포털 사이트 뉴스 서비스를 포함한 인터넷 매체 간의 상호 의제 설정 효과 연구

학위논문(석사) --서울대학교 대학원 :행정학과(정책학전공),2008.Maste

Modulation of Dopaminergic Neuronal Excitability by Zinc through the Regulation of Calcium-related Channels

Depending on the intracellular buffering of calcium by chelation, zinc has the following two apparent effects on neuronal excitability: enhancement or reduction. Zinc increased tonic activity in the depolarized state when neurons were intracellularly dialyzed with EGTA but attenuated the neuronal activity when BAPTA was used as an intracellular calcium buffer. This suggests that neuronal excitability can be modulated by zinc, depending on the internal calcium buffering capacity In this study we elucidated the mechanisms of zinc-mediated alterations in neuronal excitability and determined the effect of calcium-related channels cm zinc-mediated alterations in excitability The zinc-induced augmentation of firing activity was mediated via the inhibition of small-conductance calcium-activated potassium (SK) channels with not only the contribution of voltage-gated L-type calcium channels (VGCCs) and ryanodine receptors (Ry Rs), but also through the activation of VGCCs via melastatin-like transient receptor potential channels. We suggest that zinc modulates the dopaminergic neuronal activity by regulating not only SK channels as calcium sensors, but also VGCCs or RyRs as calcium sources. Our results suggest that the cytosolic calcium-buffering capacity can tightly regulate zinc-induced neuronal firing patterns and that local calcium-signaling domains can determine the physiological and pathological state of synaptic activity in the dopaminergic system

Marked prevention of ischemic brain injury by Neu2000, an NMDA antagonist and antioxidant derived from aspirin and sulfasalazine

Excitotoxicity and oxidative stress mediate neuronal death after hypoxic-ischemic brain injury. We examined the possibility that targeting both N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity and oxidative stress would result in enhanced neuroprotection against hypoxic-ischemia. 2-Hydroxy-5-(2,3,5,6-tetrafluoro-4-trifluoromethyl-benzylamino)-benzoic acid (Neu2000) was derived from aspirin and sulfasalazine to prevent both NMDA neurotoxicity and oxidative stress. In cortical cell cultures, Neu2000 was shown to be an uncompetitive NMDA receptor antagonist and completely blocked free radical toxicity at doses as low as 0.3 μmol/L. Neu2000 showed marked neuroprotection in a masked fashion using histology and behavioral testing in two rodent models of focal cerebral ischemia without causing neurotoxic side effects. Neu2000 protected against the effects of middle cerebral artery occlusion, even when delivered 8 h after reperfusion. Single bolus administration of the drug prevented gray and white matter degeneration and spared neurologic function for over 28 days after MACO. Neu2000 may be a novel therapy for combating both NMDA receptor-mediated excitotoxicity and oxidative stress, the two major routes of neuronal death in ischemia, offering profound neuroprotection and an extended therapeutic window. © 2007 ISCBFM All rights reserved

Attenuated effects of Neu2000 on hypoxia-induced synaptic activities in a rat hippocampus

Derivative of acetylsalicylic acid; Extracellular recording; Hypoxia; Neuronal toxicity; Oxidative stres

Effect of dopamine on a voltage-gated potassium channel in a jellyfish motor neuron

To swimming motor neurons (SMNs) of Polyorchis penicillatus, a hydrozoan medusae, dopamine (DA) acts as an inhibitory neurotransmitter by hyperpolarizing its membrane potential and decreasing its firing rate as well. Such an inhibitory action of DA is caused by an increased permeability to potassium (K) ions. To investigate whether voltage-gated K channels are directly responsible for the membrane hyperpolarization induced by DA, we employed whole-cell voltage clamp configuration. One μM DA applied to SMNs increased the peak and rear values of voltage-gated K currents by 37 and 54%, respectively, in a reversible manner. Combined with subtraction analysis, this result suggests that the outflux of K ions by DA in SMNs occurs mainly through rectifier-like K channels

한국인에서 전완부 회전 및 강력 파악 동작에 따른 척골 변이의 변화 양상

학위논문(석사)--서울대학교 대학원 :의학과 정형외과학전공,2000.Maste

Functional and morphological study on the contribution from proximal nerve stump in double end-to-side nerve repair of median nerve in the rat-comparison with classical end-toside nerve repair-

학위논문(박사) --서울대학교 대학원 :의학과 정형외과학 전공,2007.Docto

Electrophysiological evidence for the role of substance P in retinohypothalamic transmission in the rat

The retinohypothalamic tract (RHT) is a neural pathway through which photic time cues are delivered directly to the mammalian circadian pacemaker in the suprachiasmatic nucleus (SCN). Although the excitatory amino acid glutamate is the primary neurotransmitter in the RHT, other substances such as substance P (SP) also have been suggested to play a role. The present study tested the hypothesis that SP participates in retinohypothalamic transmission and selectively modulates either N-methyl-D-aspartate (NMDA) or non-NMDA receptor-mediated neurotransmission. The SP antagonist L-703,606 depressed the excitatory postsynaptic current (EPSC) evoked by optic nerve stimulation in SCN neurons in rat hypothalamic slices. The SP antagonist also had a similar depressive effect on the NMDA and non-NMDA receptor-mediated components of the EPSC. These results suggest that SP is an excitatory neuromodulator contributing to the expression of both the NMDA and non-NMDA receptor-mediated components of retinohypothalamic transmission. Copyright (C) 1999 Elsevier Science Ireland Ltd

Zinc increases the excitability of dopaminergic neurons in rat substantia nigra

The effect of zinc ions (Zn2+) on the neuronal excitability of substantia nigra (SN) where the zinc level is known higher in Parkinsonian brains than that in normal brains has not yet been elucidated. We, therefore, examined the effect of Zn2+ on the intrinsic electrical properties of dopaminergic SN neurons, using a whole-cell recording method. Zn2+ hyperpolarized dopaminergic SN neurons at resting state. Also Zn2+ shortened the duration of evoked spikes, developed a fast afterhyperpolarization, and increased their firing frequency. Voltage-clamp studies showed that Zn2+ decreased 4-aminopyridine-sensitive outward currents, suggesting that a transient A-like potassium channel be one of the major targets Zn2+ can modulate in the SN neurons. (C) 2000 Elsevier Science Ireland Ltd

Extracellular ATP mediates necrotic cell swelling in SN4741 dopaminergic neurons through P2X7 receptors

Extracellular ATP has recently been identified as an important regulator of cell death in response to pathological insults. When SN4741 cells, which are dopaminergic neurons derived from the substantia nigra of transgenic mouse embryos, are exposed to ATP, cell death occurs. This cell death is associated with prominent cell swelling, loss of ER integrity, the formation of many large cytoplasmic vacuoles, and subsequent cytolysis and DNA release. In addition, the cleavage of caspase-3, a hallmark of apoptosis, is induced by ATP treatment. However, caspase inhibitors do not overcome ATP-induced cell death, indicating that both necrosis and apoptosis are associated with ATP-induced cell death and suggesting that a necrotic event might override the apoptotic process. In this study we also found that P2X7 receptors (P2X7Rs) are abundantly expressed in SN4741 cells, and both ATP-induced swelling and cell death are reversed by pretreatment with the P2X7Rs antagonist, KN62, or by knock-down of P2X7Rs with small interfering RNAs. Therefore, extracellular ATP release from injured tissues may act as an accelerating factor in necrotic SN4741 dopaminergic cell death via P2X7Rs. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc