• 제목/요약/키워드: brain mechanism

검색결과 746건 처리시간 0.029초

조현병(調鉉病) : 뇌 연결성의 장애 (Attunement Disorder : A Disorder of Brain Connectivity)

  • 김기원;박경민;장혜련;이유상;박선철
    • 생물정신의학
    • /
    • 제20권4호
    • /
    • pp.136-143
    • /
    • 2013
  • Objectives We reviewed cellular and synaptic dysconnectivity, disturbances in micro- and macro- circuitries, and neurodevelopmentally-derived disruptions of neural connectivity in the pathogenesis of schizophrenia. Method We reviewed the selected articles about disturbances in neural circuits which had been proposed as a pathogenetic mechanism of schizophrenia. Results The literature review reveals that schizophrenia may be a disease related to disturbance in neurodevelopmental mechanism, shown as 'a misconnection syndrome of neural circuit or neural network'. In descriptive psychopathological view, definition of a disorder of brain connectivity has limitation to explain other aspects of schizophrenia including deterministic strictness in thought process. Conclusion Schizophrenia is considered as a disorder of brain connectivity as well as a neurodevelopmental disorder related with genetic and environmental factors. We could make a suggestion that "JoHyeonByung (attunement disorder)" denotes the disturbances of psychic fine-tuning which correspond to the neural correlates of brain dysconnectivity metaphorically.

잡견을 이용한 실험적 뇌사모델에서 뇌사가 혈역학적 변화와 심근손상에 미치는 영향 -제1보;급격한 뇌압의 상승에 의한 뇌사모델에서의 혈역학적 및 심전도학적 변화- (Effect of the Brain Death on Hemodynamic Changes and Myocardial Damages in Canine Brain Death Model -Hemodynamic and Electrocardiographic Changes in the Brain Death Model Caused by Sudden Increase of Intracranial Pressure-)

  • 조명찬
    • Journal of Chest Surgery
    • /
    • 제28권5호
    • /
    • pp.437-442
    • /
    • 1995
  • We developed an experimental model of brain death using dogs. Brain death was caused by increasing the intracranial pressure[ICP suddenly by injecting saline to an epidural Foley catheter in five female mongrel dogs[weight, 20-25Kg .Hemodynamic and electrocardiographic changes were evaluated continuously during the process of brain death. 1. Abrupt rise of ICP after each injection of saline followed by a rapid decline to a new steady-state level within 15 minutes and the average volume required to induce brain death was 7.6$\pm$0.8ml.2. Body temperature, heart rate, mean pulmonary arterial pressure, left ventricular[LV enddiastolic pressure and cardiac output was not changed significantly during the process of brain death, but there was an increasing tendency.3. Mean arterial pressure and LV maximum +dP/dt increased significantly at the time of brain death.4. Hemodynamic collapse was developed within 140 minutes after brain death.5. Marked sinus bradycardia followed by junctional rhythm was seen in two dogs and frequent VPB`s with ventricular tachycardia was observed in one dog at the time of brain death. Hyperdynamic state develops and arrhythmia appears frequently at the time of brain death. Studies on the effects of brain death on myocardium and its pathophysiologic mechanism should be followed in the near future.

  • PDF

Neuronal Responses in the Globus Pallidus during Subthalamic Nucleus Electrical Stimulation in Normal and Parkinson's Disease Model Rats

  • Ryu, Sang Baek;Bae, Eun Kyung;Kim, Jinhyung;Hwang, Yong Sup;Im, Changkyun;Chang, Jin Woo;Shin, Hyung-Cheul;Kim, Kyung Hwan
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제17권4호
    • /
    • pp.299-306
    • /
    • 2013
  • Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been widely used as a treatment for the movement disturbances caused by Parkinson's disease (PD). Despite successful application of DBS, its mechanism of therapeutic effect is not clearly understood. Because PD results from the degeneration of dopamine neurons that affect the basal ganglia (BG) network, investigation of neuronal responses of BG neurons during STN DBS can provide informative insights for the understanding of the mechanism of therapeutic effect. However, it is difficult to observe neuronal activity during DBS because of large stimulation artifacts. Here, we report the observation of neuronal activities of the globus pallidus (GP) in normal and PD model rats during electrical stimulation of the STN. A custom artifact removal technique was devised to enable monitoring of neural activity during stimulation. We investigated how GP neurons responded to STN stimulation at various stimulation frequencies (10, 50, 90 and 130 Hz). It was observed that activities of GP neurons were modulated by stimulation frequency of the STN and significantly inhibited by high frequency stimulation above 50 Hz. These findings suggest that GP neuronal activity is effectively modulated by STN stimulation and strongly dependent on the frequency of stimulation.

Purification and Reaction Mechanism of Rat Brain Succinic Semialdehyde Dehydrogenase

  • Kim, Kyu-Tae;Joo, Chung-No
    • BMB Reports
    • /
    • 제28권2호
    • /
    • pp.162-169
    • /
    • 1995
  • Rat brain succinic semialdehyde dehydrogenase (EC 1.2.1.24 SSADH) activity was detected in mitochondrial, cytosolic and microsomal fractions. Brain mitochondrial soluble SSADH was purified by ammonium sulfate precipitation, DEAE Sephacel, and 5'-AMP Sepharose 4B affinity chromatography. The purified enzyme was shown to consist of four identical subunits, and the molecular weight of a subunit was 55 kD. The $K_m$ for short chain aliphatic aldehydes and aromatic aldehydes were at the $10^{-3}M$ level but that for succinic semialdehyde was 2.2 ${\mu}M$. Either $NAD^+$ or $NADP^+$ can be used as a cofactor but the affinity for $NAD^+$ was 10 times higher than that for $NADP^+$. The brain cytosolic SSADH was also purified by ammonium sulfate precipitation, DEAE Sephacel, Blue Sepharose CL-6B and 5'-AMP Sepharose 4B affinity chromatography and its Km for short chain aliphatic aldehydes was at the $10^{-3}$ level but that for succinic semialdehyde was 3.3 ${\mu}M$. $NAD^+$ can be used as a cofactor for this enzyme. We suppose that both enzyme might participate in the oxidation of succinic semialdehyde, which is produced during GABA metabolism. The activity of both cytosolic and mitochondrial SSADH was markedly inhibited when the concentration of succinic semialdehyde was high. The reciprocal plot pattern of product inhibition and initial velocity indicated a sequential ordered mechanism for mitochondrial matrix SSADH. Chemical modification data suggested that amino acid residues such as cysteine, serine and lysine might participate in the SSADH reaction.

  • PDF

로봇을 위한 인공 두뇌 개발 (Artificial Brain for Robots)

  • 이규빈;권동수
    • 로봇학회논문지
    • /
    • 제1권2호
    • /
    • pp.163-171
    • /
    • 2006
  • This paper introduces the research progress on the artificial brain in the Telerobotics and Control Laboratory at KAIST. This series of studies is based on the assumption that it will be possible to develop an artificial intelligence by copying the mechanisms of the animal brain. Two important brain mechanisms are considered: spike-timing dependent plasticity and dopaminergic plasticity. Each mechanism is implemented in two coding paradigms: spike-codes and rate-codes. Spike-timing dependent plasticity is essential for self-organization in the brain. Dopamine neurons deliver reward signals and modify the synaptic efficacies in order to maximize the predicted reward. This paper addresses how artificial intelligence can emerge by the synergy between self-organization and reinforcement learning. For implementation issues, the rate codes of the brain mechanisms are developed to calculate the neuron dynamics efficiently.

  • PDF

트립토판 보강식이를 섭취한 마우스에서 serotonin 대사와 morphine 진통기작 관련성에 대한 연구(II) (A Study on the Serotonin Metabolism and the Morphine-related Analgesic Mechanism in Mice Fed Tryptophan Supplemented Deit (II))

  • 권영혜;이윤옥;김해리
    • Biomolecules & Therapeutics
    • /
    • 제9권1호
    • /
    • pp.20-25
    • /
    • 2001
  • In this study we fed control diet and tryptophan supplemented diets containing 0.35% tryptophan to ICR mice for 2 weeks. The concentrations of serotonin and 5-HIAA were changed by injection of the serotonin synthesis inhibitor, p-CPA and the serotonin precursor, serotoninP and the change of brain serotonin concentration negatively correlated with that of pain sensitivity, and p-CPA and serotoninP also changed the analgesic effect of morphine. The injection of naloxone, the opiate antagonist, resulted in an increase in the writhing frequency, but its antagonistic effect was not significant. The concentration of 5-HIAA elevated in mice brain at least 3hr after administration of morphine hydroxide indicates that the changes in brain serotonin metabolism may be associated with the acute effects of morphine analgesia. In short, these results not only suggest that tryptophan supplemented diet suppress pain sensitivity in mice, but also indicate that at least in part analgesic mechanism of serotonin may be associated with morphine analgesia.

  • PDF

Lithium-induced Increase of Synaptosomal Uptake of Norepinephrine in Rat Brain

  • Cho, Young-Wuk;Han, Seung-Ho;Kim, Chang-Ju;Min, Byung-Il
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제1권2호
    • /
    • pp.127-133
    • /
    • 1997
  • Lithium remains the most widely used therapeutic agent for bipolar affective disorder, particularly mania. Although many investigators have studied the effects of lithium on abnormalities in monoamine neuro-transmitter as a pathophysiological basis of affective disorder, the action mechanism of lithium ion remains still unknown. To explore the action mechanism of lithium in the brain, we examined the effects of lithium on the extrasynaptosomal concentrations of catecholamines and their metabolites. Synaptosomes were prepared from the rat forebrains and assays of catecholamines and metabolites were made using HPLC with an electrochemical detector. Lithium of 1mM decreased the extrasynaptosomal concentrations of NE from the control group of $3.07{\pm}1.19$ to the treated group of $0.00{\pm}0.00$ (ng/ml of synaptosomal suspension) but not that of DHPG. It can be suggested that lithium increases synaptosomal uptake of NE. Increased intraneuronal uptake of NE would decrease neurotransmission and extraneuronal metabolism of NE. Because increased brain NE metabolism and neurotransmission have been suggested as important components in the pathophysiology of bipolar affective disorder, especially mania, lithium-induced increase of intraneuronal NE uptake can be suspected as an action mechanism of therapeutic effect of lithium in manic patient, possibly in bipolar affective disorder.

  • PDF

Permeability of a Capsaicin Derivative $[{14}^C]DA-5018$ to Blood-Brain Barrier Corrected with HPLC Method

  • Kang, Young-Sook;Kim, Jong-Mi
    • Archives of Pharmacal Research
    • /
    • 제22권2호
    • /
    • pp.165-172
    • /
    • 1999
  • In the present work , the transport mechanism of a capsaicin derivative, DA-5018, through blood-brain barrier (BBB) has been investigated to evaluate the feasibility of potential drug development. The result of pharmacokinetic parameters obtained from the intravenous injection of plasma volume marker,$[3^H]RSA$ and $[{14}^C]DA-5018$, indicated that both AUC, area under the plasma concentration curve and VD, volume of distribution in brain of $[3^H]RSA$ agreed with those reported ($1620{\pm}10 $percentage injected dose minute per milliliter (%IDmin/ml) and $12.0{\pm}0.1{\mu}l/g$, respectively). Elimination half-life and AUC of $[{14}^C]DA-5018$is corrected by the PHLC analysis, 19.6$\pm$1.2 min and 7.69$\pm$0.85% IDmin/ml, respectively. The metabolic rate of $[{14}^C]DA-5018$was very rapid. The blood-brain barrier permeability surface area (PS) product of $[{14}^C]DA-5018$ was calculated to be 0.24$\pm$0.05 $\mu$l/min/g. The result of internal carotid artery perfusion and capillary depletion suggested that [14C]DA-5018 pass through BBB with the time increasingly. Investigation of transport mechanism of $[{14}^C]DA-5018$ using agonist and antagonist suggested that vanilloid (capsaicin) receptor did not exist in the BBB, and nutrient carrier system in the BBB has no effect on the transport of DA-5018. In conclusion, despite the fact that penetration of DA-5018 through BBB is significant, the intact drug found in the brain tissue is small because of a rapid metabolism. Therefore, for the central analgesic effect of DA-5018, the method to increase the metabolic stability in plasma and the brain permeability should be considered.

  • PDF

감각 정보를 이용한 뱀 로봇의 행동구현 (Snake Robot Motion Scheme Using Image and Voice)

  • 강준영;김성주;조현찬;전홍태
    • 대한전자공학회:학술대회논문집
    • /
    • 대한전자공학회 2002년도 하계종합학술대회 논문집(3)
    • /
    • pp.127-130
    • /
    • 2002
  • Human's brain action can divide by recognition and intelligence. recognition is sensing voice, image and smell and Intelligence is logical judgment, inference, decision. To this concept, Define function of cerebral cortex, and apply the result. Current expert system is lack, that reasoning by cerebral cortex and thalamus, hoppocampal and so on. In this paper, With human's brain action, wish to embody human's action artificially Embody brain mechanism using Modular Neural Network, Applied this result to snake robot.

  • PDF

Intracranial Calcification Caused by a Brain Abscess : A Rare Cause of Intracranial Calcification

  • Kim, Hyeun Sook;Kim, Dong Min;Ju, Chang Il;Kim, Seok Won
    • Journal of Korean Neurosurgical Society
    • /
    • 제54권2호
    • /
    • pp.148-150
    • /
    • 2013
  • Intracranial calcifications are relatively common computed tomographic findings in the field of neurosurgery, and cysticercosis, tuberculosis, HIV, and cryptococcus are acquired intracranial infections typically associated with calcifications. However, intracranial calcification caused by a bacterial brain abscess is rare. Here, we present a rare case of intracranial calcification caused by a bacterial brain abscess, from which staphylococcus hominis was isolated. To the best of our knowledge, no previous report has been published on intracranial calcification caused by bacterial brain abscess after decompressive craniectomy for traumatic brain injury. In this article, the pathophysiological mechanism of this uncommon entity is discussed and relevant literature reviewed.