• CELLMED
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• v.9 no.2
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• pp.2.1-2.1
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• 2019

Depression is common psychiatric diseases characterized by diverse physical and emotional symptoms including low mood, loss of interest in pleasurable activities, and feelings of worthlessness. Depression causes of death and disability. The first antidepressant was created by the idea that central serotonin mechanism. Selective serotonin reuptake inhibitor, fluoxetine is the first-line drug in the treatment of depressive disorder and their few side effects as opposed to tricyclic antidepressants. Not all people with depression respond adequately to standard treatments. Korean music playing/listening actions appear to be a reliable approach to developing recovery from depression.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.230.1-230.1
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• 2003

In case of oral application of quinupramine, antidepressants, it may cause adverse effects such as diarrhea, nausea due to transient high blood concentration. Ethylene vinyl acetate (EVA) which is heat-processible, flexible, inexpensive material was used for transdermal drug delivery. The purpose of this study was to develop the new transdermal delivery system of quinupramine using EVA polymer matrix that can provide sustained release and avoid the side effects. The EVA matrix containing quinupramine was prepared by solvent-evaporation method. (omitted)

• Korean Journal of Psychosomatic Medicine
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• v.22 no.2
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• pp.138-142
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• 2014

Burning mouth syndrome is characterized by intra-oral burning sensation without any organic abnormalities. This syndrome is associated with various etiological factors such as neuropathy, malnutrition, menopause and depression. Several medications have been tried for the treatment. Those are analgesics, hormones, anticonvulsants and antidepressants. However, optimal effective pharmacologic treatment remains still unknown. The purpose of this case study is to report the clinical effectiveness of gabapentin in the treatment of burning mouth syndrome in postmenopausal women with comorbid depression. We report two menopausal women. Antidepressants were effective for improving depressive symptoms, but it had no effects on intra-oral burning sensation. Gabapentin reduced intra-oral burning sensation effectively for all two patients. One patient reported 55% reduction(a decrease from 9 to 4 on VAS), the other patient reported 35% reduction(from 8 to 5) of the intra-oral burning sensation during 16 weeks. The minimal effective daily dose of gabapentin was 300mg. This study suggests that gabapentin might be a useful, effective therapeutic option for treating burning mouth syndrome in postmenopausal women with comorbid depression. Further prospective clinical studies are needed to investigate the effectiveness of gabapentin in patients with burning mouth syndrome.

• The Korean Journal of Pain
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• v.23 no.2
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• pp.99-108
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• 2010

Chronic pain is a multifactorial condition with both physical and psychological symptoms, and it affects around 20% of the population in the developed world. In spite of outstanding advances in pain management over the past decades, chronic pain remains a significant problem. This article provides a mechanism- and evidence-based approach to improve the outcome for pharmacologic management of chronic pain. The usual approach to treat mild to moderate pain is to start with a nonopioid analgesic. If this is inadequate, and if there is an element of sleep deprivation, then it is reasonable to add an antidepressant with analgesic qualities. If there is a component of neuropathic pain or fibromyalgia, then a trial with one of the gabapentinoids is appropriate. If these steps are inadequate, then an opioid analgesic may be added. For moderate to severe pain, one would initiate an earlier trial of a long term opioid. Skeletal muscle relaxants and topicals may also be appropriate as single agents or in combination. Meanwhile, the steps of pharmacologic treatments for neuropathic pain include (1) certain antidepressants (tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors), calcium channel ${\alpha}2-{\delta}$ ligands (gabapentin and pregabalin) and topical lidocaine, (2) opioid analgesics and tramadol (for first-line use in selected clinical circumstances) and (3) certain other antidepressant and antiepileptic medications (topical capsaicin, mexiletine, and N-methyl-d-aspartate receptor antagonists). It is essential to have a thorough understanding about the different pain mechanisms of chronic pain and evidence-based multi-mechanistic treatment. It is also essential to increase the individualization of treatment.

• The Korean Journal of Pain
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• v.27 no.1
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• pp.54-62
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• 2014

Background: The recently known analgesic action mechanisms of nefopam (NFP) are similar to those of anticonvulsants and antidepressants in neuropathic pain treatment. It is difficult to prescribe high doses of oral neuropathic drugs without titration due to adverse effects. Unfortunately, there are few available intravenous analgesics for the immediate management of acute flare-ups of the chronic neuropathic pain. The aim of this study was to determine the additional analgesic effects for neuropathic pain of NFP and its adverse effects during the titration of oral medications for neuropathic pain among inpatients with postherpetic neuralgia (PHN). Methods: Eighty inpatients with PHN were randomly divided into either the NFP or normal saline (NS) groups. Each patient received a 3-day intravenous continuous infusion of either NFP with a consecutive dose reduction of 60, 40, and 20 mg/d, or NS simultaneously while dose titrations of oral medications for neuropathic pain gradually increased every 3 days. The efficacy of additional NFP was evaluated by using the neuropathic pain symptom inventory (NPSI) score for 12 days. Adverse effects were also recorded. Results: The median NPSI score was significantly lower in the NFP group from days 1 to 6 of hospitalization. The representative alleviating symptoms of pain after using NFP were both spontaneous and evoked neuropathic pain. Reported common adverse effects were nausea, dizziness, and somnolence, in order of frequency. Conclusions: An intravenous continuous infusion of NFP reduces spontaneous and evoked neuropathic pain with tolerable adverse effects during the titration of oral medications in inpatients with PHN.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.71-80
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• 2018

In patients with epilepsy, depression is a common comorbidity but difficult to be treated because many antidepressants cause pro-convulsive effects. Thus, it is important to identify the risk of seizures associated with antidepressants. To determine whether paroxetine, a very potent selective serotonin reuptake inhibitor (SSRI), interacts with ion channels that modulate neuronal excitability, we examined the effects of paroxetine on Kv3.1 potassium channels, which contribute to high-frequency firing of interneurons, using the whole-cell patch-clamp technique. Kv3.1 channels were cloned from rat neurons and expressed in Chinese hamster ovary cells. Paroxetine reversibly reduced the amplitude of Kv3.1 current, with an $IC_{50}$ value of $9.43{\mu}M$ and a Hill coefficient of 1.43, and also accelerated the decay of Kv3.1 current. The paroxetine-induced inhibition of Kv3.1 channels was voltage-dependent even when the channels were fully open. The binding ($k_{+1}$) and unbinding ($k_{-1}$) rate constants for the paroxetine effect were $4.5{\mu}M^{-1}s^{-1}$ and $35.8s^{-1}$, respectively, yielding a calculated $K_D$ value of $7.9{\mu}M$. The analyses of Kv3.1 tail current indicated that paroxetine did not affect ion selectivity and slowed its deactivation time course, resulting in a tail crossover phenomenon. Paroxetine inhibited Kv3.1 channels in a use-dependent manner. Taken together, these results suggest that paroxetine blocks the open state of Kv3.1 channels. Given the role of Kv3.1 in fast spiking of interneurons, our data imply that the blockade of Kv3.1 by paroxetine might elevate epileptic activity of neural networks by interfering with repetitive firing of inhibitory neurons.

• Toxicological Research
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• v.26 no.4
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• pp.315-320
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• 2010

It has been clinically reported that toluene causes mental depression in humans. However, the detrimental effects of toluene exposure on brain function and the relation between features of mental depression and toluene exposure are poorly understood. This study evaluated depression-like behaviors in adult C57BL/6 mice after administration of toluene, and elucidated the effects of classical antidepressants on the depression-like behaviors. For the estimation of depression-like behaviors, tail suspension test (TST) and forcedswim test (FST) were performed 1, 4 and 16 days after toluene (0~1000 mg/kg bw) treatment. In addition, classical antidepressants such as fluoxetine (FLX, 20 mg/kg bw) and imipramine (IMI, 40 mg/kg bw) were administered 12 h and 1 h before the tests. In the TST and FST, toluene-treated mice exhibited a longer duration of immobility than vehicle-treated mice 1 and 4 days after toluene treatment. The depression-like behaviors were significantly reversed by FLX and IMI. The weight of the adrenal gland and the size of adrenocortical cells were significantly higher in toluene-treated mice compared to vehicle-treated controls. It is suggested that acute toluene exposure of adult mice is sufficiently detrimental to induce depression. In addition, this study has established a mouse model for a depressive state induced by toluene treatment.

• Korean Journal of Biological Psychiatry
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• v.8 no.2
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• pp.226-232
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• 2001

The pharmacotherapy of depression has reduced morbidity and improved outcome for many depressive patients. A wide range of classical and new antidepressants are available for their treatment. However, 30-40% of all patients do not respond sufficiently to the initial treatment and present adverse effects. Pharmacogenetics studies the genetic basis of an individual's ability to respond to pharmacotherapy. Recently, some reports on serotonin transporter gene polymorphisms and their influence on the response to antidepressive therapy provide an interesting diagnostic tool in assessing the chances of response to antidepressants. We also investigated the relationship between serotonin transprter polymorphisms(5-HTTLPR) and the long-term effect of the antidepressant treatment. 128 depressive patients were enrolled into 2nd year study. The therapeutic response of each subset was not different at 8th, 16th week, but the subset with homozygote(l/l) of long variant showed a better therapeutic response to antidepressant than the heterozygote(l/s) of long and short variant, which showed a better therapeutic response than the subset with homozygote (s/s) of short variant at 1st year and 2nd year after the antidepressant treatment. This result shows that the serotonin transporter polymorphisms may be related to the long-term effect of antidepressant treatment. The potential for pharmacogenomics, the use of genetic information to guide pharmacotherapy and improve outcome by providing individualized treatment decisions, has gained increasing attention. pharmacogenomics will contribute to individualize drug choice by using genotype to predict positive clinical outcomes, adverse reactions, and levels of drug metabolism. Personalized medicine, the use of marker-assisted diagnosis and targeted therapies derived from an individual molecular profile, will impact the antidepressant therapy and this approach will replace the traditional trial-and-error practice of medicine.

• The Korean Journal of Pharmacology
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• v.11 no.1 s.17
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• pp.55-60
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• 1975

An animal which is placed in a new environment displays a complex behavioral pattern consisting of locomotion, grooming and rearing. This behavioral pattern is influenced by endogenous and exogenous stimuli, such as hormonal secretion, level of neurohumoral transmitters, drugs and light. It is widely known that the most tranquilizers depressed spontaneous motor activity although their mechanisms of action were different, while antidepressants stimulated except imipramine which showed various action. Until the present time, the hole-board apparatus, which gives rather subjective data, has been used extensively to study the effects of drugs on general activity and exploratory behavior in mice. Recently a new apparatus for mobility measurements, called a 'Selective Activity Meter' has been introduced. This instrument supposedly produces more objective data on activity and behavior. The purpose of the present experiment was to study the influence of psychotropics on motor activity using the Selective Activity Meter. In the experiment, various psychotropic agents such as major tranquilizers(chlorpromazine, haloperidol); minor tranquilizers(meprobamate, diazepam); and antidepressants(amphetamine, imipramine) were used. In each experiment, the drug was administered to five mice and their activity was recorded. Each experiment was run five or more times and the results are based on the mean of each trial. The results are summarized as follows: 1. The group of mice treated with chlorpromazine showed markedly inhibited motor activity in comparison with controls and the inhibitory action of chlorpromazine was shown to be more intense than any of the other drugs used in the test. Haloperidol administration yielded similar results until 60 minutes, but mice showed less inhibition of motor activity than with chlorpromazine after 90 minutes. 2. In the group treated with diazepam, there was strong inhibition of motor activity until 30 minutes, but after 60 minutes the mice showed less inhibition than with chlorpromazine. In the meprobamate group, motor activity was inhibited in a manner similar to that of other tranquilizers, but the inhibition was less than that of diazepam. 3. In the group treated with imipramine, the inhibition developed gradually after ten minutes. 4. The effects of amphetamine did not appear until 30 minutes after administration, but then there was a significant increase in the motor activity.

• Journal of Ginseng Research
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• v.17 no.3
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• pp.187-195
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• 1993

We have examined the functional role of central dopaminergic processes on the behavioral pharmacological effects induced by psychotropics and red ginseng saponins of normal rats and compared with that of brain damaged rats. Desipramine and clomipramine produced, a significant depression of the locomotor activity in normal rats, but in brain damaged rats, they did not have any effect throughout the experimental period of 4 hours. Total saponin (50~200 mg/kg), PT (25~50 mg/kg), PD (25~50 mg/kg), $Rg_1$(12.5~25 mg/kg), $Rb_1$ (12.5~50 mg/kg) did not change, and high concentrations of PT (100 mg/kg), PD (100 mg/kg) and $Rg_1$ (50 mg/kg) showed a significant decrease in the locomotor activity of one hour after administration but total saponin (100 mg/kg), PD (25~50 mg/kg), Rgl (12.5 mg/kg), $Rb_1$ (12.5 mg/kg) markedly increased the locomotor activity of four hour after administration in normal rats. On the other hand, total saponin (50 mg/kg), PT (100 mg/kg) and PD (100 mg/kg) Produced a prominent stimulation of the locomotor activity in brain damaged rats. These results suggest that the inhibition of the locomotor activity induced by antidepressants was not affected by the sensitivity of cerebral DA system, whereas red ginseng saponin showed antifatigue effect and also the stimulation of the locomotor activity induced by red ginseng saponin was mediated by the inhibition of cerebral DA system. These psychotropic action of red ginseng saponins could be responsible for the beneficial effects on conditions of fatigue and decreased alertness.