• The Transactions of the Korean Institute of Electrical Engineers D
• /
• v.55 no.10
• /
• pp.458-463
• /
• 2006

The purpose of this work is to investigate the fundamental properties of the gradual muscle force potentiation. We investigated the dependence of force potentiation on both the pulse-amplitude and the pulse-duration with different ramp-up time. The experimental results showed that the force increment ratio (FIR) during constant electrical stimulation decreased with pulse-amplitude and also with pulse-duration. The FIR was greater with short ramp-up time in both the pulse-amplitude and pulse-width modulation. The feasible mechanism might be that the myosin light chain phosphorylation induces the force potentiation and it occurs only in the fast type muscle fibers which are recruited first. These observations indicate that muscle potentiation must be understood well for the accurate control of muscle force.

• Molecules and Cells
• /
• v.28 no.3
• /
• pp.167-174
• /
• 2009

Genistein has been reported to potentiate glucose-stimulated insulin secretion (GSIS). Inhibitory activity on tyrosine kinase or activation of protein kinase A (PKA) was shown to play a role in the genistein-induced potentiation effect on GSIS. The aim of the present study was to elucidate the mechanism of genistein-induced potentiation of insulin secretion. Genistein augmented insulin secretion in INS-1 cells stimulated by various energygenerating nutrients such as glucose, pyruvate, or leucine/glutamine (Leu/Gln), but not the secretion stimulated by depolarizing agents such as KCl and tolbutamide, or $Ca^{2+}$ channel opener Bay K8644. Genistein at a concentration of $50{\mu}M$ showed a maximum potentiation effect on Leu/Gln-stimulated insulin secretion, but this was not sufficient to inhibit the activity of tyrosine kinase. Inhibitor studies as well as immunoblotting analysis demonstrated that activation of PKA was little involved in genistein-induced potentiation of Leu/Gln-stimulated insulin secretion. On the other hand, all the inhibitors of $Ca^{2+}$/calmodulin kinase II tested, significantly diminished genistein-induced potentiation. Genistein also elevated the levels of $[Ca^{2+}]_i$ and phospho-CaMK II. Furthermore, genistein augmented Leu/Gln-stimulated insulin secretion in CaMK II-overexpressing INS-1 cells. These data suggest that the activation of CaMK II played a role in genistein-induced potentiation of insulin secretion.

• Proceedings of the KIEE Conference
• /
• 2006.07d
• /
• pp.2155-2156
• /
• 2006

The purpose of this work is to investigate the fundamental properties of the gradual muscle force potentiation for the prediction of muscle force and body movement from the stimulation input with musculo-skeletal model. We investigated the dependence of force potentiation on both the pulse-amplitude and the pulse-duration. The experimental result showed that the force increment ratio during electrical stimulation decreased with pulse-amplitude. The force increment ratio decreased with short pulse-duration and was maintained to be constant with pulse-duration longer than $500{\mu}s$. A new model of the muscle potentiation based on these results is desired in the future.

• Journal of Biomedical Engineering Research
• /
• v.22 no.2
• /
• pp.151-156
• /
• 2001

A computer model of the musculoskelotal system that provides accurate prediction of muscle force and body movement trom the stimulation input is desired for the effective control system design in FES. This paper aims to investigate the fundamental properties of the gradual muscle force potentiation that was not included in the previous muscle models, for future development of a model that provides vetter prediction of FES-induced muscle force and body movement. Specifically, hou the muscle length was investigated. The experimental results showed that both the force increment ratio and the time-to-peak during electrical stimulation decreased with stimulatino frequency. When the muscle potentiation state was saturated by preceding stimulation. the force did not increase any more during additive stimulation. Muscle length significantly affected the force potentiation in such a way that the force increment ratio decreased with muscle length. A new model of the muscle potentiation based on these results is desired in the future.

• The Korean Journal of Physiology and Pharmacology
• /
• v.17 no.6
• /
• pp.553-558
• /
• 2013

Spinal dorsal horn nociceptive neurons have been shown to undergo long-term synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD). Here, we focused on the spinothalamic tract (STT) neurons that are the main nociceptive neurons projecting from the spinal cord to the thalamus. Optical technique using fluorescent dye has made it possible to identify the STT neurons in the spinal cord. Evoked fast mono-synaptic, excitatory postsynaptic currents (eEPSCs) were measured in the STT neurons. Time-based tetanic stimulation (TBS) was employed to induce long-term potentiation (LTP) in the STT neurons. Coincident stimulation of both pre- and postsynaptic neurons using TBS showed immediate and persistent increase in AMPA receptor-mediated EPSCs. LTP can also be induced by postsynaptic spiking together with pharmacological stimulation using chemical NMDA. TBS-induced LTP observed in STT neurons was blocked by internal BAPTA, or $Ni^{2+}$, a T-type VOCC blocker. However, LTP was intact in the presence of L-type VOCC blocker. These results suggest that long-term plastic change of STT neurons requires NMDA receptor activation and postsynaptic calcium but is differentially sensitive to T-type VOCCs.

• The Korean Journal of Physiology
• /
• v.29 no.2
• /
• pp.243-250
• /
• 1995

A possible potentiation between cholecystokinin (CCK) and secretin in amylase secretion from isolated rat pancreatic acini was investigated. Combined treatment of acini with secretin and CCK at low concentrations, which are known to be physiological, resulted in enzyme secretion larger than the arithmetic sum of their separate effects. Such a potentiating effect also occurred between secretin and A23187 (Ca ionophore), between forskolin (adenylate cyclase activator) and CCK, and between forskolin and A23187. Staurosporin (protein kinase C inhibitor) and W7 (calmodulin antagonist) inhibited markedly the potentiated amylase release induced by the agonists, but KT5720 (protein kinase A inhibitor) did not affect the potentiated amylase release. Therefore, we concluded that the action of CCK in a physiological concentration is potentiated by secretin in a physiological concentration range and vice versa, and that the intracellular mechanism necessary for the potentiation is associated with $Ca^{2+}$. However, it is uncertain what mechanisms are involved in potentiation of amylase release after CAMP and $Ca^{2+}$.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.10a
• /
• pp.147-147
• /
• 2001

A previous study showed that sulfur amino acid deprivation (SAAD) potentiated cytotoxicity induced by arsenic (As) and that activation of ERKl/2, p38 kinase and JNK1 was responsible for the potentiation of As toxicity. In the present study, we found for the first time that deprenyl a selective monoamine oxidase B inhibitor prevented potentiation of As toxicity by SAAD in a dose-dependent manner.(omitted)

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 2008.04a
• /
• pp.33-45
• /
• 2008

Auditory fear memory is thought to be maintained by fear conditioning-induced potentiation of synaptic efficacy. The conditioning-induced potentiation has been shown to be maintained, at least in part, by enhanced expression of surface AMPA receptor (AMPAR) at excitatory synapses in the lateral amygdala (LA). Depotentiation, reversal of conditioning-induced potentiation, has been proposed as a cellular mechanism for fear extinction. However, a direct link between depotentiation and extinction has not yet been tested. To address this, we applied both ex vivo and in vivo approaches to rats in which fear memory had been consolidated. We found a novel form of ex vivo depotentiation; the depotentiation reversed conditioning-induced potentiation at thalamic input synapses onto the LA (T-LA synapses) ex vivo, and it could be induced only when both NMDA and metabotropic glutamate receptors were co-activated. Extinction returned the enhanced T-LA synaptic efficacy observed in conditioned rats to baseline and occluded the depotentiation. Consistently, extinction reversed conditioning-induced enhancement of surface expression of AMPAR subunits in LA synaptosomal preparations. A GluR2-derived peptide that blocks regulated AMPAR endocytosis inhibited depotentiation, and microinjection of a cell-permeable form of the peptide into the LA attenuated extinction. Our results are consistent with the use of depotentiation to weaken potentiated synaptic inputs onto the LA during extinction, and they provide strong evidence that AMPAR removal at excitatory synapses in the LA underlies extinction. The results described here are in line with previous findings. Neural activity in the LA has been shown to decrease after extinction in the rat and human. The NMDAR dependency of the depotentiation fits nicely with a large body of evidence that fear extinction depends upon amygdala NMDARs. Similarly, blockade of metabotropic glutamate recepotrs in the LA has recently been shown to attenuate fear extinction.

• The Korean Journal of Pharmacology
• /
• v.6 no.1
• /
• pp.27-35
• /
• 1970

1) In whole anesthetized rabbits and spinal rabbits, the potentiating effect of syrosingopine and reserpine on pressor action of norepinephrine (NE) was compared. 2) The doses of syrosingopine and reserpine were 8, 40, $200\;{\mu}g$ and 1 mg per kg of body weight. The pressor responses to NE(0.1, 0.5, 0.25, 1.2, 6.0, 30.0, $150.0\;{\mu}g/kg$) were examine at 4, 10 and 24 hours after administration of the drugs. 3) In whole rabbits, potentiation by syrosingopine of pressor effect of NE was observed after administration of above the dose of $40\;{\mu}g/kg$, potentiation by reserpine was above $8\;{\mu}g/kg$. The maximal potentiation was achieved 10 hours after administration of $200\;{\mu}g/kg$ of each agent. 4) In spinal rabbits, syrosingopine $(200\;{\mu}g/kg)$ produced slight potentiation of pressor effect of NE. The same dose of reserpine produced more pronounced potentiation. 5) In the whole rabbits carbachol inhibited the potentiation observed 4 hours after administration of $40\;{\mu}g/kg$ of reserpine and syrosingopine. 6) In spinal rabbits, the potentiation observed 10 hours after $200\;{\mu}g/kg$ of reserpine and syrosingopine was inhibited by administration of carbachol. 7) The onset of potentiation of the pressor effect of NE was within 15 min after administration of syrosingopine and reserpine (1 mg/kg, each). 8) The above data suggest that the development of NE supersensitivity by syrosingopine and reserpine in rabbits has more intimate relationship with the decrease of central catecholamine contents than with that of peripheral ones. The depression of central sympathetic tone produced by these agents seems to play an important role in development of supersensitivity.

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.4
• /
• pp.423-428
• /
• 2017

Vestibular compensation is a recovery process from vestibular symptoms over time after unilateral loss of peripheral vestibular end organs. The aim of the present study was to observe time-dependent changes in long-term potentiation (LTP) at Schaffer collateral-CA1 synapses in the CA1 area of the hippocampus during vestibular compensation. The input-output (I/O) relationships of fEPSP amplitudes and LTP induced by theta burst stimulation to Schaffer's collateral commissural fibers were evaluated from the CA1 area of hippocampal slices at 1 day, 1 week, and 1 month after unilateral labyrinthectomy (UL). The I/O relationships of fEPSPs in the CA1 area was significantly reduced within 1 week post-op and then showed a non-significant reduction at 1 month after UL. Compared with sham-operated animals, there was a significant reduction of LTP induction in the hippocampus at 1 day and 1 week after UL. However, LTP induction levels in the CA1 area of the hippocampus also returned to those of sham-operated animals 1 month following UL. These data suggest that unilateral injury of the peripheral vestibular end organs results in a transient deficit in synaptic plasticity in the CA1 hippocampal area at acute stages of vestibular compensation.