• Title/Summary/Keyword: Synaptic Plasticity

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Enhancement of GluN2B Subunit-Containing NMDA Receptor Underlies Serotonergic Regulation of Long-Term Potentiation after Critical Period in the Rat Visual Cortex

  • Joo, Kayoung;Rhie, Duck-Joo;Jang, Hyun-Jong
    • The Korean Journal of Physiology and Pharmacology
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    • v.19 no.6
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    • pp.523-531
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    • 2015
  • Serotonin [5-hydroxytryptamine (5-HT)] regulates synaptic plasticity in the visual cortex. Although the effects of 5-HT on plasticity showed huge diversity depending on the ages of animals and species, it has been unclear how 5-HT can show such diverse effects. In the rat visual cortex, 5-HT suppressed long-term potentiation (LTP) at 5 weeks but enhanced LTP at 8 weeks. We speculated that this difference may originate from differential regulation of neurotransmission by 5-HT between the age groups. Thus, we investigated the effects of 5-HT on apha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-, ${\gamma}$-aminobutyric acid receptor type A (GABAAR)-, and N-methyl-D-aspartic acid receptor (NMDAR)-mediated neurotransmissions and their involvement in the differential regulation of plasticity between 5 and 8 weeks. AMPAR-mediated currents were not affected by 5-HT at both 5 and 8 weeks. GABAAR-mediated currents were enhanced by 5-HT at both age groups. However, 5-HT enhanced NMDAR-mediated currents only at 8 weeks. The enhancement of NMDAR-mediated currents appeared to be mediated by the enhanced function of GluN2B subunit-containing NMDAR. The enhanced GABAAR- and NMDAR-mediated neurotransmissions were responsible for the suppression of LTP at 5 weeks and the facilitation of LTP at 8 weeks, respectively. These results indicate that the effects of 5-HT on neurotransmission change with development, and the changes may underlie the differential regulation of synaptic plasticity between different age groups. Thus, the developmental changes in 5-HT function should be carefully considered while investigating the 5-HT-mediated metaplastic control of the cortical network.

Effects of Serotonin on the Induction of Long-term Depression in the Rat Visual Cortex

  • Jang, Hyun-Jong;Cho, Kwang-Hyun;Park, Sung-Won;Kim, Myung-Jun;Yoon, Shin-Hee;Rhie, Duck-Joo
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.5
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    • pp.337-343
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    • 2010
  • Long-term potentiation (LTP) and long-term depression (LTD) have both been studied as mechanisms of ocular dominance plasticity in the rat visual cortex. In a previous study, we suggested that a developmental increase in serotonin [5-hydroxytryptamine (5-HT)] might be involved in the decline of LTP, since 5-HT inhibited its induction. In the present study, to further understand the role of 5-HT in a developmental decrease in plasticity, we investigated the effect of 5-HT on the induction of LTD in the pathway from layer 4 to layer 2/3. LTD was inhibited by 5-HT ($10{\mu}M$) in 5-week-old rats. The inhibitory effect was mediated by activation of 5-$HT_2$ receptors. Since 5-HT also regulates the development of visual cortical circuits, we also investigated the role of 5-HT on the development of inhibition. The development of inhibition was retarded by chronic (2 weeks) depletion of endogenous 5-HT in 5-week-old rats, in which LTD was reinstated. These results suggest that 5-HT regulates the induction of LTD directly via activation of 5-$HT_2$ receptors and indirectly by regulating cortical development. Thus, the present study provides significant insight into the roles of 5-HT on the development of visual cortical circuits and on the age-dependent decline of long-term synaptic plasticity.

Artificial Brain for Robots (로봇을 위한 인공 두뇌 개발)

  • Lee, Kyoo-Bin;Kwon, Dong-Soo
    • The Journal of Korea Robotics Society
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    • v.1 no.2
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    • pp.163-171
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    • 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.

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Dopamine-dependent synaptic plasticity in an amygdala inhibitory circuit controls fear memory expression

  • Lee, Joo Han;Kim, Joung-Hun
    • BMB Reports
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    • v.49 no.1
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    • pp.1-2
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    • 2016
  • Of the numerous events that occur in daily life, we readily remember salient information, but do not retain most less-salient events for a prolonged period. Although some of the episodes contain putatively emotional aspects, the information with lower saliency is rarely stored in neural circuits via an unknown mechanism. We provided substantial evidence indicating that synaptic plasticity in the dorsal ITC of amygdala allows for selective storage of salient emotional experiences, while it deters less-salient experience from entering long-term memory. After activation of D4R or weak fear conditioning, STDP stimulation induces LTD in the LA-ITC synapses. This form of LTD is dependent upon presynaptic D4R, and is likely to result from enhancement of GABA release. Both optogenetic abrogation of LTD and ablation of D4R at the dorsal ITC in vivo lead to heightened and over-generalized fear responses. Finally, we demonstrated that LTD was impaired at the dorsal ITC of PTSD model mice, which suggests that maladaptation of GABAergic signaling and the resultant LTD impairment contribute to the endophenotypes of PTSD. [BMB Reports 2016; 49(1): 1-2]

Effect of Fermented Garlic Extract Containing Nitric Oxide Metabolites on Impairments of Memory and of Neural Plasticity in Rat Model of Vascular Dementia (산화질소 대사체 함유 마늘 발효 추출물 이용 혈관성 치매 흰쥐 모델의 기억력 및 신경가소성 장애 개선 효과)

  • Zhang, Xiaorong;Moon, Se Jin;Kim, Yoo Ji;Jeong, Sun Oh;Kim, Min Sun
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.36 no.2
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    • pp.59-65
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    • 2022
  • Rodent model for chronic cerebral hypoperfusion caused by bilateral carotid artery occlusion (BCAO) show clinically relevant evidences for vascular dementia and impairments of synaptic plasticity in the hippocampus. The purpose of this study was to evaluate effect of fermented garlic (F-Garlic) extract with NO metabolites on cognitive behaviors, synaptic plasticity, and molecular events in the hippocampus following BCAO. Adult male Sprague-Dawley rats were randomly divided three experimental groups into: control+water; BCAO+water; BCAO+F-Garlic. Animals were treated with oral administration of F-Garlic in tap water as a drinking water after surgery for 4 weeks. On passive avoidance test and Y-maze test, BCAO+water showed a significant decrease in step-through latency and spontaneous alteration, indicating deficit of hippocampal memory formation but the treatment of F-Garlic significantly increased these cognitive behaviors. In control+water, a robust increase in the amplitude of evoked field excitatory postsynaptic potentials was observed by theta burst stimulation to hippocampal neural circuit indicating formation of long-term potentiation (LTP) in the hippocampal CA1. BCAO+water showed a highly significant deficit in LTP induction 4 weeks after BCAO. On other hand, daily oral administration of F-Garlic extract caused the marked preservation of LTP induction. Moreover, parvalbumin was markedly reduced in the CA1, especially, in the stratum radiatum of BCAO+water. In contrast, BCAO+F-Garlic mitigate a significantly reduction of the parvalbumin. In summary, these results suggest that daily oral administration of F-Garlic extract can ameliorate cognitive memory deficit through the preservation of synaptic plasticity and interneurons integrity in the hippocampus in rodent model of chronic cerebral hypoperfusion.

Long-Term Potentiation of Excitatory Synaptic Strength in Spinothalamic Tract Neurons of the Rat Spinal Cord

  • Hur, Sung Won;Park, Joo Min
    • The Korean Journal of Physiology and Pharmacology
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    • v.17 no.6
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    • pp.553-558
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    • 2013
  • Spinal dorsal horn nociceptive neurons have been shown to undergo long-term synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD). Here, we focused on the spinothalamic tract (STT) neurons that are the main nociceptive neurons projecting from the spinal cord to the thalamus. Optical technique using fluorescent dye has made it possible to identify the STT neurons in the spinal cord. Evoked fast mono-synaptic, excitatory postsynaptic currents (eEPSCs) were measured in the STT neurons. Time-based tetanic stimulation (TBS) was employed to induce long-term potentiation (LTP) in the STT neurons. Coincident stimulation of both pre- and postsynaptic neurons using TBS showed immediate and persistent increase in AMPA receptor-mediated EPSCs. LTP can also be induced by postsynaptic spiking together with pharmacological stimulation using chemical NMDA. TBS-induced LTP observed in STT neurons was blocked by internal BAPTA, or $Ni^{2+}$, a T-type VOCC blocker. However, LTP was intact in the presence of L-type VOCC blocker. These results suggest that long-term plastic change of STT neurons requires NMDA receptor activation and postsynaptic calcium but is differentially sensitive to T-type VOCCs.

Acid-sensing ion channels (ASICs): therapeutic targets for neurological diseases and their regulation

  • Kweon, Hae-Jin;Suh, Byung-Chang
    • BMB Reports
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    • v.46 no.6
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    • pp.295-304
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    • 2013
  • Extracellular acidification occurs not only in pathological conditions such as inflammation and brain ischemia, but also in normal physiological conditions such as synaptic transmission. Acid-sensing ion channels (ASICs) can detect a broad range of physiological pH changes during pathological and synaptic cellular activities. ASICs are voltage-independent, proton-gated cation channels widely expressed throughout the central and peripheral nervous system. Activation of ASICs is involved in pain perception, synaptic plasticity, learning and memory, fear, ischemic neuronal injury, seizure termination, neuronal degeneration, and mechanosensation. Therefore, ASICs emerge as potential therapeutic targets for manipulating pain and neurological diseases. The activity of these channels can be regulated by many factors such as lactate, $Zn^{2+}$, and Phe-Met-Arg-Phe amide (FMRFamide)-like neuropeptides by interacting with the channel's large extracellular loop. ASICs are also modulated by G protein-coupled receptors such as CB1 cannabinoid receptors and 5-$HT_2$. This review focuses on the physiological roles of ASICs and the molecular mechanisms by which these channels are regulated.

The Role of NMDA Receptor in Learning and Memory (학습과 기억에서 NMDA 수용체의 역할)

  • Kim, Seung-Hyun;Shin, Kyung-Ho
    • Sleep Medicine and Psychophysiology
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    • v.7 no.1
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    • pp.10-17
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    • 2000
  • To investigate the neurobiological bases of learning and memory is one of the ambitious goals of modern neuroscience. The progress in this field of recent years has not only brought us closer to understanding the molecular mechanism underlying long-lasting changes in synaptic strength, but it has also provided further evidence that these mechanisms are required for memory formation. Since twenty years ago, several studies for the tests of the hypothesis that NMDA-dependent hippocampal long-term potentiation(LTP) underlies learning have been reported. Also, in the recent year, data from mutant mice showed that a potential role for NMDA-dependent LTP in hippocampal CA1 and spatial learning. Although the current evidence for the role of NMDA receptor in learning and memory is not still obvious, NMDA receptor seems to act as a critical switch for activation of a cascade of events that underlie synaptic plasticity.

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Proteins in the Postsynaptic Density of the Central Nervous System

  • Moon, Il-Soo
    • Journal of Life Science
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    • v.9 no.2
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    • pp.34-39
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    • 1999
  • The postsynaptic density (PSD) is a cytoskeletal specialization that is involved in the regulation of synaptic signal transduction. Mainly due to the hydrophobic nature of the PSD proteins, characterization of this intriguing structure at the molecular level has been very intractable until early 1990s. However, recent development in protein microchemistry and molecular cloning techniques allowed identification and characterization of the PSD proteins. As expected, cytoskeletal proteins constitute major components of the PSD. Other major PSD proteins have been identified by protein sequencing, and their genes were used to fish out associating proteins by yeast two-hybrid system expanding our knowledge on the molecular structure of the PSD significantly. In this review, I summarize proteins that are so far identified focusing on the glutamatergic synapses.