oalib

Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99

Submit

Any time

2019 ( 154 )

2018 ( 328 )

2017 ( 303 )

2016 ( 462 )

Custom range...

Search Results: 1 - 10 of 299074 matches for " Barry J. Sessle "
All listed articles are free for downloading (OA Articles)
Page 1 /299074
Display every page Item
The Pain Crisis: What It Is and What Can Be Done
Barry J. Sessle
Pain Research and Treatment , 2012, DOI: 10.1155/2012/703947
Abstract: Chronic pain is present in epidemic proportions in most countries, is often unrelieved, and has a huge socioeconomic impact. It is not just a “medical” illness but indeed is a problem that faces all healthcare professional fields. Several steps are identified to address this crisis. These include approaches to enhance pain awareness and access to timely and effective care for pain, and educational and research approaches to improve the knowledge base of healthcare professionals and students and diagnostic and management procedures for pain. Several opportunities to enhance pain understanding, access, and management are also identified. 1. Introduction Despite recent advances in our understanding, diagnosis, and management of pain, several problems confront the pain field, especially in the case of chronic pain which remains a public health problem of epidemic proportion in most countries. This is largely due to the limited levels of (a) awareness of pain, particularly its socioeconomic impact and burden, and access to timely and appropriate care, (b) pain education, especially of health professionals, and (c) research into pain mechanisms and into ways to improve diagnostic and management approaches and healthcare delivery. This pain crisis has been highlighted over the past 2 decades by several authors and again recently by the recent report in the USA by the Institute of Medicine (IOM) [1–7]. This article will focus on these areas and provide for each some possible means to address the current crisis of chronic pain. 2. Awareness of Pain and Its Impact Pain is a subjective individual experience encompassing sensory, cognitive, emotional, and social dimensions. One person may report a moderate level of pain following an injury while another person with a similar injury may report a much higher, or lower, pain level. This individual-by-individual experience of pain depends on numerous features that include each person’s unique genetic features and cognitive, motivational, emotional, and psychological state as well as environmental factors stemming from their gender, past experiences and memories of pain, cultural and social influences, plus their general health condition. Pain does serve an important vital function as a warning signal of tissue damage, resulting from an accidental trauma, infection, or inflammation, for example. It usually disappears after the injured tissue has healed. In contrast to such acute pain episodes, chronic pain is usually considered as having no biological role but is associated with changes in the peripheral and central
Satellite glial cell P2Y12 receptor in the trigeminal ganglion is involved in lingual neuropathic pain mechanisms in rats
Ayano Katagiri, Masamichi Shinoda, Kuniya Honda, Akira Toyofuku, Barry J Sessle, Koichi Iwata
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-23
Abstract: The head-withdrawal reflex thresholds to mechanical and heat stimulation of the lateral tongue were significantly decreased in LNC-rats compared to sham-rats. These nocifensive effects were apparent on day 1 after LNC and lasted for 17 days. On days 3, 9, 15 and 21 after LNC, the mean relative number of TG neurons encircled with GFAP-immunoreactive (IR) cells significantly increased in the ophthalmic, maxillary and mandibular branch regions of TG. On day 3 after LNC, P2Y12R expression occurred in GFAP-IR cells but not neuronal nuclei (NeuN)-IR cells (i.e. neurons) in TG. After 3 days of successive administration of the P2Y12R antagonist MRS2395 into TG in LNC-rats, the mean relative number of TG neurons encircled with GFAP-IR cells was significantly decreased coincident with a significant reversal of the lowered head-withdrawal reflex thresholds to mechanical and heat stimulation of the tongue compared to vehicle-injected rats. Furthermore, after 3 days of successive administration of the P2YR agonist 2-MeSADP into the TG in na?ve rats, the mean relative number of TG neurons encircled with GFAP-IR cells was significantly increased and head-withdrawal reflex thresholds to mechanical and heat stimulation of the tongue were significantly decreased in a dose-dependent manner compared to vehicle-injected rats.The present findings provide the first evidence that the activation of P2Y12R in SGCs of TG following lingual nerve injury is involved in the enhancement of TG neuron activity and nocifensive reflex behavior, resulting in neuropathic pain in the tongue.Neuropathic pain occurs and persists in a heterogeneous group of etiologically different diseases involving a peripheral nerve lesion or dysfunction of the peripheral or central nervous system. Neuropathic pain is relatively common and frequently resistant to clinical treatment [1].Injury to trigeminal nerve branches is known to cause neuropathic pain in the orofacial region [2,3]. The lingual nerve, a branch of the t
Mechanisms involved in an increment of multimodal excitability of medullary and upper cervical dorsal horn neurons following cutaneous capsaicin treatment
Kuniya Honda, Junichi Kitagawa, Barry J Sessle, Masahiro Kondo, Yoshiyuki Tsuboi, Yoshiyuki Yonehara, Koichi Iwata
Molecular Pain , 2008, DOI: 10.1186/1744-8069-4-59
Abstract: Compared to vehicle application, capsaicin application to the lateral facial skin produced 1 hour later a flare in the skin, and also induced significantly greater nocifensive behaviors to heat, cold or mechanical stimulus of the lateral facial skin. The intrathecal (i.t.) injection of the MEK inhibitor PD98059 markedly attenuated the nocifensive behaviors to these stimuli in capsaicin-treated rats. Moreover, the number of pERK-like immunoreactive (pERK-LI) cells in Vc and C1-C2 was significantly larger following the heat, cold and mechanical stimuli in capsaicin-treated rats compared with vehicle-treated rats. The number of pERK-LI cells gradually increased following progressive increases in the heat or mechanical stimulus intensity and following progressive decrease in the cold stimulus. The ERK phosphorylation in Vc and C1-C2 neurons was strongly inhibited after subcutaneous injection of the capsaicin antagonist capsazepine in capsaicin-treated rats.The present findings revealed that capsaicin treatment of the lateral facial skin causes an enhancement of ERK phosphorylation in Vc and C1-C2 neurons as well as induces nocifensive behavior to heat, cold and mechanical simulation of the capsaicin-treated skin. The findings suggest that TRPV1 receptor mechanisms in rat facial skin influence nociceptive responses to noxious cutaneous thermal and mechanical stimuli by inducing neuroplastic changes in Vc and C1-C2 neurons that involve in the MAP kinase cascade.Thermal allodynia or hyperalgesia to heat, cold or mechanical stimuli can be produced by peripheral inflammation or peripheral nerve injury [1,2]. Capsaicin is an inflammatory irritant and a specific excitant of C- and small-diameter Aδ-fibers innervating peripheral tissues [3-5]. It is well known that capsaicin binds to the transient receptor potential (TRP) vanilloid 1 (TRPV1) channel and induces cation influx in peripheral nerve fiber terminals [6-8]. These receptors are also activated by heat stimulation of per
The effect of minocycline on the masticatory movements following the inferior alveolar nerve transection in freely moving rats
Rahman MD. Mostafeezur, Hossain MD. Zakir, Yoshiaki Yamada, Kensuke Yamamura, Koichi Iwata, Barry J. Sessle, Junichi Kitagawa
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-27
Abstract: The number of Iba1-immunoreactive (IR) cells both in prV and motV was significantly larger in IAN-X rats compared with sham rats on day 3 after IAN-X. The intraperitoneal (i.p.) administration of MC caused a significant reduction of the number of Iba1-IR cells both in prV and motV that was evident on day 14 after IAN-X. Furthermore, a significant reduction of the number of Iba1-IR cells could be observed in motV but not in prV after microinjection (m.i.) of MC into the motV of IAN-X rats. The rats also exhibited a significant decrease in the head-withdrawal threshold on the side ipsilateral to the IAN-X compared to the threshold before IAN-X and it lasted to day 14. In addition, IAN-X markedly affected the ability to rat to carry out mastication. The number of complete masticatory sequences was significantly decreased. Furthermore, the total masticatory sequence time and food preparatory (PP) period duration was significantly elongated in compared to sham rats. Although IAN-X significantly affected the total number of chewing cycles within the RC period of a masticatory sequence, it had no effect on the duration of the chewing cycles. On the other hand, systemic administration of MC (both i.p. and m.i.) in IAN-X rats significantly improved decreased head-withdrawal threshold and the impaired masticatory jaw movements.The present findings reveal that the strong modulation of masticatory jaw movements occurs following microglial cell activation after IAN-X, and the modulation recovers after inhibition of the microglial cell activation by MC, suggesting that microglial cell activation in the motV as well as in the prV has a pivotal role in modulating mastication following trigeminal nerve injury associated with orofacial neuropathic pain.
Involvement of peripheral ionotropic glutamate receptors in orofacial thermal hyperalgesia in rats
Kuniya Honda, Noboru Noma, Masamichi Shinoda, Makiko Miyamoto, Ayano Katagiri, Daiju Kita, Ming-Gang Liu, Barry J Sessle, Masafumi Yasuda, Koichi Iwata
Molecular Pain , 2011, DOI: 10.1186/1744-8069-7-75
Abstract: Glu application to the tongue or whisker pad skin caused an enhancement of head-withdrawal reflex and extracellular signal-regulated kinase (ERK) phosphorylation in Vc-C2 neurons. Head-withdrawal reflex and ERK phosphorylation were also enhanced following cold stimulation of the tongue but not whisker pad skin in Glu-injected rats, and the head-withdrawal reflex and ERK phosphorylation were enhanced following heat stimulation of the tongue or whisker pad skin. The enhanced head-withdrawal reflex and ERK phosphorylation after heat stimulation of the tongue or whisker pad skin, and those following cold stimulation of the tongue but not whisker pad skin were suppressed following ionotropic glutamate receptor antagonists administration into the tongue or whisker pad skin. Furthermore, intrathecal administration of MEK1/2 inhibitor PD98059 caused significant suppression of enhanced head-withdrawal reflex in Glu-injected rats, heat head-withdrawal reflex in the rats with Glu injection into the tongue or whisker pad skin and cold head-withdrawal reflex in the rats with Glu injection into the tongue.The present findings suggest that peripheral Glu receptor mechanisms may contribute to cold hyperalgesia in the tongue but not in the facial skin, and also contribute to heat hyperalgesia in the tongue and facial skin, and that the mitogen-activated protein kinase cascade in Vc-C2 neurons may be involved in these Glu-evoked hyperalgesic effects.It is well known from human psychophysical studies that thermal and mechanical sensitivity of the tongue is different from that of the facial skin [1-4]. Cold and heat sensory thresholds are significantly higher in the tongue compared to the facial skin. The pain threshold is also higher in tongue compared to the facial skin. Previous histological studies have also reported that cutaneous tissues are covered by orthokeratinized tissues, whereas mucosal membranes are covered by parakeratinized tissues, and mucosal surfaces are highly moist
Alteration of primary afferent activity following inferior alveolar nerve transection in rats
Kazuharu Nakagawa, Mamoru Takeda, Yoshiyuki Tsuboi, Masahiro Kondo, Junichi Kitagawa, Shigeji Matsumoto, Azusa Kobayashi, Barry J Sessle, Masamichi Shinoda, Koichi Iwata
Molecular Pain , 2010, DOI: 10.1186/1744-8069-6-9
Abstract: Fluorogold (FG) injection into the mental region 14 days after IAN transection showed massive labeling of trigeminal ganglion (TG). The escape threshold to mechanical stimulation of the mental skin was significantly lower (i.e. mechanical allodynia) at 11-14 days after IAN transection than before surgery. The background activity, mechanically evoked responses and afterdischarges of IAN Aδ-fibers were significantly higher in IAN-transected rats than naive. The small/medium diameter TG neurons showed an increase in both tetrodotoxin (TTX)-resistant (TTX-R) and -sensitive (TTX-S) sodium currents (INa) and decrease in total potassium current, transient current (IA) and sustained current (IK) in IAN-transected rats. The amplitude, overshoot amplitude and number of action potentials evoked by the depolarizing pulses after 1 μM TTX administration in TG neurons were significantly higher, whereas the threshold current to elicit spikes was smaller in IAN-transected rats than naive. Resting membrane potential was significantly smaller in IAN-transected rats than that of naive.These data suggest that the increase in both TTX-S INa and TTX-R INa and the decrease in IA and Ik in small/medium TG neurons in IAN-transected rats are involved in the activation of spike generation, resulting in hyperexcitability of Aδ-IAN fibers innervating the mental region after IAN transection.Numerous papers have described how peripheral nerve injury causes a variety of functional deficits in sensory processing [1-7]. Neuropathic pain also may occur after nerve injury [8-11], and whereas the injured tissue does usually repair, the neuropathic pain frequently persists [12-14]. One mechanism that is considered to underlie the abnormal pain after nerve damage involves regenerating nerve fibers. Injured nerves regenerate several weeks after nerve damage [15-17]. Some clinical reports have noted that areas innervated by the regenerated nerves show an altered sensitivity to a variety of stimuli compared
Mechanisms involved in extraterritorial facial pain following cervical spinal nerve injury in rats
Azusa Kobayashi, Masamichi Shinoda, Barry J Sessle, Kuniya Honda, Yoshiki Imamura, Suzuro Hitomi, Yoshiyuki Tsuboi, Akiko Okada-Ogawa, Koichi Iwata
Molecular Pain , 2011, DOI: 10.1186/1744-8069-7-12
Abstract: The head withdrawal threshold to mechanical stimulation of the lateral facial skin and head withdrawal latency to heating of the lateral facial skin were significantly lower and shorter respectively in CNX rats compared to Sham rats. These nocifensive effects were apparent within 1 day after CNX and lasted for more than 21 days. The numbers of pERK-like immunoreactive (LI) cells in superficial laminae of Vc and C1-C2 were significantly larger in CNX rats compared to Sham rats following noxious and non-noxious mechanical or thermal stimulation of the lateral facial skin at day 7 after CNX. Two peaks of pERK-LI cells were observed in Vc and C1-C2 following mechanical and heat stimulation of the lateral face. The number of pERK-LI cells in C1-C2 was intensity-dependent and increased when the mechanical and heat stimulations of the face were increased. The decrements of head withdrawal latency to heat and head withdrawal threshold to mechanical stimulation were reversed during intrathecal (i.t.) administration of MAPK/ERK kinase 1/2 inhibitor PD98059. The area of activated astroglial cells was significantly higher in CNX rats (at day 7 after CNX). The heat and mechanical nocifensive behaviors were significantly depressed and the number of pERK-LI cells in Vc and C1-C2 following noxious and non-noxious mechanical stimulation of the face was also significantly decreased following i.t. administration of the astroglial inhibitor fluoroacetate.The present findings have demonstrated that mechanical allodynia and thermal hyperalgesia occur in the lateral facial skin after CNX and also suggest that ERK phosphorylation of Vc and C1-C2 neurons and astroglial cell activation are involved in orofacial extraterritorial pain following cervical nerve injury.It has been reported that peripheral nerve injury causes marked neuronal excitability and gene expression in the central nervous system (CNS) as well as in the peripheral nervous system (PNS) [1,2]. Whole or partial peripheral nerv
Purinergic receptors are involved in tooth-pulp evoked nocifensive behavior and brainstem neuronal activity
Kazunori Adachi, Kohei Shimizu, James W Hu, Ikuko Suzuki, Hiroshi Sakagami, Noriaki Koshikawa, Barry J Sessle, Masamichi Shinoda, Makiko Miyamoto, Kuniya Honda, Koichi Iwata
Molecular Pain , 2010, DOI: 10.1186/1744-8069-6-59
Abstract: Genioglossus (GG) muscle activity was evoked by pulpal application of 100 mM α,β-meATP and was significantly larger than GG activity following vehicle (phosphate-buffered saline PBS) application (p < 0.01). The enhanced GG muscle activity following 100 mM α,β-meATP was significantly reduced (p < 0.05) by co-application of 1 mM TNP-ATP (P2X1, P2X3 and, P2X2/3 antagonist). A large number of pERK-LI cells were expressed in the Vc, Vi/Vc, C1/C2 and Pa5 at 5 min following pulpal application of 100 mM α,β-meATP compared to PBS application to the pulp (p < 0.05). The pERK-LI cell expression and GG muscle activity induced by 100 mM α,β-meATP pulpal application were significantly reduced after intrathecal injection of the MAPK/ERK kinase (MEK) inhibitor PD 98059 and by pulpal co-application of 1 mM TNP-ATP (p < 0.05).The present findings suggest that activation of P2X3 and P2X2/3 receptors in the tooth pulp is sufficient to elicit nociceptive behavioral responses and trigeminal brainstem neuronal activity.Adenosine 5'-triphosphate (ATP) is considered a neuro-modulator in primary afferent neurons. Release of ATP from sympathetic nerve terminals, endothelial, Merkel or tumor cells is known to be involved in excitation of unmyelinated primary afferent neurons [1]. One of ATP receptors activated by ATP binding is the P2X family of ATP receptors; it has been classified into seven subtypes, P2X1-7 (for review, see [2-8]). All of them, except the P2X7 receptor, are expressed in various primary sensory neurons including tooth pulp neurons [9-13]. In particular, the P2X3 homomeric and P2X2/3 heteromeric receptors have been associated with peripheral nociceptive mechanisms, since these subtypes occur in a subset of putative nociceptive sensory neurons [10-12,14-16], and their activation produces nocifensive behavior that can be attenuated by peripheral [17-20] or central [16,21] administration of P2X3,2/3 receptor antagonists. Also activation of pulpal P2X3,2/3 receptors produces cent
Involvement of ERK Phosphorylation of Trigeminal Spinal Subnucleus Caudalis Neurons in Thermal Hypersensitivity in Rats with Infraorbital Nerve Injury
Ikuko Suzuki, Yoshiyuki Tsuboi, Masamichi Shinoda, Kazuo Shibuta, Kuniya Honda, Ayano Katagiri, Masaaki Kiyomoto, Barry J. Sessle, Shingo Matsuura, Kinuyo Ohara, Kentaro Urata, Koichi Iwata
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0057278
Abstract: To evaluate the involvement of the mitogen-activated protein kinase (MAPK) cascade in orofacial neuropathic pain mechanisms, this study assessed nocifensive behavior evoked by mechanical or thermal stimulation of the whisker pad skin, phosphorylation of extracellular signal-regulated kinase (ERK) in trigeminal spinal subnucleus caudalis (Vc) neurons, and Vc neuronal responses to mechanical or thermal stimulation of the whisker pad skin in rats with the chronic constriction nerve injury of the infraorbital nerve (ION-CCI). The mechanical and thermal nocifensive behavior was significantly enhanced on the side ipsilateral to the ION-CCI compared to the contralateral whisker pad or sham rats. ION-CCI rats had an increased number of phosphorylated ERK immunoreactive (pERK-IR) cells which also manifested NeuN-IR but not GFAP-IR and Iba1-IR, and were significantly more in ION-CCI rats compared with sham rats following noxious but not non-noxious mechanical stimulation. After intrathecal administration of the MEK1 inhibitor PD98059 in ION-CCI rats, the number of pERK-IR cells after noxious stimulation and the enhanced thermal nocifensive behavior but not the mechanical nocifensive behavior were significantly reduced in ION-CCI rats. The enhanced background activities, afterdischarges and responses of wide dynamic range neurons to noxious mechanical and thermal stimulation in ION-CCI rats were significantly depressed following i.t. administration of PD98059, whereas responses to non-noxious mechanical and thermal stimulation were not altered. The present findings suggest that pERK-IR neurons in the Vc play a pivotal role in the development of thermal hypersensitivity in the face following trigeminal nerve injury.
Mechanisms Underlying Ectopic Persistent Tooth-Pulp Pain following Pulpal Inflammation
Shingo Matsuura, Kohei Shimizu, Masamichi Shinoda, Kinuyo Ohara, Bunnai Ogiso, Kuniya Honda, Ayano Katagiri, Barry J. Sessle, Kentaro Urata, Koichi Iwata
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0052840
Abstract: In order to clarify the peripheral mechanisms of ectopic persistent pain in a tooth pulp following pulpal inflammation of an adjacent tooth, masseter muscle activity, phosphorylated extracellular signal-regulated protein kinase (pERK) and TRPV1 immunohistochemistries and satellite cell activation using glial fibrillary acidic protein (GFAP) immunohistochemistry in the trigeminal ganglion (TG) were studied in the rats with molar tooth-pulp inflammation. And, Fluorogold (FG) and DiI were also used in a neuronal tracing study to analyze if some TG neurons innervate more than one tooth pulp. Complete Freund’s adjuvant (CFA) or saline was applied into the upper first molar tooth pulp (M1) in pentobarbital-anesthetized rats, and capsaicin was applied into the upper second molar tooth pulp (M2) on day 3 after the CFA or saline application. Mean EMG activity elicited in the masseter muscle by capsaicin application to M2 was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats. The mean number of pERK-immunoreactive (IR) TG cells was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats. Application of the satellite cell inhibitor fluorocitrate (FC) into TG caused a significant depression of capsaicin-induced masseter muscle activity and a significant reduction of satellite cell activation. The number of TRPV1-IR TG cells innervating M2 was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats, and that was decreased following FC injection into TG. Furthermore, 6% of TG neurons innervating M1 and/or M2 innervated both M1 and M2. These findings suggest that satellite cell activation following tooth pulp inflammation and innervation of multiple tooth pulps by single TG neurons may be involved in the enhancement of the activity of TG neurons innervating adjacent non-inflamed teeth that also show enhancement of TRPV1 expression in TG neurons, resulting in the ectopic persistent tooth-pulp pain following pulpal inflammation of adjacent teeth.
Page 1 /299074
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.