• 제목/요약/키워드: noradrenergic system

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주정의존 환자에서 Sodium Lactate 정주 후에 유발되는 공황 발작의 빈도 및 Clonidine에 의한 성장 호르몬 둔화 반응 (Frequency of Sodium Lactate Induced Panic Attacks and Blunted Growth Hormone Responses After Clonidine Infusions in Alochol Dependence Patients)

  • 최인근;현동훈;유태혁
    • 정신신체의학
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    • 제4권1호
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    • pp.13-20
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    • 1996
  • This study was performed to explore the frequency of panic attack induced by sodium lactate in alcohol dependence patients and to compare the extent of blunted growth hormone reponses after clonidine infusion with that of normal controls. The authors investigated 10 alcohol dependence patients receiving inpatient care in Hangang Sacred Heart Hospital from March 2, 1993 to August 31, 1993 and 10 normal controls. The disagnosis of alcohol dependence was based on DSM-III-R. Thirty minutes after the sodium lactate infusions clonidins were administrated. Venous bloods were sampled before the sodium lactate infusions, and 30, 45, 60, 90 minutes after the administrations of clonidine. Plasma growth hormone levels were measured by RIA method. The results were as follows : 1) In the questionaires of Hamilton Anxiety Rating Scale, Hamilton Depression Raing Scale, CAGE, Korean MAST, the scores of alcohol dependent patients were higher than those of normal controls. 2) Sixty percent of alcohol dependence patients and twenty percent of normal controls had panic attacks induced by sodium lactate. 3) All panic attacks induced by sodium lactate were relieved after clonidine infusions. 4) There were blunted growth hormone responses after clonidine infusions in alcohol dependence patients who had sodium lactate induced panic attacks like panic disorder patients. These results suggest that alcohol dependence patients may have noradrenergic abnormality same as panic disorder patients and two disorder may have high biological correlations each other.

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Chronic Administration of Catechin Decreases Depression and Anxiety-Like Behaviors in a Rat Model Using Chronic Corticosterone Injections

  • Lee, Bombi;Sur, Bongjun;Kwon, Sunoh;Yeom, Mijung;Shim, Insop;Lee, Hyejung;Hahm, Dae-Hyun
    • Biomolecules & Therapeutics
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    • 제21권4호
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    • pp.313-322
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    • 2013
  • Previous studies have demonstrated that repeated administration of the exogenous stress hormone corticosterone (CORT) induces dysregulation in the hypothalamic-pituitary-adrenal (HPA) axis and results in depression and anxiety. The current study sought to verify the impact of catechin (CTN) administration on chronic CORT-induced behavioral alterations using the forced swimming test (FST) and the elevated plus maze (EPM) test. Additionally, the effects of CTN on central noradrenergic systems were examined by observing changes in neuronal tyrosine hydroxylase (TH) immunoreactivity in rat brains. Male rats received 10, 20, or 40 mg/kg CTN (i.p.) 1 h prior to a daily injection of CORT for 21 consecutive days. The activation of the HPA axis in response to the repeated CORT injections was confirmed by measuring serum levels of CORT and the expression of corticotrophin-releasing factor (CRF) in the hypothalamus. Daily CTN administration significantly decreased immobility in the FST, increased open-arm exploration in the EPM test, and significantly blocked increases of TH expression in the locus coeruleus (LC). It also significantly enhanced the total number of line crossing in the open-field test (OFT), while individual differences in locomotor activities between experimental groups were not observed in the OFT. Taken together, these findings indicate that the administration of CTN prior to high-dose exogenous CORT significantly improves helpless behaviors, possibly by modulating the central noradrenergic system in rats. Therefore, CTN may be a useful agent for the treatment or alleviation of the complex symptoms associated with depression and anxiety disorders.

인간의 성대조직에서 자율신경 전달물질의 분포 (Distribution of Autonomic Neurotransmitters in the Human Vocal Fold)

  • 조정일;박정선;김영모
    • 대한후두음성언어의학회지
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    • 제10권1호
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    • pp.37-42
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    • 1999
  • The vocal fold has three major function-phonation, respiration and protection, and is richly innervated. The vocal 1314 its autonomic innervation-adrenergic and cholinergic from superior cervical ganglion and the vagus nerve, respectively. The action of both system account for vasoregulation and glandular activity. In e vocal fold several kin of neuropeptides, including SP, CGRP, VIP, TH, NPY, ENK have been reported at the animal including cat or dog. But information regarding the distribution of autonomic nerve fibers containing neuropeptides in the human vocal fold is lacking. Two neuropeptides are of special interest : 1) vasoactive intestinal polypeptide(VIP)that is known to be contained in the parasympathetic(cholinergic) neuron. 2) tyrosine hydroxylase(TH)is located in the cytoplasm of noradrenergic neuron and is the rate-limiting enzyme in noradrenaline synthesis. To understand specific autonomic function of vocal fold we did immunohistochemical examination of VIP and TH in the human vocal fold.

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Nicotine Addiction: Neurobiology and Mechanism

  • Tiwari, Raj Kumar;Sharma, Vikas;Pandey, Ravindra Kumar;Shukla, Shiv Shankar
    • 대한약침학회지
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    • 제23권1호
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    • pp.1-7
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    • 2020
  • Nicotine, primary component of tobaco produces craving and withdrawal effect both in humans and animals. Nicotine shows a close resemblance to other addictive drugs in molecular, neuroanatomical and pharmacological, particularly the drugs which enhances the cognitive functions. Nicotine mainly shows its action through specific nicotinic acetylcholine receptors located in brain. It stimulates presynaptic acetylcholine receptors thereby enhancing Ach release and metabolism. Dopaminergic system is also stimulated by it, thus increasing the concentration of dopamine in nuclear accumbens. This property of nicotine according to various researchers is responsible for reinforcing behavioral change and dependence of nicotine. Various researchers have also depicted that some non dopaminergic systems are also involved for rewarding effect of nicotinic withdrawal. Neurological systems such as GABAergic, serotonergic, noradrenergic, and brain stem cholinergic may also be involved to mediate the actions of nicotine. Further, the neurobiological pathway to nicotine dependence might perhaps be appropriate to the attachment of nicotine to nicotinic acetylcholine receptors, peruse by stimulation of dopaminergic system and activation of general pharmacological changes that might be responsible for nicotine addiction. It is also suggested that MAO A and B both are restrained by nicotine. This enzyme helps in degradation dopamine, which is mainly responsible for nicotinic actions and dependence. Various questions remain uninsurable to nicotine mechanism and require more research. Also, various genetic methods united with modern instrumental analysis might result for more authentic information for nicotine addiction.

Synthesis and Studies on Anticonvulsant and Antidepressant Activities of 5-Alkoxy-tetrazolo[1,5-a]quinolines

  • Deng, Xian-Qing;Wei, Cheng-Xi;Song, Ming-Xia;Chai, Kyu-Yun;Sun, Zhi-Gang;Quan, Zhe-Shan
    • Bulletin of the Korean Chemical Society
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    • 제31권2호
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    • pp.447-452
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    • 2010
  • A series of 5-alkoxy-tetrazolo[1,5-a]quinolines were synthesized to evaluate their anticonvulsant and antidepressant effects. Anticonvulsant effects and neurotoxicity of the compounds when injected intraperitoneally to mice were determined by a maximal electroshock (MES) test and a rotarod test, respectively. Only three of the synthesized compounds (4a, 4b, 4c) displayed anticonvulsant activity at a dose of 300 mg/kg. Most of the compounds significantly reduced immobility times during the forced swimming test (FST) at a dose of 100 mg/kg, indicative of antidepressant activity. Among the compounds, 5-(2-fluorobenzyloxy)tetrazolo[1,5-a]quinoline (4k) reduced immobility time by 66.85% at 30 mg/kg compared with the same dose of Fluoxetine, which reduced immobility time by 52.30%. According to the results of the 5-Hydroxytryptophan induced head-twitch test and yohimbine toxicity potentiation test, the noradrenergic system seems not to be involved in the antidepressant-like effect of compound 4k while the serotonergic system seems a little to be involved.

The mechanism of action of pulsed radiofrequency in reducing pain: a narrative review

  • Park, Donghwi;Chang, Min Cheol
    • Journal of Yeungnam Medical Science
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    • 제39권3호
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    • pp.200-205
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    • 2022
  • Pain from nervous or musculoskeletal disorders is one of the most common complaints in clinical practice. Corticosteroids have a high pain-reducing effect, and their injection is generally used to control various types of pain. However, they have various adverse effects including flushing, hyperglycemia, allergic reactions, menstrual changes, immunosuppression, and adrenal suppression. Pulsed radiofrequency (PRF) is known to have a pain-reducing effect similar to that of corticosteroid injection, with nearly no major side effects. Therefore, it has been widely used to treat various types of pain, such as neuropathic, joint, discogenic, and muscle pain. In the current review, we outlined the pain-reducing mechanisms of PRF by reviewing previous studies. When PRF was first introduced, it was supposed to reduce pain by long-term depression of pain signaling from the peripheral nerve to the central nervous system. In addition, deactivation of microglia at the level of the spinal dorsal horn, reduction of proinflammatory cytokines, increased endogenous opioid precursor messenger ribonucleic acid, enhancement of noradrenergic and serotonergic descending pain inhibitory pathways, suppression of excitation of C-afferent fibers, and microscopic damage of nociceptive C- and A-delta fibers have been found to contribute to pain reduction after PRF application. However, the pain-reducing mechanism of PRF has not been clearly and definitely elucidated. Further studies are warranted to clarify the pain-reducing mechanism of PRF.

주의력결핍 과잉행동장애의 신경생물학적 병태생리 (Neurobiological Pathophysiology of Attention Deficit Hyperactivity Disorder)

  • 박형배;주열
    • Journal of Yeungnam Medical Science
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    • 제17권2호
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    • pp.108-122
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    • 2000
  • Background: Models of attention deficit hyperactivity disorder(ADHD) that have proposed a hypodopaminergic state resulting in hypofunction of the prefrontal circuitry have assumed a unitary dopamine system, which largely ignores the distinct functional differences between mesocortical dopamine system and nigrostriatal dopamine system. Purpose: The author's goal was to develop a pathophysiological model for ADHD with greater explanotory power than dopaminergic hypofunction hypothesis in prefronal circuitry. Material and Methods: Published clinical findings on ADHD were integrated with data from genetic, pharmacological, neuroimaging studies in human and animals. Results: Molecular genetic studies suggest that three genes may increase the susceptibility to ADHD. The three candidate genes associated with ADHD are each involved in dopaminergic function, and this consistent with the neurobiologic studies implicating catecholamines in the etiology of ADHD. Pharmacological data also provide compelling support for dopamine and noradrenergic hypothesis of ADHD. Neuroimaging studies lend substantial support for the hypothesis that right-sided abnormalities of prefrontal-basal ganglia circuit would be found in ADHD. Conclusions: The present hypothesis takes advantage of the major differences between the two pertinent dopamine systems. Mesocortical dopamine system, which largely lacks inhibitory autoreceptors, is ideally positioned to regulate cortical inputs, thus improving the signal-to-noise ratio for biologically valued signals. In this circuit, therapeutic doses of stimulants are hypothesized to increase postsynaptic dopamine effects and enhance executive functions. By contrast, symptoms of hyperactivity/impulsivity in ADHD are hypothesized to be associated with relative overactivity of nigrostriatal circuit. This nigrostriatal circuit is tightly regulated by inhibitory autoreceptoors as well as by long distance feedback from the cortex, and slow diffusion of therapeutic doses of stimulant via oral administration is hypothesized to produce a net inhibition of dopaminergic neurotransmission and improves hyperactivity.

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Effect of Ginsenoside Re on Depression- and Anxiety-Like Behaviors and Cognition Memory Deficit Induced by Repeated Immobilization in Rats

  • Lee, Bom-Bi;Shim, In-Sop;Lee, Hye-Jung;Hahm, Dae-Hyun
    • Journal of Microbiology and Biotechnology
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    • 제22권5호
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    • pp.708-720
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    • 2012
  • In this study, we assessed the effects of ginsenoside Re (GRe) administration on repeated immobilization stress-induced behavioral alterations using the forced swimming test (FST), the elevated plus maze (EPM), and the active avoidance conditioning test (AAT). Additionally, we examined the effect of GRe on the central adrenergic system by observing changes in neuronal tyrosine hydroxylase (TH) immunoreactivity and brain-derived neurotrophic factor (BDNF) mRNA expression in the rat brain. Male rats received 10, 20, or 50 mg/kg GRe (i.p.) 30 min before daily exposures to repeated immobilization stress (2 h/day) for 10 days. Activation of the hypothalamic-pituitary-adrenal (HPA) axis in response to repeated immobilization was confirmed by measuring serum levels of corticosterone (CORT) and the expression of corticotrophin-releasing factor (CRF) in the hypothalamus. Repeated immobilization stress increased immobility in the FST and reduced open-arm exploration in the EPM test. It also increased the probability of escape failures in the AAT test, indicating a reduced avoidance response. Daily administration of GRe during the repeated immobilization stress period significantly inhibited the stress-induced behavioral deficits in these behavioral tests. Administration of GRe also significantly blocked the increase in TH expression in the locus coeruleus (LC) and the decrease in BDNF mRNA expression in the hippocampus. Taken together, these findings indicate that administration of GRe prior to immobilization stress significantly improved helpless behaviors and cognitive impairment, possibly through modulating the central noradrenergic system in rats. These findings suggest that GRe may be a useful agent for treating complex symptoms of depression, anxiety, and cognitive impairment.

Alpha-Asarone, a Major Component of Acorus gramineus, Attenuates Corticosterone-Induced Anxiety-Like Behaviours via Modulating TrkB Signaling Process

  • Lee, Bombi;Sur, Bongjun;Yeom, Mijung;Shim, Insop;Lee, Hyejung;Hahm, Dae-Hyun
    • The Korean Journal of Physiology and Pharmacology
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    • 제18권3호
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    • pp.191-200
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    • 2014
  • We investigated the anxiolytic-like activity of ${\alpha}$-asarone (AAS) from Acorus gramineus in an experimental rat model of anxiety induced by repeated administration of the exogenous stress hormone corticosterone (CORT). The putative anxiolytic effect of AAS was studied in behavioral tests of anxiety, such as the elevated plus maze (EPM) test and the hole-board test (HBT) in rats. For 21 consecutive days, male rats received 50, 100, or 200 mg/kg AAS (i.p.) 30 min prior to a daily injection of CORT. Dysregulation of the HPA axis in response to the repeated CORT injections was confirmed by measuring serum levels of CORT and the expression of corticotrophin-releasing factor (CRF) in the hypothalamus. Daily AAS (200 mg/kg) administration increased open-arm exploration significantly in the EPM test, and it increased the duration of head dipping activity in the HBT. It also blocked the increase in tyrosine hydroxylase (TH) expression in the locus coeruleus (LC) and decreased mRNA expression of brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, in the hippocampus. These results indicated that the administration of AAS prior to high-dose exogenous CORT significantly improved anxiety-like behaviors, which are associated with modification of the central noradrenergic system and with BDNF function in rats. The current finding may improve understanding of the neurobiological mechanisms responsible for changes in emotions induced by repeated administration of high doses of CORT or by elevated levels of hormones associated with chronic stress. Thus, AAS did exhibit an anxiolytic-like effects in animal models of anxiety.

아동기 외상의 정신과적 개관 (CHILDHOOD TRAUMA:PSYCHIATRIC OVERVIEW)

  • 한성희
    • Journal of the Korean Academy of Child and Adolescent Psychiatry
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    • 제13권1호
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    • pp.3-14
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    • 2002
  • 아동에 가해지는 정신적 외상의 충격은 아동의 심리발달에 지울 수 없는 상처를 남김으로써 향후 심각한 정신장애를 일으키는 결정적 원인이 된다. 아동기 외상의 현상학적 특징과 외상에 관여하는 신경생물학적 기전을 살펴보았고, 아동기에 경험하는 외상이 인격의 발달에 미치는 영향과 그와 관련한 정신병리를 알아보았다. 외상에 노출된 아동은 공통적으로 자신이 경험한 공포사건을 시각적으로 재경험하거나 그 기억을 반복하며, 놀이나 행동을 통해서도 외상사건을 반복하려는 경향을 보인다. 일회의 충격적 사건에 노출된 아동은 사건에 대한 지나친 기억과 집착을 보이고 지각왜곡이 심한 반면 장기간 반복되는 외상을 경험하는 아동은 정신적 무감각과 자기최면, 해리, 분노의 경향이 두드러진다. 소아·청소년에서는 외상 후 퇴행이 보다 현저하고 시간감각의 왜곡이 더 심하게 나타나며 아동의 연령이 어릴수록 자율신경계의 반응성이 증가하는 경향을 보인다. 외상적 충격에 노출되면 뇌내에서 즉각적이고 방대한 신경전달물질의 방출이 있게되는데, 자율신경계, 면역계, 시상하부-뇌하수체-부신피질 축(hypothalamic-pituitary-adrenal axis)이 활성화된다. 외상시 internal opiate가 활발한 작용을 하면서 아동으로 하여금 외상에 반응하지 않도록 하고 외상에 대한 감정반응 자체를 봉쇄할 수 있도록 해준다. 아동기 외상의 경우 central noradrenergic system에 변화가 초래되어 카테콜아민에 대해 과민감한 비정상적 소견을 보이게 된다. 체내 순환되는 cortisol 수치는 감소하고, glucocorticoid 수용체 농도와 반응성이 증가한다. 외상 후 발견되는 기억력 장애는 해마의 구조적 변화와 관련이 있는 것으로 보고되고 있다. 아동기 외상은 자기(self)와 대상(object)에 대한 내적 표상(internal representation)이 지속적으로 분화 발전하는 발달과정에서 일어난다는 점에서 인격의 발달에 심각한 영향을 미치게 된다. 해리, 신체화, 자학성, 자기애 장애의 정신병리로 발전하면서 경계성 인격장애, 자기애성 인격장애, 다중인격장애 등을 초래하게 된다.

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