• The Korean Journal of Physiology and Pharmacology
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• 제8권1호
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• pp.7-15
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• 2004

Nitric oxide (NO) system has been implicated in a wide range of physiological functions in the nervous system. However, the role of NO in regulating the neural activity in the gustatory zone of nucleus tractus solitarius (NTS) has not been established. The present study was aimed to investigate the role of NO in the gustatory NTS neurons. Sprague-Dawley rats, weighing about 50 g, were used. Whole cell patch recording and immunohistochemistry were done to determine the electrophysiological characteristics of the rostral gustatory nucleus of the tractus solitaries and distribution of NO synthases (NOS). Neuronal NOS (nNOS) immunoreactivity was strongly detected along the solitary tract extending from rostral to caudal medulla. Resting membrane potentials of NTS neurons were $-49.2{\pm}2\;mV$ and action potential amplitudes were $68.5{\pm}2\;mV$ with a mean duration measured at half amplitude of $1.7{\pm}0.3\;ms$. Input resistance, determined from the response to a 150 ms, -100 pA hyperpolarizing current pulse, was $385{\pm}15\;M{\Omega}$, Superfusion of SNAP or SNP, NO donors, produced either hyperpolarization (68%), depolarization (5%), or no effect (27%). The hyperpolarization was mostly accompanied by a decrease in input resistance. The hyperpolarization caused by SNAP or SNP increased the time to initiate the first action potential, and decreased the number of action potentials elicited by current injection. SNP or SNAP also markedly decreased the number of firing neural discharges of the spontaneous NTS neural activity under zero current. Superfusion of L-NAME, a NOS inhibitor, slightly depolarized the membrane potential and increased the firing rate of NTS neurons induced by current injection. ODQ, a soluble guanylate cyclase inhibitor, ameliorated the SNAP-induced changes in membrane potential, input resistance and firing rates. 8-Br-cGMP, a non-degradable cell-permeable cGMP, hyperpolarized the membrane potential and decreased the number of action potentials. It is suggested that NO in the gustatory NTS has an inhibitory role on the neural activity of NTS through activating soluble guanylate cyclase.

• International Journal of Oral Biology
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• 제48권4호
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• pp.33-44
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• 2023

In this review, the regulatory mechanisms of autophagy were described, and its interaction with apoptosis was identified. The role of autophagy in embryogenesis, tooth development, and cell differentiation were also investigated. Autophagy is regulated by various autophagy-related genes and those related to stress response. Highly active autophagy occurrences have been reported during cell differentiation before implantation after fertilization. Autophagy is involved in energy generation and supplies nutrients during early birth, essential to compensate for their deficient supply from the placenta. The contribution of autophagy during tooth development, such as the shape of the crown and root formation, ivory, and homeostasis in cells, was also observed. Genes control autophagy, and studying the role of autophagy in cell differentiation and development was useful for understanding human aging, illness, and health. In the future, the role of specific mechanisms in the development and differentiation of autophagy may increase the understanding of the pathological mechanisms of disease and development processes and is expected to reduce the treatment of various diseases by modulating the autophagic phenomenon.

• 대한치과마취과학회지
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• 제3권2호
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• pp.71-79
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• 2003

• The Korean Journal of Physiology and Pharmacology
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• 제19권6호
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• pp.507-514
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• 2015

Nitric oxide (NO) is important in the regulation of bone remodeling, whereas high concentration of NO promotes cell death of osteoblast. However, it is not clear yet whether NO-induced autophagy is implicated in cell death or survival of osteoblast. The present study is aimed to examine the role of NO-induced autophagy in the MC3T3-E1 cells and their underlying molecular mechanism. The effect of sodium nitroprusside (SNP), an NO donor, on the cytotoxicity of the MC3T3-E1 cells was determined by MTT assay and expression of apoptosis or autophagy associated molecules was evaluated by western blot analysis. The morphological observation of autophagy and apoptosis by acridine orange stain and TUNEL assay were performed, respectively. Treatment of SNP decreased the cell viability of the MC3T3-E1 cells in dose- and time-dependent manner. SNP increased expression levels of p62, ATG7, Beclin-1 and LC3-II, as typical autophagic markers and augmented acidic autophagolysosomal vacuoles, detected by acridine orange staining. However, pretreatment with 3-methyladenine (3MA), the specific inhibitor for autophagy, decreased cell viability, whereas increased the cleavage of PARP and caspase-3 in the SNP-treated MC3T3-E1 cells. AMP-activated protein kinase (AMPK), a major autophagy regulatory kinase, was activated in SNP-treated MC3T3-E1 cells. In addition, pretreatment with compound C, an inhibitor of AMPK, decreased cell viability, whereas increased the number of apoptotic cells, cleaved PARP and caspase-3 levels compared to those of SNP-treated MC3T3-E1 cells. Taken together, it is speculated that NO-induced autophagy functions as a survival mechanism via AMPK activation against apoptosis in the MC3T3-E1 cells.

• The Korean Journal of Physiology and Pharmacology
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• 제12권6호
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• pp.315-321
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• 2008

Eugenol is widely used in dentistry to relieve pain. We have recently demonstrated voltage-gated $Na^+$ and $Ca^{2+}$ channels as molecular targets for its analgesic effects, and hypothesized that eugenol acts on $P2X_3$, another pain receptor expressed in trigeminal ganglion (TG), and tested the effects of eugenol by whole-cell patch clamp and $Ca^{2+}$ imaging techniques. In the present study, we investigated whether eugenol would modulate 5'-triphosphate (ATP)-induced currents in rat TG neurons and $P2X_3$-expressing human embryonic kidney (HEK) 293 cells. ATP-induced currents in TG neurons exhibited electrophysiological properties similar to those in HEK293 cells, and both ATP- and $\alpha$, $\beta$-meATP-induced currents in TG neurons were effectively blocked by TNP-ATP, suggesting that $P2X_3$ mediates the majority of ATP-induced currents in TG neurons. Eugenol inhibited ATP-induced currents in both capsaicin-sensitive and capsaicin-insensitive TG neurons with similar extent, and most ATP-responsive neurons were IB4-positive. Eugenol inhibited not only $Ca^{2+}$ transients evoked by $\alpha$, $\beta$-meATP, the selective $P2X_3$ agonist, in capsaicin-insensitive TG neurons, but also ATP-induced currents in $P2X_3$-expressing HEK293 cells without co-expression of transient receptor potential vanilloid 1 (TRPV1). We suggest, therefore, that eugenol inhibits $P2X_3$ currents in a TRPV1-independent manner, which contributes to its analgesic effect.

• International Journal of Oral Biology
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• 제37권3호
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• pp.121-129
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• 2012

Previous clinical studies have demonstrated that gabapentin, a drug that binds to the voltage-gated calcium channel ${\alpha}2{\delta}1$ subunit proteins, is effective in the management of neuropathic pain, but there is limited evidence that addresses the participation of glial cells in the antiallodynic effects of this drug. The present study investigated the participation of glial cells in the anti-nociceptive effects of gabapentin in rats with trigeminal neuropathic pain produced by mal-positioned dental implants. Under anesthesia, the left mandibular second molar was extracted and replaced by a miniature dental implant to induce injury to the inferior alveolar nerve. Mal-positioned dental implants significantly decreased the air-puff thresholds both ipsilateral and contralateral to the injury site. Gabapentin was administered intracisternally beginning on postoperative day (POD) 1 or on POD 7 for three days. Early or late treatment with 0.3, 3, or 30 ${\mu}g$ of gabapentin produced significant anti-allodynic effect in the rats with mal-positioned dental implants. On POD 9, in the mal-positioned dental implants group, OX-42, a microglia marker, and GFAP, an astrocyte marker, were found to be up-regulated in the medullary dorsal horn, compared with the naive group. However, the intracisternal administration of gabapentin (30 ${\mu}g$) failed to reduce the number of activated microglia or astrocytes in the medullary dorsal horn. These findings suggest that gabapentin produces significant antinociceptive effects, which are not mediated by the inhibition of glial cell function in the medullary dorsal horn, in a rat model of trigeminal neuropathic pain.

• 대한치과의사협회지
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• 제19권3호통권142호
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• pp.233-237
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• 1981

• 대한치과의사협회지
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• 제34권2호통권321호
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• pp.92-98
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• 1996

• 대한치과마취과학회:학술대회논문집
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• 대한치과마취과학회 2003년도 제3차 학술대회
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• pp.43-44
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• 2003

• International Journal of Oral Biology
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• 제36권1호
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• pp.23-29
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• 2011

Porphyromonas gingivalis, one of the major periodontal pathogens, is implicated in the initiation and progression of periodontal disease. The initial stages of periodontal inflammation are accompanied by vascular hyperpermeability. In our present study, we report that the P. gingivalis lipopolysaccharide (LPS) increases the mRNA expression of interleukin-8 (IL-8), a major inducer of vascular permeability, in vascular endothelial cells. P. gingivalis LPS also stimulated the induction of IL-8 secretion in endothelial cells. The P. gingivalis LPS-induced expression of IL-8 was primarily modulated by nuclear factor-${\kappa}$B(NF-${\kappa}$B). P. gingivalis LPS significantly enhanced the vascular permeability both in vitro and in vivo, and a blockade of the IL-8 receptor decreased the P. gingivalis LPS-induced vascular permeability. Taken together, these results suggest that P. gingivalis LPS increases vascular permeability through the NF-${\kappa}$B-dependent production of IL-8 in vascular endothelial cells.