In addition to the heat sensor function, ... ...

Abstract	Thermosensitive transient receptor potential (thermo TRP) channels are important for sensory transduction. Among them, TRPV2 has an interesting characteristic of being activated by very high temperature (>52 °C). In addition to the heat sensor function, TRPV2 also acts as a mechanosensor, an osomosensor and a lipid sensor. It has been reported that TRPV2 is expressed in heart, intestine, pancreas and sensory nerves. In the central nervous system, neuronal TRPV2 expression was reported, however, glial expression and the precise roles of TRPV2 have not been determined. To explore the functional expression of TRPV2 in astrocytes, the expression was determined by histological and physiological methods. Interestingly, TRPV2 expression was detected in plasma membrane of astrocytes, and the astrocytic TRPV2 was activated by very high temperature (>50 °C) consistent with the reported characteristic. We revealed that the astrocytic TRPV2 was also activated by lysophosphatidylcholine, a known endogenous lipid ligand for TRPV2, suggesting that astrocytic TRPV2 might regulate neuronal activities in response to lipid metabolism. Thus, for the first time we revealed that TRPV2 is functionally expressed in astrocytes in addition to neurons.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Calcium/metabolism ; Calcium Channels/biosynthesis ; Calcium Channels/genetics ; Cerebellum/cytology ; Cerebellum/metabolism ; Hot Temperature ; Humans ; Lysophosphatidylcholines/pharmacology ; Mice ; Mice, Inbred C57BL ; TRPV Cation Channels/biosynthesis ; TRPV Cation Channels/genetics
Chemical Substances	Calcium Channels ; Lysophosphatidylcholines ; TRPV Cation Channels ; Trpv2 protein, mouse ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2013-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.10.046
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Article ; Online: A new method to study sensory modulation of locomotor networks by activation of thermosensitive cutaneous afferents using a hindlimb attached spinal cord preparation.

Mandadi, Sravan / Whelan, Patrick J

Journal of neuroscience methods

2009 Volume 182, Issue 2, Page(s) 255–259

Abstract: The use of isolated in vitro spinal cord preparations to examine the underlying networks that control locomotion has become popular. It is also well known that afferent feedback can excite and modulate these networks. However, it is often difficult to ... ...

Abstract	The use of isolated in vitro spinal cord preparations to examine the underlying networks that control locomotion has become popular. It is also well known that afferent feedback can excite and modulate these networks. However, it is often difficult to selectively activate classes of afferents that subserve specific modalities using in vitro preparations. Here, we describe a technique where afferent receptors that detect temperature were selectively activated. To accomplish this we used an in vitro preparation of the mouse where the spinal cord was isolated (T5-cauda equina) with one hind limb left attached. We designed a special chamber allowing the hind paw to be placed in such a way that it remained attached to the spinal cord but received a separate supply of artificial cerebrospinal fluid (aCSF). This allowed us to alter the temperature of the hind limb compartment without affecting the temperature of the central compartment containing the spinal cord. We also demonstrate using this approach that agonists which activate receptors which detect noxious heat could be intradermally injected into the hind limb without it diffusing into the central compartment.
MeSH term(s)	Animals ; Capsaicin/pharmacology ; Cauda Equina/physiology ; Cold Temperature ; Dopamine/pharmacology ; Electrophysiology ; Excitatory Amino Acid Agonists/pharmacology ; Hindlimb/innervation ; Hindlimb/physiology ; Hot Temperature ; Locomotion/physiology ; Mice ; N-Methylaspartate/pharmacology ; Nerve Net/drug effects ; Nerve Net/physiology ; Neurons, Afferent/drug effects ; Neurons, Afferent/metabolism ; Neurons, Afferent/physiology ; Sensation/drug effects ; Sensation/physiology ; Serotonin/pharmacology ; Skin/innervation ; Spinal Cord/physiology ; Stimulation, Chemical ; TRPV Cation Channels/physiology ; Thermoreceptors/drug effects ; Thermoreceptors/physiology ; Transient Receptor Potential Channels/physiology
Chemical Substances	Excitatory Amino Acid Agonists ; TRPV Cation Channels ; TRPV1 protein, mouse ; Transient Receptor Potential Channels ; Serotonin (333DO1RDJY) ; N-Methylaspartate (6384-92-5) ; Capsaicin (S07O44R1ZM) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2009-09-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	282721-9
ISSN	1872-678X ; 0165-0270
ISSN (online)	1872-678X
ISSN	0165-0270
DOI	10.1016/j.jneumeth.2009.06.011
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Article: Real-Time Translocation and Function of PKCβII Isoform in Response to Nociceptive Signaling via the TRPV1 Pain Receptor.

Mandadi, Sravan / Armati, Patricia J / Roufogalis, Basil D

Pharmaceuticals (Basel, Switzerland)

2011 Volume 4, Issue 11, Page(s) 1503–1517

Abstract: Serine/threonine protein kinase C βII isoform (PKCβII) or the pain receptor transient receptor potential vanilloid 1 (TRPV1) have been separately implicated in mediating heat hyperalgesia during inflammation or diabetic neuropathy. However, detailed ... ...

Abstract	Serine/threonine protein kinase C βII isoform (PKCβII) or the pain receptor transient receptor potential vanilloid 1 (TRPV1) have been separately implicated in mediating heat hyperalgesia during inflammation or diabetic neuropathy. However, detailed information on the role of PKC βII in nociceptive signaling mediated by TRPV1 is lacking. This study presents evidence for activation and translocation of the PKC βII isoform as a signaling event in nociception mediated by activation of TRPV1 by capsaicin. We show that capsaicin induces translocation of cytosolic PKCβII isoform fused with enhanced green fluorescence protein (PKCβII-EGFP) in dorsal root ganglion (DRG) neurons. We also show capsaicin-induced translocation in Chinese Hamster Ovarian (CHO) cells co-transfected with TRPV1 and PKCβII-EGFP, but not in CHO cells expressing PKCβII-EGFP alone. By contrast, the PKC activator phorbol-12-myristate-13-acetate (PMA) induced translocation of PKCβII-EGFP which was sustained and independent of calcium or TRPV1. In addition PMA-induced sensitization of TRPV1 to capsaicin response in DRG neurons was attenuated by PKCβII blocker CGP 53353. Capsaicin response via TRPV1 in the DRG neurons was confirmed by TRPV1 antagonist AMG 9810. These results suggested a novel and potential signaling link between PKCβII and TRPV1. These cell culture models provide a platform for investigating mechanisms of painful neuropathies mediated by nociceptors expressing the pain sensing gene TRPV1, and its regulation by the PKC isoform PKCβII.
Language	English
Publishing date	2011-11-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph4111503
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Article ; Online: Protein kinase C modulation of thermo-sensitive transient receptor potential channels: Implications for pain signaling.

Mandadi, Sravan / Armati, Patricia J / Roufogalis, Basil D

Journal of natural science, biology, and medicine

2011 Volume 2, Issue 1, Page(s) 13–25

Abstract: A variety of molecules are reported to be involved in chronic pain. This review outlines the specifics of protein kinase C (PKC), its isoforms and their role in modulating thermo-sensitive transient receptor potential (TRP) channels TRPV1-4, TRPM8, and ... ...

Abstract	A variety of molecules are reported to be involved in chronic pain. This review outlines the specifics of protein kinase C (PKC), its isoforms and their role in modulating thermo-sensitive transient receptor potential (TRP) channels TRPV1-4, TRPM8, and TRPA1. Anatomically, PKC and thermo-sensitive TRPs are co-expressed in cell bodies of nociceptive dorsal root ganglion (DRG) neurons, which are used as physiological correlates of peripheral and central projections involved in pain transmission. In the past decade, modulation of painful heat-sensitive TRPV1 by PKC has received the most attention. Recently, PKC modulation of other newly discovered thermo-sensitive pain-mediating TRPs has come into focus. Such modulation may occur under conditions of chronic pain resulting from nerve damage or inflammation. Since thermo-TRPs are primary detectors of acute pain stimuli, their modulation by PKC can severely alter their function, resulting in chronic pain. Comprehensive knowledge of pain signaling involving interaction of specific isoforms of PKC with specific thermo-sensitive TRP channels is incomplete. Such information is necessary to dissect out modality specific mechanisms to better manage the complex polymodal nature of chronic pain. This review is an attempt to update the readers on current knowledge of PKC modulation of thermo-sensitive TRPs and highlight implications of such modulation for pain signaling.
Language	English
Publishing date	2011-10-12
Publishing country	India
Document type	Journal Article
ZDB-ID	2638867-4
ISSN	2229-7707 ; 0976-9668
ISSN (online)	2229-7707
ISSN	0976-9668
DOI	10.4103/0976-9668.82311
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Article ; Online: Control of neonatal spinal networks by nociceptors: a potential role for TRP channel based therapies.

Mandadi, Sravan / Hong, Peter / Dhoopar, Arjun Sunny / Whelan, Patrick

Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques

2013 Volume 16, Issue 2, Page(s) 313–320

Abstract: Pediatric spinal cord injury (SCI) often leads to increased nociceptive input resulting in aberrant motor output like tremor and spasticity. Acute plasticity within spinal pain and motor networks following pediatric SCI may result in long-term ... ...

Abstract	Pediatric spinal cord injury (SCI) often leads to increased nociceptive input resulting in aberrant motor output like tremor and spasticity. Acute plasticity within spinal pain and motor networks following pediatric SCI may result in long-term sensorimotor disabilities. Despite this, pediatric SCI remains poorly understood. Part of the problem lies in the paucity of detailed studies aimed at defining sensorimotor control by nociceptors during development. This review provides an overview of work that highlights afferent control of sensorimotor networks by defined nociceptors in the developing spinal cord. Here, we focus on the well established and widely used neonatal sensorimotor model called sacrocaudal afferent (SCA) pathway. Until recently, the identity of specific subclasses of nociceptive afferents in the SCA pathway controlling developing sensorimotor networks was unknown. We highlight here the use of members of the Transient Receptor Potential (TRP) ion channels and mouse genetics to identify specific subsets of nociceptive afferents in the SCA pathway. In addition, we highlight the use of mouse genetics to map sensorimotor networks during development and potential future applications. A neonatal spinal cord model of central neuropathic pain via a defined set of nociceptors is presented as a probe into potential therapeutic avenues in neonatal SCI. Finally, knowledge translation from neonatal basic research to the pediatric population in the clinic is described. In conclusion, studies in neonatal models may lead to therapeutic strategies and pharmaceuticals for chronic pain and motor dysfunction after SCI during development.
MeSH term(s)	Animals ; Humans ; Neuralgia/physiopathology ; Nociceptors/physiology ; Spinal Cord/physiology ; Spinal Cord Injuries/physiopathology ; Transient Receptor Potential Channels/physiology
Chemical Substances	Transient Receptor Potential Channels
Language	English
Publishing date	2013-08-13
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1482-1826
ISSN (online)	1482-1826
DOI	10.18433/j3w02s
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Article: ThermoTRP channels in nociceptors: taking a lead from capsaicin receptor TRPV1.

Mandadi, Sravan / Roufogalis, Basil D

Current neuropharmacology

2006 Volume 6, Issue 1, Page(s) 21–38

Abstract: Nociceptors with peripheral and central projections express temperature sensitive transient receptor potential (TRP) ion channels, also called thermoTRP's. Chemosensitivity of thermoTRP's to certain natural compounds eliciting pain or exhibiting thermal ... ...

Abstract	Nociceptors with peripheral and central projections express temperature sensitive transient receptor potential (TRP) ion channels, also called thermoTRP's. Chemosensitivity of thermoTRP's to certain natural compounds eliciting pain or exhibiting thermal properties has proven to be a good tool in characterizing these receptors. Capsaicin, a pungent chemical in hot peppers, has assisted in the cloning of the first thermoTRP, TRPV1. This discovery initiated the search for other receptors encoding the response to a wide range of temperatures encountered by the body. Of these, TRPV1 and TRPV2 encode unique modalities of thermal pain when exposed to noxious heat. The ability of TRPA1 to encode noxious cold is presently being debated. The role of TRPV1 in peripheral inflammatory pain and central sensitization during chronic pain is well known. In addition to endogenous agonists, a wide variety of chemical agonists and antagonists have been discovered to activate and inhibit TRPV1. Efforts are underway to determine conditions under which agonist-mediated desensitization of TRPV1 or inhibition by antagonists can produce analgesia. Also, identification of specific second messenger molecules that regulate phosphorylation of TRPV1 has been the focus of intense research, to exploit a broader approach to pain treatment. The search for a role of TRPV2 in pain remains dormant due to the lack of suitable experimental models. However, progress into TRPA1's role in pain has received much attention recently. Another thermoTRP, TRPM8, encoding for the cool sensation and also expressed in nociceptors, has recently been shown to reduce pain via a central mechanism, thus opening a novel strategy for achieving analgesia. The role of other thermoTRP's (TRPV3 and TRPV4) encoding for detection of warm temperatures and expressed in nociceptors cannot be excluded. This review will discuss current knowledge on the role of nociceptor thermoTRPs in pain and therapy and describes the activator and inhibitor molecules known to interact with them and modulate their activity.
Language	English
Publishing date	2006-05-15
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2192352-8
ISSN	1875-6190 ; 1570-159X
ISSN (online)	1875-6190
ISSN	1570-159X
DOI	10.2174/157015908783769680
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Article: Astrocytes express functional TRPV2 ion channels

Shibasaki, Koji / Ishizaki, Yasuki / Mandadi, Sravan

Biochemical and biophysical research communications. 2013 Nov. 15, v. 441, no. 2

2013

Abstract: Thermosensitive transient receptor potential (thermo TRP) channels are important for sensory transduction. Among them, TRPV2 has an interesting characteristic of being activated by very high temperature (>52°C). In addition to the heat sensor function, ... ...

Abstract	Thermosensitive transient receptor potential (thermo TRP) channels are important for sensory transduction. Among them, TRPV2 has an interesting characteristic of being activated by very high temperature (>52°C). In addition to the heat sensor function, TRPV2 also acts as a mechanosensor, an osomosensor and a lipid sensor. It has been reported that TRPV2 is expressed in heart, intestine, pancreas and sensory nerves. In the central nervous system, neuronal TRPV2 expression was reported, however, glial expression and the precise roles of TRPV2 have not been determined. To explore the functional expression of TRPV2 in astrocytes, the expression was determined by histological and physiological methods. Interestingly, TRPV2 expression was detected in plasma membrane of astrocytes, and the astrocytic TRPV2 was activated by very high temperature (>50°C) consistent with the reported characteristic. We revealed that the astrocytic TRPV2 was also activated by lysophosphatidylcholine, a known endogenous lipid ligand for TRPV2, suggesting that astrocytic TRPV2 might regulate neuronal activities in response to lipid metabolism. Thus, for the first time we revealed that TRPV2 is functionally expressed in astrocytes in addition to neurons.
Keywords	astrocytes ; central nervous system ; heart ; heat ; intestines ; ion channels ; lipid metabolism ; lysophosphatidylcholine ; nerve tissue ; neurons ; pancreas ; plasma membrane ; temperature
Language	English
Dates of publication	2013-1115
Size	p. 327-332.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.10.046
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Article ; Online: Real-Time Translocation and Function of PKCβII Isoform in Response to Nociceptive Signaling via the TRPV1 Pain Receptor

Basil D. Roufogalis / Patricia J. Armati / Sravan Mandadi

Pharmaceuticals, Vol 4, Iss 11, Pp 1503-

2011 Volume 1517

Abstract	Serine/threonine protein kinase C βII isoform (PKCβII) or the pain receptor transient receptor potential vanilloid 1 (TRPV1) have been separately implicated in mediating heat hyperalgesia during inflammation or diabetic neuropathy. However, detailed information on the role of PKC βII in nociceptive signaling mediated by TRPV1 is lacking. This study presents evidence for activation and translocation of the PKC βII isoform as a signaling event in nociception mediated by activation of TRPV1 by capsaicin. We show that capsaicin induces translocation of cytosolic PKCβII isoform fused with enhanced green fluorescence protein (PKCβII-EGFP) in dorsal root ganglion (DRG) neurons. We also show capsaicin-induced translocation in Chinese Hamster Ovarian (CHO) cells co-transfected with TRPV1 and PKCβII-EGFP, but not in CHO cells expressing PKCβII-EGFP alone. By contrast, the PKC activator phorbol-12-myristate-13-acetate (PMA) induced translocation of PKCβII-EGFP which was sustained and independent of calcium or TRPV1. In addition PMA-induced sensitization of TRPV1 to capsaicin response in DRG neurons was attenuated by PKCβII blocker CGP 53353. Capsaicin response via TRPV1 in the DRG neurons was confirmed by TRPV1 antagonist AMG 9810. These results suggested a novel and potential signaling link between PKCβII and TRPV1. These cell culture models provide a platform for investigating mechanisms of painful neuropathies mediated by nociceptors expressing the pain sensing gene TRPV1, and its regulation by the PKC isoform PKCβII.
Keywords	pain ; protein kinase C ; transient receptor potential vanilloid-1 ; real-time translocation ; dorsal root ganglion neurons ; nociceptive signaling ; Medicine ; R ; Pharmacy and materia medica ; RS1-441
Subject code	500
Language	English
Publishing date	2011-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Identification of multisegmental nociceptive afferents that modulate locomotor circuits in the neonatal mouse spinal cord.

Mandadi, Sravan / Hong, Peter / Tran, Michelle A / Bráz, Joao M / Colarusso, Pina / Basbaum, Allan I / Whelan, Patrick J

The Journal of comparative neurology

2013 Volume 521, Issue 12, Page(s) 2870–2887

Abstract: Compared to proprioceptive afferent collateral projections, less is known about the anatomical, neurochemical, and functional basis of nociceptive collateral projections modulating lumbar central pattern generators (CPG). Quick response times are ... ...

Abstract	Compared to proprioceptive afferent collateral projections, less is known about the anatomical, neurochemical, and functional basis of nociceptive collateral projections modulating lumbar central pattern generators (CPG). Quick response times are critical to ensure rapid escape from aversive stimuli. Furthermore, sensitization of nociceptive afferent pathways can contribute to a pathological activation of motor circuits. We investigated the extent and role of collaterals of capsaicin-sensitive nociceptive sacrocaudal afferent (nSCA) nerves that directly ascend several spinal segments in Lissauer's tract and the dorsal column and regulate motor activity. Anterograde tracing demonstrated direct multisegmental projections of the sacral dorsal root 4 (S4) afferent collaterals in Lissauer's tract and in the dorsal column. Subsets of the traced S4 afferent collaterals expressed transient receptor potential vanilloid 1 (TRPV1), which transduces a nociceptive response to capsaicin. Electrophysiological data revealed that S4 dorsal root stimulation could evoke regular rhythmic bursting activity, and our data suggested that capsaicin-sensitive collaterals contribute to CPG activation across multiple segments. Capsaicin's effect on S4-evoked locomotor activity was potent until the lumbar 5 (L5) segments, and diminished in rostral segments. Using calcium imaging we found elevated calcium transients within Lissauer's tract and dorsal column at L5 segments when compared to the calcium transients only within the dorsal column at the lumbar 2 (L2) segments, which were desensitized by capsaicin. We conclude that lumbar locomotor networks in the neonatal mouse spinal cord are targets for modulation by direct multisegmental nSCA, subsets of which express TRPV1 in Lissauer's tract and the dorsal column. J. Comp. Neurol. 521:2870-2887, 2013. © 2013 Wiley Periodicals, Inc.
MeSH term(s)	Afferent Pathways/physiology ; Animals ; Animals, Newborn ; Calcium/metabolism ; Capsaicin/pharmacology ; Evoked Potentials/drug effects ; Evoked Potentials/physiology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; In Vitro Techniques ; Locomotion/genetics ; Locomotion/physiology ; Mice ; Mice, Transgenic ; Neurofilament Proteins/metabolism ; Nociception/physiology ; Periodicity ; Physical Stimulation ; Sensory Receptor Cells/drug effects ; Sensory Receptor Cells/physiology ; Sensory System Agents/pharmacology ; Spinal Cord/cytology ; Spinal Cord/physiology ; TRPV Cation Channels/genetics
Chemical Substances	Neurofilament Proteins ; Sensory System Agents ; TRPV Cation Channels ; TRPV1 protein, mouse ; enhanced green fluorescent protein ; neurofilament protein H (108688-71-7) ; Green Fluorescent Proteins (147336-22-9) ; Capsaicin (S07O44R1ZM) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2013-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.23321
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Article ; Online: Anandamide modulates carotid sinus nerve afferent activity via TRPV1 receptors increasing responses to heat.

Roy, Arijit / Mandadi, Sravan / Fiamma, Marie-Noelle / Rodikova, Ekaterina / Ferguson, Erin V / Whelan, Patrick J / Wilson, Richard J A

Journal of applied physiology (Bethesda, Md. : 1985)

2012 Volume 112, Issue 1, Page(s) 212–224

Abstract: Abnormal respiratory chemosensitivity is implicated in recurrent apnea syndromes, with the peripheral chemoreceptors, the carotid bodies, playing a particularly important role. Previous work suggests that supraphysiological concentrations of the ... ...

Abstract	Abnormal respiratory chemosensitivity is implicated in recurrent apnea syndromes, with the peripheral chemoreceptors, the carotid bodies, playing a particularly important role. Previous work suggests that supraphysiological concentrations of the endocannabinoid endovanilloid and TASK channel blocker anandamide (ANA) excite carotid bodies, but the mechanism(s) and physiological significance are unknown. Given that carotid body output is temperature-sensitive, we hypothesized that ANA stimulates carotid body chemosensory afferents via temperature-sensitive vanilloid (TRPV1) receptors. To test this hypothesis, we used the dual-perfused in situ rat preparation to confirm that independent perfusion of carotid arteries with supraphysiological concentrations of ANA strongly excites carotid sinus nerve afferents and that this activity is sufficient to increase phrenic activity. Next, using ex vivo carotid body preparations, we demonstrate that these effects are mediated by TRPV1 receptors, not CB1 receptors or TASK channels: in CB1-null mouse preparations, ANA increased afferent activity across all levels of Po(2), whereas in TRPV1-null mouse preparations, the stimulatory effect of ANA was absent. In rat ex vivo preparations, ANA's stimulatory effects were mimicked by olvanil, a nonpungent TRPV1 agonist, and suppressed by the TRPV1 antagonist AMG-9810. The specific CB1 agonist oleamide had no effect. Physiological levels of ANA had no effect alone but increased sensitivity to mild hyperthermia. AMG-9810 blocked ANA's effect on the temperature response. Immunolabeling and RT-PCR demonstrated that TRPV1 receptors are not expressed in carotid body glomus cells but reside in petrosal sensory afferents. Together, these results suggest that ANA plays a physiological role in augmenting afferent responses to mild hyperthermia by activating TRPV1 receptors on petrosal afferents.
MeSH term(s)	Animals ; Arachidonic Acids/pharmacology ; Arachidonic Acids/physiology ; Cannabinoids/pharmacology ; Carotid Sinus/drug effects ; Carotid Sinus/physiology ; Endocannabinoids ; Hot Temperature ; In Vitro Techniques ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons, Afferent/drug effects ; Neurons, Afferent/physiology ; Polyunsaturated Alkamides/pharmacology ; Rats ; Rats, Sprague-Dawley ; TRPV Cation Channels/agonists ; TRPV Cation Channels/metabolism
Chemical Substances	Arachidonic Acids ; Cannabinoids ; Endocannabinoids ; Polyunsaturated Alkamides ; TRPV Cation Channels ; Trpv1 protein, rat ; anandamide (UR5G69TJKH)
Language	English
Publishing date	2012-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.01303.2010
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