• The Korean Journal of Pain
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• 제9권1호
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• pp.26-38
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• 1996

In a normal state, sympathetic efferent activity does not elicit discharges of sensory neurons, whereas it becomes associated with and excites sensory neurons in a pathophysiological state such as injury to a peripheral nerve. Although this sympathetic-sensory interaction is reportedly adrenergic, involved subtypes of adrenoreceptors are not yet clearly revealed. The purpose of this study was to determine which adrenorceptor subtypes were involved in sympathetic-sensory interaction that was developed in rats with an experimental peripheral neuropathy. Using rats that received a tight ligation of one or two of L4-L6 spinal nerves 10~15 days previously, a recording was made from afferent fibers in microfilaments teased from the dorsal root that was in continuity with the ligated spinal nerve. Electrical stimulation of sympathetic preganglionic fibers in T13 or L1 ventral root (50 Hz, 2-5 mA. 0.5 ms pulse duration, 10 sec) was made to see if the activity of recorded afferents was modulated. About half of afferents showing spontaneous discharges responded to sympathetic stimulation, and had the conduction velocities in the A-fiber range. Most of the sympathetically induced afferent responses were excitation. This sympathetically induced excitation occurred in the dorsal root ganglion (DRG), and was blocked by yohimbine (${\alpha}_2$ blocker), neither by propranolol ($\beta$ blocker) not by prazosine (${\alpha}_1$ blocker). The results suggest that after spinal nerve ligation, sympathetic efferents interact with sensory neurons having A-fiber axons in DRG where adrenaline released from sympathetic nerve endings excites the activity of sensory neurons by acting on 2-adrenoreceptors. This 2-adrenoreceptor mediated excitation of sensory neurons may account for sympathetic involvement in neuropathic pain.

• The Korean Journal of Pain
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• 제36권1호
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• pp.4-10
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• 2023

Herpes zoster (HZ) is a common disease in the aging population and immunocompromised individuals, with a lifetime risk of 20%-30% that increases with age. HZ is caused by reactivation of the varicella-zoster virus (VZV), which remains latent in the spinal dorsal root ganglia and cranial sensory ganglia after resolution of the primary VZV infection. The main focus of HZ management is rapid recovery from VZV infection as well as the reduction and prevention of zoster-associated pain (ZAP) and postherpetic neuralgia (PHN). The use of antivirals against VZV is essential in the treatment of HZ. However, limited antivirals are only licensed clinically for the treatment of HZ, including acyclovir, valacyclovir, famciclovir, brivudine, and amenamevir. Fortunately, some new antivirals against different types of Herpesviridae have been investigated and suggested as novel drugs against VZV. Therefore, this review focuses on discussing the difference in efficacy and safety in the currently licensed antivirals for the treatment of HZ, the applicability of future novel antivirals against VZV, and the preventive or therapeutic effects of these antivirals on ZAP or PHN.

• 동의생리병리학회지
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• 제32권1호
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• pp.30-34
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• 2018

This research was practiced to comparative investigate the distribution of sensory and motor neuron linkaged with Yangji(TE4) by using neural-tracer technology. A total 16 S-D rats were used in the present research. After anesthesia, the rats received micro-injection of $6{\mu}{\ell}$ of cholera toxin B subunit(CTB) into the relation positions of the Yangji(TE4), in the human body for observing the distribution of the linkaged sensory neurons in dorsal root ganglia(DRGs) and motor neurons in the spinal cord(C3~T4) and sympathetic ganglia. 3 days after the micro injection, the rats were anesthetized and transcardially perfused saline and 4% paraformaldehyde, followed by routine section of the DRGs, sympathetic chain ganglia(SCGs) and spinal cord. Marked neurons and nerve fibers were detected by immunohistochemical method and observed by light microscope. The marked neurons were recorded and counted. From this study the distribution of primary sensory and motor neurons linkaged with Yangji(TE4) were concluded as follows. Yangji(TE4) dominated by spinal segments of C5~T1, C6~T4, individually.

• Korean Journal of Acupuncture
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• 제32권3호
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• pp.136-143
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• 2015

This study was performed to comparative investigate the distribution of primary sensory and motor neurons associated with Cheonji(PC1) acupoint by using neural tracing technique. A total 4 SD rats were used in the present study. After anesthesia, the rats received microinjection of $6{\mu}l$ of cholera toxin B subunit(CTB) into the corresponding sites of the acupoints Cheonji(PC1) in the human body for observing the distribution of the related primary sensory neurons in dorsal root ganglia(DRGs) and motor neurons in the spinal cord(C3~T4) and sympathetic ganglia. Three days after the microinjection, the rats were anesthetized and transcardially perfused saline and 4% paraformaldehyde, followed by routine section of the DRGs, sympathetic chain ganglia(SCGs) and spinal cord. Labeled neurons and nerve fibers were detected by immunohistochemical method and observed by light microscope equipped with a digital camera. The labeled neurons were recorded and counted. From this research, the distribution of primary sensory and motor neurons associated with Cheonji(PC1) acupoints were concluded as follows. Muscle meridian related Cheonji(PC1) are controlled by spinal segments of C5~T1, C6~T4, respectively.

• The Korean Journal of Pain
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• 제37권3호
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• pp.233-246
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• 2024

Background: Ferrostatin-1 and liproxstatin-1, both ferroptosis inhibitors, protect cells. Liproxstatin-1 decreases morphine tolerance. Yet, ferrostatin-1's effect on morphine tolerance remains unexplored. This study aimed to evaluate the influence of ferrostatin-1 on the advancement of morphine tolerance and understand the underlying mechanisms in male rats. Methods: This experiment involved 36 adult male Wistar albino rats with an average weight ranging from 220 to 260 g. These rats were categorized into six groups: Control, single dose ferrostatin-1, single dose morphine, single dose ferrostatin-1 + morphine, morphine tolerance (twice daily for five days), and ferrostatin-1 + morphine tolerance (twice daily for five days). The antinociceptive action was evaluated using both the hot plate and tail-flick tests. After completing the analgesic tests, tissue samples were gathered from the dorsal root ganglia (DRG) for subsequent analysis. The levels of glutathione, glutathione peroxidase 4 (GPX4), and nuclear factor erythroid 2-related factor 2 (Nrf2), along with the measurements of total oxidant status (TOS) and total antioxidant status (TAS), were assessed in the tissues of the DRG. Results: After tolerance development, the administration of ferrostatin-1 resulted in a significant decrease in morphine tolerance (P < 0.001). Additionally, ferrostatin-1 treatment led to elevated levels of glutathione, GPX4, Nrf2, and TOS (P < 0.001), while simultaneously causing a decrease in TAS levels (P < 0.001). Conclusions: The study found that ferrostatin-1 can reduce morphine tolerance by suppressing ferroptosis and reducing oxidative stress in DRG neurons, suggesting it as a potential therapy for preventing morphine tolerance.

• Journal of Korean Neurosurgical Society
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• 제29권7호
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• pp.877-885
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• 2000

Objective : The NOS inhibitors exhibit antinociceptive activity in rat model of neuropathic pain. NOS activity increases in the dorsal root ganglia(DRG) in neurop-athic pain. However, NOS activity decreases in the dorsal horn of spinal cord in the nerve injury models of neuropathic pain. To investigate whether the mechanism of decrease of NOS expression in the dorsal horn is related to a secondary effect resulting from increased NO production and likewise in the spinal DRG in the spinal nerve ligation model of neuropathic pain. Methods : We conducted behavioral tests for neuropathic pain, and nNOS immunohistochemistry and NADPH-diaphorase histochemistry after tight ligation of the 5th lumbar(L5) and 6th lumbar(L6) spinal nerves and L5 dorsal rhizotomy. Results : Typical neuropathic pain behaviors occurred 7 days after post-ligation in the neuropathic surgery group, but neuropathic pain behaviors in the dorsal rhizotomy group were absent or weak 7 days after post-operation. There was a decrease in the number of nNOS immunoreactive dorsal horn neurons on the both side(especially ipsilateral side) 7 days after post-ligation. The number of nNOS immunoreactive neurons in both side of the dorsal horn was not decreased 7 days after L5 dorsal rhizotomy. Conclusion : These data indicate that the changes in the injured DRG is essential for development and maintenance of neuropathic pain, and mechanism of decrease of nNOS expression in the dorsal horn is a secondary effect against the changes in the DRG including increased NO production in the spinal nerve ligation model of neuropathic pain.

• 대한한의학회지
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• 제18권1호
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• pp.58-71
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• 1997

In order to the location and local arrangement of nerve cell bodies and nerve fibers projecting to the meridian points related to facial nerve paralysis in the rat using the neural tracers, CTB and WGA-HRP, labeled neurons the were investigated by immunohistochemical and HRP histochemical methods following injection of 2.5% WGA-HRP and 1% CTB into Hyopko$(S_6)$. Chichang$(S_4)$, Sugu$(GV_{26})$, Sajukkong$(TE_{23})$ and Yangbaek$(G_{14})$. Following injection of Hyopko$(S_6)$, Chichang$(S_4)$, labeled motor neurons were founded in facial nucleus, trigeminal motor nucleus, reticular nucleus and hypoglossal nucleus. labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in mesencephalic trigeminal tract, sensory root of trigeminal nerve, oral, interpolar and caudal part of trigeminal nucleus, area postrema, nucleus tractus solitarius, lateral reticular nucleus and $C_{1-2}$ spinal ganglia. Following injection of Sugu$(GV_{26})$, labeled motor neurons were founded in facial nucleus. Labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. Sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in spinal trigeminal tract, trigeminal motor nucleus, mesencephalic trigeminal tract, oral. interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius, lateral reticular nucleus, dorsal part of reticular part and $C_{1-2}$ spinal ganglia. Following injection of Sajukkong$(TE_{23})$ and Yangbaek$(G_{14})$, labeled motor neurons were founded in facial nucleus, trigeminal motor nucleus. Labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in oral, interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius, inferior olovary nucleus, medullary reticular field and lamina I-IV of $C_{1-2}$ spinal cord. Location of nerve cell body and nerve fibers projecting to the meridian points related to the facial nerve paralysis in the rats were found in facial nucleus and trigeminal motor nucleus. Sensory neurone were found in trigeminal ganglia and $C_{1-2}$ spinal ganglia. Sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in mesencephalic trigeminal tract, oral, interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius. lateral reticular nucleus, medullary reticular field.

• Archives of Pharmacal Research
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• 제27권11호
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• pp.1154-1160
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• 2004

We investigated the neurotoxic effects of capsaicin (CAP) on pain sensitivity and on the expression of capsaicin receptor, the vanilloid receptor (VR1), in rats. High-dose application of CAP has been known to degenerate a large fraction of the sensory neurons. Although the neurotoxic effects of CAP are well documented, the effects of CAP on the vanilloid receptor (VR1) are not yet known. In this paper, we investigated the effects of high-dose application of CAP on the expression of VR1 in rats. Thermal and mechanical pain sensitivity was reduced when neonatal rats were treated with a high dose of CAP. This reduction of pain sensitivity was significantly decreased after initiating carrageenan-induced inflammation. The expression of VR1 in dorsal root ganglia (DRG) isolated from the CAP-treated rats was reduced compared to that from the vehicle-treated rats. Therefore, we can conclude that the neurotoxic effect of CAP is related to the decrease of VR1 expression.

• Animal cells and systems
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• 제15권3호
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• pp.181-187
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• 2011

Transient receptor potential vanilloid type 1 (TRPV1) receptor plays an important role as a molecular detector of noxious signals in primary sensory neurons. Activity of TRPV1 can be modulated by the change in the environment such as redox state and extracellular cations. In the present study, we investigated the effect of the mercury chloride ($HgCl_2$) on the activity of TRPV1 in rat dorsal root ganglia (DRG) neurons using whole-cell patch clamp technique. Extracellular $HgCl_2$ reversibly reduced the magnitudes of capsaicin-activated currents ($I_{cap}$) in DRG neurons in a dose-dependent manner. The blocking effect of $HgCl_2$ was prevented by pretreatment with the reducing agent dithiothreitol (DTT). Inhibition of $I_{cap}$ by $HgCl_2$ was abolished by point mutation of individual cysteine residues located on the extracellular surface of TRPV1. These results suggest that three extracellular cysteines of TRPV1, Cys616, Cys634 and Cys621, are responsible for the oxidative modulation of $I_{cap}$ by $HgCl_2$.

• 한국정보기술학회 영문논문지
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• 제10권2호
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• pp.199-214
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• 2020

An important technique of the present invention is primarily to parallel light detection, self-pulse therapy after diagnosis. Herpes zoster is a disease caused by varicella zoster virus, and the virus that has been latent in the dorsal root ganglion that controls the skin segment loses its immune system and physically damages it. It is an acute skin disease in which acute pain and bullous rash occur along the sensory ganglia, which are rehab by inducers such as malignant tumors. Dorsal root ganglion after complete recovery of varicella, relapsed after incubation in brain ganglion, latent virus sometimes suppressed activity by cell mediated immunity, and in cell ganglion with reduced cellular immunity. It proliferates and destroys neurons, causing pain while forming a rash and blisters. This can reduce cell necrosis and increase the phagocytosis and enzymatic activity through the movement of ions through the cell membrane, depolarization and membrane potential change, growth factor secretion, calcium ion transfer, chondrocyte synthesis, etc., And may offer treatment options for lesions of herpes zoster and post-herpetic neuralgia (PHN).Therefore, according to the present research, the diagnosis and treatment device of treating paing for herpes zoster and post-herpetic pain can be implemented in the early stage of herpes zoster, and conventional analgesic regulation, anti-inflammatory effect, post-herpetic neuralgia.