• 대한전기학회논문지:시스템및제어부문D
• /
• 제55권10호
• /
• 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
• /
• 제28권3호
• /
• 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.

• 대한전기학회:학술대회논문집
• /
• 대한전기학회 2006년도 제37회 하계학술대회 논문집 D
• /
• 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.

• 대한의용생체공학회:의공학회지
• /
• 제22권2호
• /
• pp.151-156
• /
• 2001

기능적 전기자극(FES)에 의한 사지운동의 효과적인 제어를 위해서는, 전기자극을 입력으로 하여 근력 및 운동을 정확히 출력하는 근골격모델이 요망된다. 이 연구에서는 FES에 의한 근력 및 운동을 보다 정확히 예측할 수 있는 모델을 작성하기 위하여, 기존의 근육모델에서는 포함되지 않았던 근력의 점진적 강화현상에 대한 기초적 성질을 조사하는 것을 목적으로 한다. 구체적으로는, 일정강도의 표면자극에 대한 근력의 강화현상이 주파수, 자극이력, 근육길이에 어떻게 의존하는지를 조사하였다. 실험결과로부터, 자극의 주파수가 높을수록 초기근력에 대한 자극중의 근력의 증가도는 작아지고 근력의 피크에 도달하는 시간이 짧아지는 것을 알 수 있었다. 선행 자극에 의해 근육의 내부적인 강화상태가 포화되면 근력은 추가적인 자극에 대해서도 더 이상 증가하지 않았다. 자극시의 근육의 길이는 근력강화에 큰 영향을 미쳤으며, 근육의 길이가 짧을수록 증가도가 컸다. 장래에는 이러한 결과를 토대로 한 새로운 근력강화의 모델이 요망된다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제17권6호
• /
• 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
• /
• 제29권2호
• /
• 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 $Ca^{2+}$.

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
• /
• 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)

• 한국응용약물학회:학술대회논문집
• /
• 한국응용약물학회 2008년도 Proceedings of the Convention
• /
• 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.

• 대한약리학회지
• /
• 제6권1호
• /
• pp.27-35
• /
• 1970

1) 전신가토(全身家兎) 및 척수가토(脊髓家兎)에 있어서 syrosingopine(S) 및 reserpine(R) 처리후(處理後)에 일어나는 norepinephrine(NE)에 대한 혈압반응(血壓反應)의 강화(强化)를 비교(比較)하였다. 2) 사용(使用)한 S 및 R의 양(量)은 체중(體重) 1kg당(當) 8, 40, $200\;{\mu}g$ 및 1 mg이었으며 S 또는 R 주사후(注射後) 4, 10 및 24 시간후(時間後)에 NE(0.1, 0.5, 0.25, 1.2, 6.0, 30.0, $150.0\;{\mu}g/kg$)에 대한 반응(反應)을 보았다. 3) 전신가토(全身家兎)에 있어서 S에 의한 NE 승압반응(昇壓反應)의 강화(强化)는 $40\;{\mu}g/kg$으로써, R에 의한 강화(强化)는 $8\;{\mu}g/kg$으로써 일어났으며, S 및 R 모두 $200\;{\mu}g/kg$, 10 시간후(時間後)에 최고강화(最高强化)를 볼 수 있었다. 4) 척수가토(脊髓家兎)에 있어서는 $S(200\;{\mu}g/kg)$에 의한 NE 승압반응(昇壓反應)의 강화(强化)는 미약(微弱)하였으나 $R(200\;{\mu}g/kg)$로써는 일부(一部) NE량(量)(1.2, $6.0\;{\mu}g/kg$)에 대한 반응(反應)의 강화(强化)는 현저(顯著)하였다. 5) 전신가토(全身家兎)에서 S 및 R, 각각 $40\;{\mu}g/kg$ 투여(投與) 4 시간후(時間後)에 일어나는 NE 효과(?果)의 강화(强化)는 carbachol 처리(處理)로써 현저(顯著)히 억제(抑制)되었다. 6) 척수가토(脊髓家兎)에서 S 및 R 각각 $S(200\;{\mu}g/kg)$ 투여 10 시간후(時間後)에 보는 NE에 대한 반응증가(反應增加)는 carbachol 처리(處理)로써 억제(抑制)되었다. 7) 전신가토(全身家兎)에서 S 및 R(1 mg/kg)에 의한 NE에 대한 반응(反應)의 강화(强化)는 주사(注射) 15 분후(分後) 부터 볼 수 있었다. 8) S 및 R에 의한 NE-supersensitivity 발생(發生)에는 이들 물질(物質)의 말초조직(末梢組織)의 catecholamine 함량(含量)에 미치는 영향(影響)보다 중추(中樞)의 catecholamine 함량(含量)에 미치는 영향(影響)이 더 큰 의의(意義)가 있으며, 중추(中樞)에 대한 작용결과(作用結果) 일어나는 교감신경계(交感神經系)의 tone의 약화(弱化)가 큰 역할(役割)을 하는 것으로 생각된다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제21권4호
• /
• 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.