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Park, Kyungpyo,Kim, Joong-Soo,Lee, Jong-Heun Korean Academy of Oral Biology and the UCLA Dental 1997 International Journal of Oral Biology Vol.22 No.4
Functional neurotransmitter receptors which elevate intracellular free calcium concentration ([Ca^2+]_1) have been identified in freshly isolated trigeminal ganglion (TG) neurons in neonatal rat pups. Measurement of [Ca^2+]_1 was performed using fura-2 acetoxymethyl ester (Fura-2) based ratio microspectrofluorimetry. In our experiments only small sized neurons (<30μm) according to somatic diameter were used. In single intact neurons, the expression percentage and magnitudes of [Ca^2+]_1 increase responding to each agonist were determined. Application of bradykinin (BK), substance P (SP), calcitonin gene related peptide (CGRP), ATP and capsaicin elevated [Ca^2+]_1 in the expression percentages of 24%, 37%, 31%, 77% and 50%, respectively, and elevated [Ca^2+]_1 from 1.63±0.04 (Mean±S.E) to 1.92±0.05, from 1.36±0.08 to 1.88±0.12, from 1.33±0.03 to 1.61±0.09, from 1.35±0.04 to 2.2±0.15 and from 1.26±0.06 to 2.9±0.26, respectively. The purinergic receptor which respond to ATP was most frequently expressed (77%). A [Ca^2+]_1 increase in response to all neurotransmitters was transient in nature, except in response to capsaicin. Increase of [Ca^2+]_1 evoked by capsaicin was not transient: [Ca^2+]_1 was maintained at a higher concentration than the prestimulus level. The magnitude of [Ca^2+]_1 increase evoked by capsaicin was bigger than for any other neuroransmitters. Our results show that a subpopulation of trigeminal ganglion neurons with small diameter express functional receptors responsible for elevating [Ca^2+]_1 coexisting with other neurotransmitter receptors in the early neonatal stage. Our data may have implications for studying orofacial pain transmission which is associated with intracellular calcium increase.
Park, Chanhee,Lee, Soojin,Cho, Ik-Hyun,Lee, Hyun Kyoung,Kim, Donghoon,Choi, Se-Young,Oh, Seog Bae,Park, Kyungpyo,Kim, Joong Soo,Lee, Sung Joong Wiley Subscription Services, Inc., A Wiley Company 2006 GLIA Vol.53 No.3
<P>Viral infection is one of the leading causes of brain encephalitis and meningitis. Recently, it was reported that Toll-like receptor-3 (TLR3) induces a double-stranded RNA (dsRNA)-mediated inflammatory signal in the cells of the innate immune system, and studies suggested that dsRNA may induce inflammation in the central nervous system (CNS) by activating the CNS-resident glial cells. To explore further the connection between dsRNA and inflammation in the CNS, we have studied the effects of dsRNA stimulation in astrocytes. Our results show that the injection of polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, into the striatum of the mouse brain induces the activation of astrocytes and the expression of TNF-α, IFN-β, and IP-10. Stimulation with poly(I:C) also induces the expression of these proinflammatory genes in primary astrocytes and in CRT-MG, a human astrocyte cell line. Furthermore, our studies on the intracellular signaling pathways reveal that poly(I:C) stimulation activates IκB kinase (IKK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) in CRT-MG. Pharmacological inhibitors of nuclear factor-κB (NF-κB), JNK, ERK, glycogen synthase kinase-3β (GSK-3β), and dsRNA-activated protein kinase (PKR) inhibit the expression of IL-8 and IP-10 in astrocytes, indicating that the activation of these signaling molecules is required for the TLR3-mediated chemokine gene induction. Interestingly, the inhibition of PI3 kinase suppressed the expression of IP-10, but upregulated the expression of IL-8, suggesting differential roles for PI3 kinase, depending on the target genes. These data suggest that the TLR3 expressed on astrocytes may initiate an inflammatory response upon viral infection in the CNS. © 2005 Wiley-Liss, Inc.</P>
K^+ Channels in Mucous Cells Isolated from the Rat Sublingual Gland
Park, Kyungpyo,Kim, Joong-Soo,Lee, Jong-Heun Korean Academy of Oral Biology and the UCLA Dental 1998 International Journal of Oral Biology Vol.23 No.1
The basolateral, voltage dependent K^+ channels of mucous cells dissociated from rat sublingual gland were studied using the patch-clamp technique. In the cell-attached mode, two types of K^+ channels could be observed in these cells. One had a large conductance of 222±13 pS (mean±SEM, n=4), and the other had a small conductance of 43±7 pS (n=3). Acetylcholine (ACh; 10^-5 M) activated both K^+ channels by increasing the open probability (Po). Open probability for the large conductance channel increased from 0.18 in the control solution to a maximum value of 0.85 after addition of Ach. Whereas, Po for the small conductance channels increased from 0.002 in the control solution to a maximum value of 0.31. K^+ channel activation by 10^-5 M Ach was observed in 2 other mucous cells. When the osmolarity of bath solution was reduced to 60% of control, both large and small conductance K^+ channels were activated. Open probability for the large and small conductance K^+ channels increased significantly (P<0.05) from 0.006±0.001 (n=4) and 0.002±0.001 (n=4) in the control solution to a maximum value of 0.30±0.04 and 0.12±0.03 in the hypotonic solution, respectively. It is concluded that both K^+ channels may play a crucial role in secretion induced by muscarinic receptor activation and in regulatory volume decrease (RVD).
Park, Kyungpyo,Kim, Seong-Ah,Nam, Sang Chae,Kim, Joong-Soo,Lee, Jong-Heun Korean Academy of Oral Biology and the UCLA Dental 2000 International Journal of Oral Biology Vol.25 No.3
Medually dorsal horn〔MDH〕neurons, known as the sensory neurons, are involved in orofacial pain transmission. In the present study, we investigated the types of neurotransmitters that affect intracellular free calcium concentration〔[Ca^2+]_i〕, and which modulate pain sensation in the trigeminal sensory pathway. [Ca^2+]_i was measured in fura-2 acetoxymethyl eser (fura-2) loaded MDH neurons in neonatal rat pups by microspectrofluorimetry. Most of the neurons〔97.7%〕responded to L-glutamate by increasing [Ca^2+]_i and this response was reversible and consistent. [Ca^2+]_i increase was dose dependent, i.e., 0.24±0.06〔ΔF_340/F_380 ratio, n=2〕, 1.77±0.35 (n=10) and 1.82±0.15(n=2), at 30μM, 300μM and 1mM of glutamate, respectively. Substance P〔SP, 1nM〕also evoked a [Ca^2+]_i increase〔1.6±0.62, n=2〕in MDH neurons; however, this occurred in only 18.2% of neurons tested. In contrast to glutamate, the SP receptor showed a rapid desensitization. N-methyl-D-aspartate〔NMDA〕also increased [Ca^2+]_i in 21.1% of the neurons tested. NMDA-induced [Ca^2+]_i increase was not observed in the absence of extracellular Ca^2+. The coexpression of the SP and NMDA receptors with the glutamate receptor or the SP receptor with the NMDA receptor was observed in these neurons, although both expression percentages were low. In conclusion, L-glutamate, SP and NMDA functional receptors are expressed early in neonatal MDH neurons and may act as excitatory modulators in MDH neurons by increasing [Ca^2+]_i.
Effects of Pain-Inducing Agents on Voltage Dependent Calcium Currents in the Trigeminal Ganglion
Park, Kyungpyo,Kim, Seong-Ah,Kim, Youn Bae,Kim, Joong-Soo,Lee, Jong-Heun Korean Academy of Oral Biology and the UCLA Dental 2001 International Journal of Oral Biology Vol.26 No.1
Trigeminal ganglion (TG) neurons are primary sensory neurons involved in the transmission of orofacial sensation, including pain. It is known that intracellular free calcium concentration plays a critical role in neurotransmitter release. In the present study, we examined the effects of pain-inducing agents, bradykinin and histamine, on voltage dependent Ca^2+ current (I_Ca) and compared these with the effects of the analgesic agent, eugenol. I_Ca was measured using a whole-cell patch clamp method. Bradykinin (10μM) inhibited I_Ca in TG neurons. Maximum inward I_Ca was reduced by 26% by bradykinin compared with the controls (n=13, p<0.05). Decreased I_Ca induced by bradykinin did not recover to the prestimulus level after washing out bradykinin. In contrast, histamine (100μM) increased I_Ca by 25% compared with controls (n=7,p<0.05) in an irreversible manner. Eugenol (250μM), commonly used to produce analgesia in dental clinics, decreased I_Ca to 22.6% (n=9,p<0.05) and this effect on the I_Ca was reversible. although the effect of eugenol on the I_Ca was consistent, the effects of the two pain-inducing agents, bradykinin and histamine, were different. Our results suggest that the modulation of I_Ca in TG neurons is not a decisive factor underlying the pain mechanism evoked by pain-inducing agents.
Effects of Excitatory Amino Acid Antagonists on Locus Coeruleus Neuronal Activity
Park, Kyungpyo,Kim, Joong-Soo,Lee, Jong-Heun Korean Academy of Oral Biology and the UCLA Dental 1997 International Journal of Oral Biology Vol.22 No.2
It is known that firing rate of Locus coeruleus (LC) neurons is increased during opiate withdrawal and associated with the behavioral symptoms. The purpose of this study is to elucidate cellular mechanisms in LC neurons during opiate withdrawal. Rats were given morphine by daily subcutaneous injection (15㎎/㎏) for 5 days. Opiate withdrawal was induced by intraperitoneal naltrexone (NTX) adminstration (1㎎/㎏) on the fifth day. The resulting opiate abstinence syndrome was quantitated by the use of a composite score of five behaviors. Behavioral symptoms of abstinence were consistently elicited (n=7). Administration of physiological saline instead of NTX on the fifth day (n=4) or only NTX administraton without chronic morphine administration (n=4), both used as control goups, failed to induce opiate abstinence syndrome. After confirming opiate withdrawal through behavioral experiments, we investigated the effects of various excitatory amino acid (EAA) antagonists on LC neuronal activity induced by naloxone (NLX) administered intravenously (0.2㎎/㎏). NLX increased LC firing rates in most of morphine addicted rats. At the plateau of NLX-induced maximal activity of LC neuron, vehicle (artificial cerebrospinal fluid), as a control or EAA antagonists, i.e, kynurenic acid, 6-cyano-7-nitroquinoxaline-2, 3,-dione (CNQX) and 2-amino-5-phosphonopentanoic acid (AP-5), were administered intracerebroventricularlly. 1mM kynurenic acid, a non-specific EAA antagonist, and 0.5mM CNQX, a non-NMDA(N-methyl-D-aspartate) receptor antagonist, significantly decreased LC firing rate in contrast to vehicle injection, which had no effect on LC neuronal activity. AP-5, a NMDA receptor antagonist, was the least effective on the LC neuronal activity-neither 0.1mM nor 1mM of AP-5 had effect on LC firing rate. Only at the concentration of 5mM of AP-5 could decrease rate. These results indicate that daily subcutaneous injection of morphine could be one of opiate dependent models and LC hyperactivity during opiate withdrawal is mediated by an augmented EAA input to LC, mainly by acting on non-NMDA receptors.