• Proceedings of the Korean Biophysical Society Conference
• /
• 1999.06a
• /
• pp.66-66
• /
• 1999

The negative chronotropic effect of ACh on heart fades in the continuous presence of ACh, which is known as a phenomenon called "vagal escape". The underlying mechanism of vagal escape is not entirely clear, but desensitization of acetylcholine-activated $K^{＋}$ currents ($K_{ACh}$) was suggested, at least in part, to be responsible.(omitted)d)

• The Korean Journal of Pharmacology
• /
• v.32 no.2
• /
• pp.151-158
• /
• 1996

Following the subcutaneous administration of $R(-)N^6-(2-phenylisopropyl)adenosine(600\;nmol/kg/hr)$ to rats for 1 week using t$Alzet^{\circledR}$ mini-osmotic pumps, $A_1$ adenosine receptor functions were determined using $[^3H]DPCPX$ binding, $[^{35}S]GTP_{\gamma}S$ binding, and adenylyl cyclase assays. $A_1$ adenosine receptor binding and the inhibition of adenylyl cyclase activity by PIA was not altered in cerebrocortical membranes prepared from PIA-treated rats. However, there was a significant decrease in the $A_1$ adenosine receptor-mediated stimulation of $[^{35}S]GTP_{\gamma}S$ binding to cerebrocortical membranes prepared from PIA-treated rats(22.0% decrease in basal activity; 19.7% decrease in maximal activity). These results suggest that the desensitization of $A_1$ adenosine receptors following chronic administration involves agonist-induced uncoupling of the receptors from G proteins rather than alteration of $A_1$ adenosine receptor molecules. It is also suggested that the determination of stimulation of $[^{35}S]GTP_{\gamma}S$ binding to G proteins is a suitable tool in studying the receptor regulation including desensitization

• Biomolecules & Therapeutics
• /
• v.2 no.2
• /
• pp.114-119
• /
• 1994

[$^3$H]Ouabain binding parameters ( $K_{D}$ and $B_{max}$) to control rat ventricular strips and Langendorff preparations which were not previously exposed to ouabain were compared with those to both preparations that had been first exposed to a complete ouabain dose range of dose-response curve (10$^{-8}$ to 10$^{4}$M). In rat ventricular strips and Langendorff perfused heart preparations, cumulative dose-response curves of ouabain revealed biphasic positive inotropic effects, a "low-dose" effect and a "high-dose" effect with E $d_{50}$ values of 0.5 $\mu$M and 35 $\mu$M ouabain, respectively. The "low-dose" effect in ventricular strip disappeared or was diminished significantly when the ouabain dose-response curve was repeated after the washout of the effects of the first dose-response curve, whereas there were no significant differences in the maximal "high-dose"effect in both exposures to oubain. However, both of the control and ouabain-preexposed Langendorff perfused hearts revealed the same low-dose effects. The $K_{D}$ value for [$^3$H] ouabain binding and the ouabain binding site concentration ( $B_{max}$) estimated by [$^3$H]ouabain displacement assay in control preparations were 230 nM and 2 pmol/mg protein, respectively. [$^3$H]Ouabain binding parameters were not changed by repeated exposure to high concentrations of ouabain. These results suggest that digitalis receptor desensitization in the rat ventricular strip may due to the change of post-receptor events induced by ouabain binding to a high affinity site ($\alpha$$_2$isoform).).).).).

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.5
• /
• pp.461-469
• /
• 1999

Glutamate and ${\gamma}-aminobutyric$ acid (GABA) are major excitatory and inhibitory neurotransmitters in the vertebrate retina, respectively. Using the whole-cell patch clamp technique and a rapid solution changer, glutamate and GABA receptors have been extensively investigated in carp retina. Glutamate receptors on both horizontal and amacrine cells may be an AMPA preferring subtype, which predominantly consists of flop splice variants. $GABA_A$ and $GABA_C$ receptors coexist in bipolar cells and they both show significant desensitization. Kinetics analysis demonstrated that activation, deactivation and desensitization of the $GABA_C$ receptor-mediated response of these cells are overall slower than those of the $GABA_A$ response. Endogenous modulator $Zn^{2+}$ in the retina was found to differentially modulate the kinetic characteristics of the $GABA_C$ and $GABA_A$ responses.

• Proceedings of the KWS Conference
• /
• 1991.11a
• /
• pp.21-25
• /
• 1991

• 대한불안의학회:학술대회논문집
• /
• 2003.11a
• /
• pp.13-22
• /
• 2003

• Anxiety and mood
• /
• v.2 no.2
• /
• pp.142-146
• /
• 2006

People who were exposed to chronic interpersonal traumas in their early life consistently demonstrate complex psychological disturbances and many of them meet the criteria for proposed diagnosis of complex posttraumatic stress disorder (complx PTSD). The author reports a case of the successful sequential integrative treatment mainly composed of eye movement desensitization and reprocessing (EMDR) in a complex PTSD patient. The patient did not respond to the previous treatment with psychotropic medications and supportive psychotherapy. Twelve sessions of EMDR and three sessions of supportive psychotherapy were done for the patient. Psychological assessments were performed before starting the treatment and a week after completing the treatment. After the treatment, the patient improved on all the psychological scales and behavioral measures. This case suggests that the sequential integrative treatment mainly composed of EMDR may be effective for complex PTSD patients.

• Journal of Korean Medical Science
• /
• v.33 no.48
• /
• pp.306.1-306.6
• /
• 2018

This study examined the add-on efficacy of eye movement desensitization and reprocessing (EMDR) therapy among adult civilians with post-traumatic stress disorder (PTSD) who continued to be symptomatic after more than 12 weeks of initial antidepressant treatment. Scores for the Clinician Administered PTSD Scale (CAPS) were rated pre- and post-EMDR and at a 6-month follow-up. After an average of six sessions of EMDR treatment, seven of 14 patients (50%) showed more than a 30% decrease in CAPS score and eight (57%) no longer met the criteria for PTSD. Our results indicate that EMDR could be successfully added after failure of initial pharmacotherapy for PTSD.

• Proceedings of the Optical Society of Korea Conference
• /
• 2005.02a
• /
• pp.352-353
• /
• 2005

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.2
• /
• pp.169-177
• /
• 2017

Lamotrigine is an antiepileptic drug widely used to treat epileptic seizures. Using whole-cell voltage clamp recordings in combination with a fast drug application approach, we investigated the effects of lamotrigine on 5-hydroxytryptamine $(5-HT)_3$ receptors in NCB-20 neuroblastoma cells. Co-application of lamotrigine ($1{\sim}300{\mu}M$) resulted in a concentration-dependent reduction in peak amplitude of currents induced by $3{\mu}m$ of 5-HT for an $IC_{50}$ value of $28.2{\pm}3.6{\mu}M$ with a Hill coefficient of $1.2{\pm}0.1$. These peak amplitude decreases were accompanied by the rise slope reduction. In addition, $5-HT_3$-mediated currents evoked by 1 mM dopamine, a partial $5-HT_3$ receptor agonist, were inhibited by lamotrigine co-application. The $EC_{50}$ of 5-HT for $5-HT_3$ receptor currents were shifted to the right by co-application of lamotrigine without a significant change of maximal effect. Currents activated by 5-HT and lamotrigine co-application in the presence of 1 min pretreatment of lamotrigine were similar to those activated by 5-HT and lamotrigine co-application alone. Moreover, subsequent application of lamotrigine in the presence of 5-HT and 5-hydroxyindole, known to attenuate $5-HT_3$ receptor desensitization, inhibited $5-HT_3$ receptor currents in a concentration-dependent manner. The deactivation of $5-HT_3$ receptor was delayed by washing with an external solution containing lamotrigine. Lamotrigine accelerated the desensitization process of $5-HT_3$ receptors. There was no voltage-dependency in the inhibitory effects of lamotrigine on the $5-HT_3$ receptor currents. These results indicate that lamotrigine inhibits $5-HT_3$-activated currents in a competitive manner by binding to the open state of the channels and blocking channel activation or accelerating receptor desensitization.