• 제목/요약/키워드: Potentiation

검색결과 207건 처리시간 0.033초

시냅스 가소성에 관한 고찰 (Review of Synaptic Plasticity)

  • 김석범;김진상
    • The Journal of Korean Physical Therapy
    • /
    • 제13권1호
    • /
    • pp.229-235
    • /
    • 2001
  • Clinical interest has lately been roused by evidence that comprehension of synaptic plasticity may be based on the theoretical opinion. This paper describes perception of synaptic plasticity. Especially processes of long term potentiation(LTP) and long term depression(LTD) are discussed. Recently, it is assessed to genetical parts from development of molecular biology. Therefore this review also represents aspect of molecular events of synaptic plasticity.

  • PDF

Potentiation of COX-2 Induction by C2-ceramide, a Potential Cell Death Marker

  • Kim, Sang-Geon
    • 한국독성학회:학술대회논문집
    • /
    • 한국독성학회 2003년도 춘계학술대회 논문집
    • /
    • pp.13-14
    • /
    • 2003
  • Ceramide, a potential cell death marker formed by sphingomyelinase, is involved in the expression of cyclooxygenase-2 (COX-2). This study examines the effect of C2-ceramide (C2), a cell-permeable ceramide analog, on the LPS-inducible COX-2 expression and signaling pathways. C2 did not induce COX-2, but potentiated LPS-inducible COX-2 expression in Raw264.7 cells, whereas dihydro-C2 was inactive.(omitted)

  • PDF

EFFECTS OF DICHLOROMETHANE ON CARBON TETRACHLORIDE HEPATOTOXICITY IN RATS

  • Kim, Dae B.;Kim, Baik H.
    • Toxicological Research
    • /
    • 제5권1호
    • /
    • pp.37-41
    • /
    • 1989
  • A non-hepatotoxic dose of dichloromethane (DCM) was examined for potential effects on the hepatotoxicity of carbon tetrachloride (CT) in adult male rats. A concomitant treatment of DCM (0.45ml/kg, po) significantly potentiated the hepatotoxicity of CT at varing doses (0.06 to 0.63 ml/kg, po) as determined by increase in SGOT and SGPT activities 24 hn following the treatments. The carboxyhemoglobin (COHb) saturation induced by DCM was significantly decreased by CT treatments. The potentiation of CT hepatotoxicity by DCM does not appear to be associated with increased metabolism of CT.

  • PDF

Elucidation of the profound antagonism of contractile action of phenylephrine in rat aorta effected by an atypical sympathomimetic decongestant

  • Rizvic, Eldina;Jankovic, Goran;Savic, Miroslav M.
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제21권4호
    • /
    • pp.385-395
    • /
    • 2017
  • Vasoconstrictive properties of sympathomimetic drugs are the basis of their widespread use as decongestants and possible source of adverse responses. Insufficiently substantiated practice of combining decongestants in some marketed preparations, such are those containing phenylephrine and lerimazoline, may affect the overall contractile activity, and thus their therapeutic utility. This study aimed to examine the interaction between lerimazoline and phenylephrine in isolated rat aortic rings, and also to assess the substrate of the obtained lerimazoline-induced attenuation of phenylephrine contraction. Namely, while lower concentrations of lerimazoline ($10^{-6}M$ and especially $10^{-7}M$) expectedly tended to potentiate the phenylephrine-induced contractions, lerimazoline in higher concentrations ($10^{-4}M$ and above) unexpectedly and profoundly depleted the phenylephrine concentration-response curve. Suppression of NO with NO synthase (NOS) inhibitor $N^w$-nitro-L-arginine methyl ester (L-NAME; $10^{-4}M$) or NO scavanger $OHB_{12}$ ($10^{-3}M$), as well as non-specific inhibition of $K^+$-channels with tetraethylammonium (TEA; $10^{-3}M$), have reversed lerimazoline-induced relaxation of phenylephrine contractions, while cyclooxygenase inhibitor indomethacin ($10^{-5}M$) did not affect the interaction between two vasoconstrictors. At the receptor level, non-selective 5-HT receptor antagonist methiothepin reversed the attenuating effect of lerimazoline on phenylephrine contraction when applied at $3{\times}10^{-7}$ and $10^{-6}M$, but not at the highest concentration ($10^{-4}M$). Neither the 5-$HT_{1D}$-receptor selective antagonist BRL 15572 ($10^{-6}M$) nor 5-$HT_7$ receptor selective antagonist SB 269970 ($10^{-6}M$) affected the lerimazoline-induced attenuation of phenylephrine activity. The mechanism of lerimazoline-induced suppression of phenylephrine contractions may involve potentiation of activity of NO and $K^+$-channels and activation of some methiothepin-sensitive receptors, possibly of the 5-$HT_{2B}$ subtype.

Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission

  • Park, Hye Jin;Lee, Seungheon;Jung, Ji Wook;Lee, Young Choon;Choi, Seong-Min;Kim, Dong Hyun
    • Biomolecules & Therapeutics
    • /
    • 제24권4호
    • /
    • pp.433-437
    • /
    • 2016
  • Consumption of high doses of ethanol can lead to amnesia, which often manifests as a blackout. These blackouts experienced by ethanol consumers may be a major cause of the social problems associated with excess ethanol consumption. However, there is currently no established treatment for preventing these ethanol-induced blackouts. In this study, we tested the ethanol extract of the roots of Salvia miltiorrhiza (SM) for its ability to mitigate ethanol-induced behavioral and synaptic deficits. To test behavioral deficits, an object recognition test was conducted in mouse. In this test, ethanol (1 g/kg, i.p.) impaired object recognition memory, but SM (200 mg/kg) prevented this impairment. To evaluate synaptic deficits, NMDA receptor-mediated excitatory postsynaptic potential (EPSP) and long-term potentiation (LTP) in the mouse hippocampal slices were tested, as they are known to be vulnerable to ethanol and are associated with ethanol-induced amnesia. SM (10 and $100{\mu}g/ml$) significantly ameliorated ethanol-induced long-term potentiation and NMDA receptor-mediated EPSP deficits in the hippocampal slices. Therefore, these results suggest that SM prevents ethanol-induced amnesia by protecting the hippocampus from NMDA receptor-mediated synaptic transmission and synaptic plasticity deficits induced by ethanol.