• Clinical and Experimental Pediatrics
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• v.53 no.9
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• pp.845-851
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• 2010

Purpose: Recombinant human growth hormone (rhGH) has been widely used to treat short stature. However, there are some concerns that growth hormone treatment may induce skeletal maturation and early onset of puberty. In this study, we investigated whether rhGH can directly affect the neuronal activities of of gonadotropin-releasing hormone (GnRH). Methods: We performed brain slice gramicidin-perforated current clamp recording to examine the direct membrane effects of rhGH on GnRH neurons, and a whole-cell voltage-clamp recording to examine the effects of rhGH on spontaneous postsynaptic events and holding currents in immature (postnatal days 13-21) and adult (postnatal days 42-73) mice. Results: In immature mice, all 5 GnRH neurons recorded in gramicidin-perforated current clamp mode showed no membrane potential changes on application of rhGH (0.4, $1{\mu}g/mL$). In adult GnRH neurons, 7 (78%) of 9 neurons tested showed no response to rhGH ($0.2-1{\mu}g/mL$) and 2 neurons showed slight depolarization. In 9 (90%) of 10 immature neurons tested, rhGH did not induce any membrane holding current changes or spontaneous postsynaptic currents (sPSCs). There was no change in sPSCs and holding current in 4 of 5 adult GnRH neurons. Conclusion: These findings demonstrate that rhGH does not directly affect the GnRH neuronal activities in our experimental model.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.14 no.1
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• pp.183-190
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• 2010

We propose an eFuse one-time programmable (OTP) memory cell based on a logic process, which is programmable by an external program voltage. For the conventional eFuse OTP memory cell, a program datum is provided with the SL (Source Line) connected to the anode of the eFuse going through a voltage drop of the SL driving circuit. In contrast, the gate of the NMOS program transistor is provided with a program datum and the anode of the eFuse with an external program voltage (FSOURCE) of 3.8V without any voltage drop for the newly proposed eFuse cell. The FSOURCE voltage of the proposed cell keeps either 0V or the floating state at read mode. We propose a clamp circuit for being biased to 0V when the voltage of FSOURCE is in the floating state. In addition, we propose a VPP switching circuit switching between the logic VDD (=1.8V) and the FSOURCE voltage. The layout size of the designed eFuse OTP memory IP with Dongbu HiTek's $0.15{\mu}m$ generic process is $359.92{\times}90.98{\mu}m^2$.

• Journal of the Korean Institute of Illuminating and Electrical Installation Engineers
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• v.20 no.5
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• pp.49-56
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• 2006

The bi-directional converter interfaces the low voltage battery to the inverter do link of FC generation system. When power flows from the low voltage side(battery: 48[V]) to the high voltage side(dc link: 380[V]), the circuit works in discharge mode (boost) to power the high voltage side load; otherwise, it works in charge mode (buck) to charge the low voltage side battery. In this paper, the 1.5[kW] active clamp current-fed full bridge converter employing MOSFETs is operated to discharge the battery whereas a voltage-fed half bridge converter employing IGBTs is operated to charge the battery.

• The Korean Journal of Physiology
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• v.27 no.2
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• pp.115-122
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• 1993

There is evidence that noradrenaline enhances spontaneous contractions dose-dependently in guinea-pig antral circular muscle. To investigate the mechanism of this excitatory action, slow waves and membrane currents were recorded using conventional microelectrode techniques in muscle strips and the whole cell patch clamp technique in isolated gastric myocytes. On recording slow waves, noradrenaline $(10^{-5}\;M)$ induced the hyperpolarization of the membrane potential, although the shape of the slow waves became tall and steep. Also, spike potentiaIs occurred at the peaks of slow waves. These changes were completely reversed by administration of phentolamine $(10^{-5}\;M),\;an\;{\alpha}-adrenoceptor$ blocker. Noradrenaline-induced hyperpolarization was blocked by apamin $(10^{-7}\;M)$, a blocker of a class of $Ca^{2+}\;-dependent\;K^+$ channels. To investigate the mechanisms for these effects, we performed whole cell patch clamp experiments. Norndrenaline increased voltage-dependent $Ca^{2+}$ currents in the whole range of test potentials. Noradrenaline also increased $Ca^{2+}\;-dependent\;K^+$\;currents, and this effects was abolished by apamin. These results suggest that the increase in amplitude and the generation of spike potentials on slow waves was caused by the activation of voltage-dependent $Ca^{2+}$ channel via adrenoceptors, and hyperpolarization of the membrane potential was mediated by activation of apamin-sensitive $Ca^{2+}\;-dependent\;K^+\;channels$.

• Development and Reproduction
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• v.4 no.2
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• pp.243-250
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• 2000

To find the mechanism underlying the ADP-induced increase in the outward current in ovulated mouse oocytes, we examined changes in voltage-dependent currents using the whole cell voltage clamp technique and the internal perfusion technique. Eggs were collected from the oviduct of superovulated mice with PMSG and hCG. Membrane potential was held at -60 mV (or -80 mV in the case of recording $Ca^{2＋}$ currents) and step depolarizations or hyperpolarizations were applied for 300 ms. By step depolarizations, outward currents comprising steady-state and time-dependent components were elicited. They were generated in response to the positive potential more than 20 mV with severe outward rectification and were blocked by external TEA, a specific $K^{＋}$ channel blocker, suggesting that they be carried via $K^{＋}$ channels. Internally-perused 5 mM ADP gradually increased outward $K^{＋}$ currents (IK) 1 min after perfusion of ADP and reached slowly to maximum (150~170％) 5 min later over the positive potential range, implying that ADP might not be acted directly to the $K^{＋}$ channels. IK were decreased by 5 mM ATP without affecting the steady-state component of outward current. In contrast to the effect of ADP and ATP on IK, both effect of ATP and ADP on inward $Ca^{2＋}$ currents (ICa) could not be detected due to the continuous decrease in current amplitudes with time-lapse ("run-down" phenomena). To check if there is a G protein-involved regulation in the ionic current of mouse oocytes, 1 mM GTP was applied to the cytoplasmic side, and the outward current and inward currents were recorded. ICa was promptly increased in the presence of GTP whereas IK was not changed. from these results, it is concluded that the ATP-dependent regulation is likely linked in the ADP-induced increase in the outward $K^{＋}$ current, and G protein-involved cellular signalling might affect ion channels carrying $Ca^{2＋}$ and $K^{＋}$ in mouse oocytes.

• Journal of Korean Neurosurgical Society
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• v.29 no.11
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• pp.1429-1436
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• 2000

Objectives : This study was performed in cultured rat hippocampal neurons to investigate the acute electrophysiological features of ionotropic glutamate receptors which act as a major excitatory neurotransmitter in mammalian brain. Method : Glutamate receptor agonists were applied into the bath solution embedding in whole-cell patch-clamp recording of single hippocampal neuron. Results : In voltage-clamped at -60mV and the presence of 1mmol $Mg^{2+}$, extracellulary applied NMDA did not induce any inward current. Both the elimination of $Mg^{2+}$ and addition of glycine in bath, however, elicited a NMDAinduced inward current. $Mg^{2+}$ block current was increased gradually in more negative potentials from -30mV, showing a negative slope in I-V plot with $Mg^{2+}$. Glutamate-induced current represented an outward rectification. A non-NMDA receptor component occupied about 40% of glutamate-induced current in the voltage range of -80mV to +60mV. Conclusion : Present study suggests that glutamate activates acutely the non-NMDA receptors which induces an inward current in the level of resting membrane potential. This makes the membrane potential increase and can activate the NMDA receptors that permit calcium influx against $Mg^{2+}$ block. At the depolarized state of neuron, there may be recovery mechanisms of membrane potential to repolarize irrespective of voltage-dependent potassium channels in the hippocampal neurons.

• The Korean Journal of Physiology
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• v.26 no.1
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• pp.27-35
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• 1992

We used the whole cell patch clamp technique to examine the ionic basis for the tail current after depolarizing pulse in single atrial myocytes of the rabbit. We recorded the tail currents during various repolarizations after short depolarizing pulse from a holding potential of -70 mV. The potassium currents were blocked by external 4-aminopyridine and replacement of internal potassium with cesium. The current was reversed to the outward direction above +10 mV. High concentrations of intracellular calcium buffer inhibited the activation of the current. Diltiazem and ryanodine blocked it too. These data suggest that the current is activated by intracellular calcium released from sarcoplasmic reticulumn. When the internal chloride concentration was increased, the inward tail current was increased. The current was partially blocked by the anion transport blocker niflumic acid. The current voltage curve of the niflumic acid sensitive current component shows outward rectification and is well fitted to the current voltage curve of the theoretically predicted chloride current calculated from the constant field equation. The currents recorded in rabbit atrial myocytes, with the method showing isolated outward Na Ca exchange current in ventricular cells of the guinea pig, suggested that chloride conductance could be activated with the activation of Na/ca exchange current. From the above results it is concluded that a chloride sensitive component which is activated by intracellular calcium contributes to tail currents in rabbit atrial cells.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.5
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• pp.585-595
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• 2018

Amitriptyline, a tricyclic antidepressant, is commonly used to treat depression and neuropathic pain, but its mechanism is still unclear. We tested the effect of amitriptyline on 5-hydroxytryptamine 3 ($5-HT_3$) receptor currents and studied its blocking mechanism because the clinical applications of amitriptyline overlapped with $5-HT_3$ receptor therapeutic potentials. Using a whole-cell voltage clamp method, we recorded the currents of the $5-HT_3$ receptor when 5-HT was applied alone or co-applied with amitriptyline in cultured NCB-20 neuroblastoma cells known to express $5-HT_3$ receptors. To elucidate the mechanism of amitriptyline, we simulated the $5-HT_3$ receptor currents using Berkeley $Madonna^{(R)}$ software and calculated the rate constants of the agonist binding and receptor transition steps. The $5-HT_3$ receptor currents were inhibited by amitriptyline in a concentration-dependent, voltage-independent manner, and a competitive mode. Amitriptyline accelerated the desensitization of the $5-HT_3$ receptor. When amitriptyline was applied before 5-HT treatment, the currents rose slowly until the end of 5-HT treatment. When amitriptyline was co-applied with 5-HT, currents rose and decayed rapidly. Peak current amplitudes were decreased in both applications. All macroscopic currents recorded in whole cell voltage clamping experiments were reproduced by simulation and the changes of rate constants by amitriptyline were correlated with macroscopic current recording data. These results suggest that amitriptyline blocks the $5-HT_3$ receptor by close and open state blocking mechanisms, in a competitive manner. We could expand an understanding of pharmacological mechanisms of amitriptyline related to the modulation of a $5-HT_3$ receptor, a potential target of neurologic and psychiatric diseases through this study.

• The Korean Journal of Physiology
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• v.17 no.1
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• pp.1-11
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• 1983

1) The two microelectrode method was used to voltage clamp small preparations of rabbit sinoatrial node. The kinetics of hyperpolarization activated inward current, $i_f$ were analysed. 2) The hrperpolarization pulses activated $i_f$ current in the presence of $10^{-7}g/ml$ TTX and 2 mM $Mn^{2+}$. The activation range was in between -45 mV to -75 mV. The current magnitude was increased and time course was faster by strong hyperpolarization pulses. 3) Standard envelope tests indicated that this current is exponentially controlled by single gate. 4) Semilogarithmic plot of $i_f$ activation versus time was found to be linear in the activation range. The decrease in current magnitude and the shifts in activation curve and rate constants curve to the hyperpolarizing direction were obtained with $Ba^{2+}$, indicating that $Ba^{2+}$ shifts the voltage dependence of the gating kinetics, were partially reversed by 24 mM $K^+$.

• The Korean Journal of Physiology
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• v.20 no.2
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• pp.165-174
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• 1986

The voltage clamp studies were undertaken to elucidate the properties of the slow inward current, $i_{si}$, in the small preparations of the rabbit sinoatrial node. The slow inward current, $i_{si}$, which is known to be responsible for the late one-third of pacemaker potential and whole range of upstroke phase of action potential was analysed with the effects of isoprenaline, cobalt, ouabain and higenamine. The results obtained are as follows; 1) Voltage of SA node preparation was held at zero current level, usually-40mV and the slow inward current, $i_{si}$, was activated by depolarizing clamp pulses. Peak values of $i_{si}$, in steady state were at $-10{\pm}0mV$ in most preparations. 2) Isoprenaline, ${\beta}-agonist$ increased $i_{si}$ and no shift was noticed in voltage-dependency. 3) Cobalt ion in the concentration of 1 mM abolished is, in entire range of membrane potential and the difference of two current levels before and after $Co^{2+}$ treatment could be considered as pure $i_{si}$ magnitude. 4) In the therapeutic concentration of ouabain $(5{\times}10^{-8}M)$ slightly increased is, and reduced the time to reach the peak value. 5) Higenamine $(10^{-6}M)$ changed the configurations of action potential (i. e. rapid upstroke phase and notch in the spike) and increase spontaneous rate. It also increased is, and the effect of higenamine was blocked ${\beta}-blocker$, propranolol $(10^{-6}M)$.