Differential development of TRPV1-expressing sensory nerves in peripheral organs

Funakoshi, Kengo; Nakano, Masato; Atobe, Yoshitoshi; Goris, Richad C.; Kadota, Tetsuo; Yazama, Futoshi

doi:10.1007/s00441-005-0013-3

Cited by 44 publications

(37 citation statements)

References 77 publications

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“…CGRP and other vasodilators are co-localized in TRPV1 sensory containing terminals (Eguchi et al, 2004). The activation of TRPV1 and the subsequent depolarization of the sensory terminals caused the release of these vasodilators which enter the vascular smooth muscle layer (Caterina et al, 1997;Bernardini et al, 2004;Funakoshi et al, 2006). CGRP is one of the most powerful microvascular vasodilators (Brain et al, 1985).…”

Section: Antidromic Mechanism-mentioning

confidence: 99%

“…However, neuropeptides including CGRP and NO, as well as TRPV1 containing sensory fibers exist and play important roles in the regulation of cardiovascular system (Ferdinardy et al, 1997;Chottova Dvorakova et al, 2005;Funakoshi et al, 2006;Zyara et al, 2006;Ye et al, 2006). One explanation is that SCS does not activate TRPV1 containing sensory fibers resulting in vasodilation, but stimulates other types of fibers that regulate the cardiac nervous system (see section 2.2.4).…”

Section: Mechanisms For Changes In Blood Flow-mentioning

confidence: 99%

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Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

Linderoth

Foreman

2008

Autonomic Neuroscience

159

106

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Spinal cord stimulation (SCS) is a widely used clinical technique to treat ischemic pain in peripheral, cardiac and cerebral vascular diseases. The use of this treatment advanced rapidly during the late 80's and 90's, particularly in Europe. Although the clinical benefits of SCS are clear and the success rate remains high, the mechanisms are not yet completely understood. SCS at lumbar spinal segments (L2-L3) produces vasodilation in the lower limbs and feet which is mediated by antidromic activation of sensory fibers and decreased sympathetic outflow. SCS at thoracic spinal segments (T1-T2) induces several benefits including pain relief, reduction in both frequency and severity of angina attacks, and reduced short-acting nitrate intake. The benefits to the heart are not likely due to an increase, or redistribution of local blood flow, rather, they are associated with SCS-induced myocardial protection and normalization of the intrinsic cardiac nervous system. At somewhat lower cervical levels (C3-C6), SCS induces increased blood flow in the upper extremities. SCS at the upper cervical spinal segments (C1-C2) increased cerebral blood flow, which is associated with a decrease in sympathetic activity, an increase in vasomotor center activity and a release of neurohumoral factors. This review will summarize the basic science studies that have contributed to our understanding about mechanisms through which SCS produces beneficial effects when used in the treatment of vascular diseases. Furthermore, this review will particularly focus on the antidromic mechanisms of SCS-induced vasodilation in the lower limbs and feet.

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Section: Antidromic Mechanism-mentioning

confidence: 99%

Section: Mechanisms For Changes In Blood Flow-mentioning

confidence: 99%

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

Linderoth

Foreman

2008

Autonomic Neuroscience

159

106

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“…Within the DRG and trigeminal ganglia, TRPV1 is most abundantly expressed in small diameter C-fibers that express CGRP, SP and IB4. It is also found within sensory fibers that innervate the viscera, urinary bladder and airways [17,42,43,76,93,139]. Consistent with the central projections of these neurons, TRPV1 immunoreactivity is localized to CNS regions such as the superficial laminae (I and II) of the dorsal horn of the spinal cord and nucleus of the solitary tract [50,139].…”

Section: Trpv1 and Noxious Heat Detectionmentioning

confidence: 69%

“…Two groups have studied the role of TRPV4 in mediating acute noxious heat detection and inflammatory thermal hyperalgesia by analyzing TRPV4-/-mice [81,138]. In the first study, acute noxious heat sensation of TRPV4-/-mice appears intact, with no significant difference compared to wildtype in escape latencies in hot plate (35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50) o C) or radiant heat tests [138]. In this same study, TRPV4-/-mice display longer escape latencies from hot plate compared to wildtype following hindpaw injection of carrageenan, indicating that TRPV4 plays a role in mediating inflammation induced thermal hyperalgesia.…”

Section: Role Of Warmth-activated Thermotrpvs In Acute and Inflammatomentioning

confidence: 99%

The Emerging Role of TRP Channels in Mechanisms of Temperature and Pain Sensation

Story¹

2006

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Abstract:Pain is universal and vital to survival. It is an essential component of our sense of touch; together, touch and pain have evolved to enable our awareness of the intricacies of our environment and to warn us of danger and possible injury. There is a clear link between temperature sensation and pain-painful temperature sensations occur acutely and are a hallmark of inflammatory and chronic pain disorders of the nervous system. Mounting evidence suggests a subset of Transient Receptor Potential (TRP) ion channels activated by temperature (thermoTRPs) are important molecular players in acute, inflammatory and chronic pain states. Varying degrees of heat activate four of these channels (TRPV1-4), while cooling temperatures ranging from pleasant to painful activate two distantly related thermoTRP channels (TRPM8 and TRPA1). ThermoTRP channels are also chemosensitive, being activated and or modulated by plant-derived small molecules and endogenous inflammatory mediators. All thermoTRPs are expressed in tissues essential to cutaneous thermal and pain sensation. This review examines the contribution of thermoTRP channels to our understanding of temperature and pain transduction at the molecular level.Key Words: ThermoTRP, pain, DRG, skin, inflammation, TRPA1, TRPV. TRP CHANNELS: A PRIMERThe detection of temperature and pain stimuli is initiated at the level of primary afferent neurons that terminate as free nerve endings embedded in target tissues such as the dermal and epidermal layers of the skin, the oral and nasal mucosa and joints. The cell bodies of these neurons originate from cranial nerve ganglia and dorsal root ganglia (DRG). They relay information regarding environmental stimuli to the central nervous system via central processes projecting to the dorsal horn of the spinal cord. The conduction properties of neurons that respond to stimuli such as heat, cold and mechanical pressure are characteristic of C-and A fibers [91]. These neurons express the receptor tyrosine kinase trkA, are dependent on nerve growth factor (NGF) during development and are peptidergic, expressing nociceptive markers such as calcitonin gene-related peptide (CGRP) and substance P (SP) [121]. A portion of these neurons express c-ret postnatally, are dependent on glial-derived neurotrophic factor (GDNF) and are non-peptidergic. Instead they are distinguished by their ability to bind the plant lectin, isolectin-B4 (IB4) [95,133,164]. Until relatively recently, the mechanisms of how these sensory neurons detect thermal and pain stimuli were poorly understood.Caterina et al. achieved a breakthrough in our molecular understanding of thermal and pain sensation by identifying the "capsaicin receptor" [24]. Hot chili peppers produce this deterrent vanilloid molecule, which induces a burning sensation when coming in contact with mucous membranes of the mouth and eyes. This biological effect results from the excitation of a sub-population of nociceptive neurons [136] TRPV1 is the founding mammalian member of the superfamily of outwardly r...

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“…[136][137][138][139] By regulating Ca 2+ and other second messengers, the TRP channels may contribute to the survival and differentiation of cells and tissues, especially in the early embryonic stages. Indeed, expression of some TRP channels, like TRPV1 in the early embryonic stages has been reported, 136,140 and the expression of several TRP channels co-relate with the differentiation of the stem cells. 141 Being non-selective Ca 2+ channels, TRP channels can regulate the Ca 2+ -signaling events including Ca 2+ -waves.…”

Section: Meeting Reportmentioning

confidence: 99%

Transient Receptor Potential Channels: What is happening? Reflections in the wake of the 2009 TRP meeting, Karolinska Institutet, Stockholm

Goswami¹,

Islam²

2010

Channels

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Role of TRP channels in thermosensation.The abilities of sensing and differentiating environmental temperatures are important functions performed by almost all organisms. However, different organisms handle this fundamental function by different mechanisms and by recruiting different sets of molecules that can sense different temperatures. 6,7 In this context, TRP channels are particularly interesting since some TRP channels can be activated by different temperatures.8-10 Such thermo-sensitive TRP channels are quite selective for different temperature ranges in which they can be activated.11 Such temperature ranges cover from noxious cold to noxious heat. It has, therefore, been speculated that the thermo-sensitive TRP channels are responsible for thermosensation and for the maintenance of the normal body temperature.12-14 However, the molecular mechanisms by which these thermo-sensitive TRP channels recognize different temperatures remain unanswered.15,16 Recent electrophysiological and knockout studies show that the molecular mechanism of thermosensation can not be solely dependent on the TRP channels. Molecules other than TRP channels are also involved in this process in a more complex manner than it was thought before. [17][18][19][20][21] In fact many of the animals lacking TRP channels show normal thermosensation. 22,23 On the other hand, some animals genetically lacking molecules other than the TRP channels also manifest altered thermosensation. For example mice lacking P2Y2 receptor reveals abnormal thermal nociception. 24 Taking together, these studies indicate that a complex network is operating behind the molecular mechanisms of thermosensation.Previously it has been shown that swapping the C-terminal cytoplasmic domain of a cold receptor (TRPM8) with a hot receptor (TRPV1) makes the cold receptor recognize high temperature and vice versa. 25 This indicated that the C-terminal TRP channelsWhat's happening? Reflections in the wake of the 2009 TRP Meeting, Karolinska Institutet, Stockholm

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Differential development of TRPV1-expressing sensory nerves in peripheral organs

Cited by 44 publications

References 77 publications

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

The Emerging Role of TRP Channels in Mechanisms of Temperature and Pain Sensation

Transient Receptor Potential Channels: What is happening? Reflections in the wake of the 2009 TRP meeting, Karolinska Institutet, Stockholm

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