• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.69-76
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• 2004

A variety of G protein coupled receptors (GPCRs) are expressed in the presynaptic terminals of central and peripheral synapses and play regulatory roles in transmitter release. The patch-clamp whole-cell recording technique, applied to the calyx of Held presynaptic terminal in brainstem slices of rodents, has made it possible to directly examine intracellular mechanisms underlying the GPCR-mediated presynaptic inhibition. At the calyx of Held, bath-application of agonists for GPCRs such as $GABA_B$ receptors, group III metabotropic glutamate receptors (mGluRs), adenosine $A_1$ receptors, or adrenaline ${\alpha}2$ receptors, attenuate evoked transmitter release via inhibiting voltage-activated $Ca^{2+}$ currents without affecting voltage-activated $K^+$ currents or inwardly rectifying $K^+$ currents. Furthermore, inhibition of voltage-activated $Ca^{2+}$ currents fully explains the magnitude of GPCR-mediated presynaptic inhibition, indicating no essential involvement of exocytotic mechanisms in the downstream of $Ca^{2+}$ influx. Direct loadings of G protein ${\beta}{\gamma}$ subunit $(G{\beta}{\gamma})$ into the calyceal terminal mimic and occlude the inhibitory effect of a GPCR agonist on presynaptic $Ca^{2+}$ currents $(Ip_{Ca})$, suggesting that $G{\beta}{\gamma}$ mediates presynaptic inhibition by GPCRs. Among presynaptic GPCRs glutamate and adenosine autoreceptors play regulatory roles in transmitter release during early postnatal period when the release probability (p) is high, but these functions are lost concomitantly with a decrease in p during postnatal development.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.81-85
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• 2002

Conventional views of synaptic transmission generally overlook the possibility of 'postfusional-control' the regulation of the speed or completeness of transmitter release upon vesicular fusion. However, such regulation often occurs in non-neuronal cells where the dynamics of fusion-pore opening is critical for the speed of transmitter release. In case of synapses, the slower the transmitter release, the smaller the size and rate-of-rise of postsynaptic responses would be expected if postsynaptic neurotransmitter receptors were not saturated. This prediction was tested at hippocampal synapses where postsynaptic AMPA-type glutamate receptors (AMPAR) were not generally saturated. Here, we found that the small miniature excitatory postsynaptic currents (mEPSCs) showed significantly slower rise times than the large mEPSCs when the sucrose-induced mEPSCs recorded in cyclothiazide (CTZ), a blocker for AMPAR desensitization, were sorted by size. The slow rise time of the small mEPSCs might result from slow release through a non-expanding fusion pore, consistent with postfusional control of neurotransmitter release at central synapses.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.72-74
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• 2003

Excitatory amino acid (EAA) receptor, particularly NMDA receptor, are now known to be one of major transmitter receptors involved in synaptic excitation. Excessive release of EAA neurotransmitter, glutamate, is an important causative factor in the neurodegenerative processes and can cause neuronal damage and cell death. This excitotoxicity has been shown to be $Ca^{++}$ dependent. (omitted)

• BMB Reports
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• v.40 no.3
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• pp.302-314
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• 2007

N type calcium channels (CaV2.2) play a key role in the gating of transmitter release at presynaptic nerve terminals. These channels are generally regarded as parts of a multimolecular complex that can modulate their open probability and ensure their location near the vesicle docking and fusion sites. However, the proteins that comprise this component remain poorly characterized. We have carried out the first open screen of presynaptic CaV2.2 complex members by an antibody-mediated capture of the channel from purified rat brain synaptosome lysate followed by mass spectroscopy. 589 unique peptides resulted in a high confidence match of 104 total proteins and 40 synaptosome proteome proteins. This screen identified several known CaV2.2 interacting proteins including syntaxin 1, VAMP, protein phosphatase 2A, $G_{o\alpha}$, G$\beta$ and spectrin and also a number of novel proteins, including clathrin, adaptin, dynamin, dynein, NSF and actin. The unexpected proteins were classified within a number of functional classes that include exocytosis, endocytosis, cytoplasmic matrix, modulators, chaperones, and cell-signaling molecules and this list was contrasted to previous reports that catalogue the synaptosome proteome. The failure to detect any postsynaptic density proteins suggests that the channel itself does not exhibit stable trans-synaptic attachments. Our results suggest that the channel is anchored to a cytoplasmic matrix related to the previously described particle web.

• Journal of Chest Surgery
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• v.28 no.8
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• pp.742-746
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• 1995

The present study was aimed at investigating possible transmitter mechanisms in the endothelial cell layer in regulating the tone of the vascular smooth muscle. The thoracic aorta was isolated from the anesthetized male white rabbits and its helical strips were prepared. Electrical field stimulation was delivered to platinum wire electrodes positioned parallel to the vessel segment preconstricted with phenylephrine [3.5x10-6 mol/L at a distance of 1.5-2.0 mm. The electrical stimulation [70 V, 5 msec, 0.5-200 Hz caused either relaxation only [34% or a biphasic response [prolonged relaxation following a weak and transient contraction, 66% . The relaxation response was frequency- dependent, and at 200 Hz a complete relaxation was noted. Mechanical rubbing of the endothelial layer abolished or greatly attenuated the relaxation. The relaxation was also markedly attenuated in the presence of NG-nitro- L-arginine methyl ester [10-3mol/L or procaine hydrochloride [3.5x10-4mol/L . Tetrodotoxin,guanethidine, atropine or indomethacin failed to block or enhance the relaxation response to electrical field stimulation. It is concluded that the vascular endothelium in the aorta contains diffusible substances that regulates the function of the smooth muscle layer, in which relaxation is more prominent than contraction. Their release by the electrical stimualtion in vitro may not involve classic neuronal transmitter release mechanisms or metabolism of arachidonic acids by cyclooxygenase. The release of the relaxing agents may require an increase in cytosolic calcium level. The chemical nature of the relaxant may be, to a large extent, nitric oxide.

• Journal of Photoscience
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• v.9 no.2
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• pp.47-50
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• 2002

Raft is a distinctive membrane domain enriched in a certain class of lipids, cholesterol, and proteins observed on the plasma membrane. Growing evidence has revealed that such membrane domains play key roles in signal transduction, fertilization, development, transmitter release, and so on. Recently, we have isolated raft-like detergent-resistant membrane (DRM) fraction from bovine photoreceptor rod outer segments. Transducin and its effecter, cGMP-phosphodiesterase, elicited stimulus-dependent translocation between detergent-soluble membrane and DRM. This suggested potential importance of such distinct membrane domains in vertebrate phototransduction. Here, we will discuss physiological meaning of the translocation of major components of cGMP cascade to raft-like membrane in phototransduction. We would like to propose a hypothesis that raft-like membrane domains on the disk membrane are the place where cGMP cascade system could be quenched.

• Journal of the Korean Society of Fisheries and Ocean Technology
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• v.55 no.1
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• pp.29-38
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• 2019

In order to investigate the behavioral characteristics of Pacific cod (Gadus macrocephalus) released at the entrance of Jinhae Bay, Korea, the direction and range of movement, swimming speed of the fish were measured with an acoustic telemetry techniques in winter, 2015. Three wild Pacific codes WC1 to WC3 (total length 66.0, 75.0, 76.0 cm; body weight 2.84, 2.79, 3.47 kg, respectively) were tagged with the acoustic transmitter. WC1 tagged with an acoustic transmitter internally by surgical method, WC2 and WC3, externally with the acoustic data logger and a micro data logger for recording audible sound waves including timer release unit. The movement routes of the tagged fish were measured more than five hours using VR100 receiver and a directional hydrophone. The directionality of the fish movement was tested by Rayleigh's z-Test, the statistical analysis, and a statistical program SPSS. Three tagged fishes were individually released on the sea surface around the entrance to the Jinhae Bay on 10 to 24 January 2015. WC1 moved about 13.32 km with average swimming speed of 0.63 m/s for six hours. The average swimming depth and water depth of the seabed on the route of WC1 were 7.2 and 32.9 m, respectively. The movement range of WC2 and WC3 were 7.95 and 11.06 km, approximately, with average swimming speed of 0.44 and 0.58 m/s for 5.1 and 5.3 hours, respectively. The average swimming depth of WC2 and WC3 were 18.7 and 5.0 m, and the water depth on the route, 34.4 and 29.8 m, respectively. Three fishes WC1 to WC3 were shown significant directionality in the movement (p < 0.05). Movement mean angles of WC1 to WC3 were 77.7, 76.3 and $88.1^{\circ}$, respectively. There was no significant correlation between the movement direction of fish (WC1 and WC2) and the tidal currents during the experimental period (p >= 0.05). Consequently, three tagged fishes were commonly moved toward outside of the entrance and headed for eastward of the Korean Peninsula, approximately, after release. It may estimate positively that the tidal current speed may affect to the swimming speed of the Pacific cod during the spring tide than the neap tide.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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• pp.461-467
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• 2009

The auditory cortex (A1) encodes the acquired significance of sound for the perception and interpretation of sound. Nitric oxide (NO) is a gas molecule with free radical properties that functions as a transmitter molecule and can alter neural activity without direct synaptic connections. We used whole-cell recordings under voltage clamp to investigate the effect of NO on spontaneous GABAergic synaptic transmission in mechanically isolated rat auditory cortical neurons preserving functional presynaptic nerve terminals. GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) in the A1 were completely blocked by bicuculline. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), reduced the GABAergic sIPSC frequency without affecting the mean current amplitude. The SNAP-induced inhibition of sIPSC frequency was mimicked by 8-bromoguanosine cyclic 3',5'-monophosphate, a membrane permeable cyclic-GMP analogue, and blocked by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger. Blockade of presynaptic $K^+$ channels by 4-aminopyridine, a $K^+$ channel blocker, increased the frequencies of GABAergic sIPSCs, but did not affect the inhibitory effects of SNAP. However, blocking of presynaptic $Ca^{2+}$ channels by $Cd^{2+}$, a general voltage-dependent $Ca^{2+}$ channel blocker, decreased the frequencies of GABAergic sIPSCs, and blocked SNAP-induced reduction of sIPSC frequency. These findings suggest that NO inhibits spontaneous GABA release by activation of cGMP-dependent signaling and inhibition of presynaptic $Ca^{2+}$ channels in the presynaptic nerve terminals of A1 neurons.

• KSII Transactions on Internet and Information Systems (TIIS)
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• v.15 no.8
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• pp.2923-2943
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• 2021

The double helix structure of DNA makes it diverse, stable and can store information with high density, and these characteristics are consistent with the requirements of molecular communication for transport carriers. In this paper, a specific structure of molecular communication system based on DNA length coding is proposed. Transmitter (Tx) adopts the multi-layer golden foil design to control the release of DNA molecules of different lengths accurately, and receiver (Rx) adopts an effective and sensitive design of nanopore, and the biological information can be converted to the electric signal at Rx. The effect of some key factors, e.g., the length of time slot, transmission distance, the number of releasing molecules, the priori probability, on channel capacity is demonstrated exhaustively. Moreover, we also compare the transmission capacity of DNA-based molecular communication (DNA-MC) system and concentration-based molecular communication (MC) system under the same parameter setting, and the peak value of capacity of DNA-MC system can achieve 0.08 bps, while the capacity of MC system remains 0.025 bps. The simulation results show that DNA-MC system has obvious advantages over MC system in saving molecular resources and improving transmission stability.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.1
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• pp.39-48
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• 2023

Spinal nerve injury causes mechanical allodynia and structural imbalance of neurotransmission, which were typically associated with calcium overload. Storeoperated calcium entry (SOCE) is considered crucial elements-mediating intracellular calcium homeostasis, ion channel activity, and synaptic plasticity. However, the underlying mechanism of SOCE in mediating neuronal transmitter release and synaptic transmission remains ambiguous in neuropathic pain. Neuropathic rats were operated by spinal nerve ligations. Neurotransmissions were assessed by whole-cell recording in substantia gelatinosa. Immunofluorescence staining of STIM1 with neuronal and glial biomarkers in the spinal dorsal horn. The endoplasmic reticulum stress level was estimated from qRT-PCR. Intrathecal injection of SOCE antagonist SKF96365 dose-dependently alleviated mechanical allodynia in ipsilateral hind paws of neuropathic rats with ED₅₀ of 18 ㎍. Immunofluorescence staining demonstrated that STIM1 was specifically and significantly expressed in neurons but not astrocytes and microglia in the spinal dorsal horn. Bath application of SKF96365 inhibited enhanced miniature excitatory postsynaptic currents in a dosage-dependent manner without affecting miniature inhibitory postsynaptic currents. Mal-adaption of SOCE was commonly related to endoplasmic reticulum (ER) stress in the central nervous system. SKF96365 markedly suppressed ER stress levels by alleviating mRNA expression of C/ EBP homologous protein and heat shock protein 70 in neuropathic rats. Our findings suggested that nerve injury might promote SOCE-mediated calcium levels, resulting in long-term imbalance of spinal synaptic transmission and behavioral sensitization, SKF96365 produces antinociception by alleviating glutamatergic transmission and ER stress. This work demonstrated the involvement of SOCE in neuropathic pain, implying that SOCE might be a potential target for pain management.