• The Korean Journal of Physiology and Pharmacology
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• 제16권5호
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• pp.293-296
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• 2012

Memory reconsolidation is ubiquitous across species and various memory tasks. It is a dynamic process in which memory is modified and/or updated. In experimental conditions, memory reconsolidation is usually characterized by the fact that the consolidated memory is disrupted by a combination of memory reactivation and inhibition of protein synthesis. However, under some experimental conditions, the reactivated memory is not disrupted by inhibition of protein synthesis. This so called "boundary condition" of reconsolidation may be related to memory strength. In Pavlovian fear conditioning, the intensity of unconditional stimulus (US) determines the strength of the fear memory. In this study, we examined the effect of the intensity of US on the reconsolidation of contextual fear memory. Strong contextual fear memory, which is conditioned with strong US, is not disrupted by inhibition of protein synthesis after its reactivation; however, a weak fear memory is often disrupted. This suggests that a US of strong intensity can inhibit reconsolidation of contextual fear memory.

• 생물정신의학
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• 제18권2호
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• pp.80-89
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• 2011

Pavlovian fear conditioning has been extensively studied for the understanding of neurobiological basis of memory and emotion. Pavlovian fear conditioning is an associative memory which forms when conditioned stimulus (CS) is paired with unconditioned stimulus (US) once or repeatedly. This behavioral model is also important for the understanding of anxiety disorders such as posttraumatic stress disorder. Here we describe the neural circuitry involved in fear conditioning and the molecular mechanisms underlying fear memory formation. During consolidation some memories fade out but other memories become stable and concrete. Emotion plays an important role in determining which memories will survive. Memory becomes unstable and editable again immediately after retrieval. It opens the possibility for us of modulating the established fear memory. It provides us with very efficient tools to improve the efficacy of cognitive-behavior therapy and other exposure-based therapy treating anxiety disorders.

• 대한불안의학회지
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• 제6권2호
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• pp.102-108
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• 2010

Objective : Although studies have explored responses to fear had been assessed using various psychophysiological methods, results have been inconsistent. The present study examined psychophysiological responses in healthy subjects after viewing fear stimuli in a video clip for set up future fear related psychophysiological studies. Methods : We monitored three psychophysiological variables (electroencephalography, skin temperature, and heart rate variability) in adults who watched either a control stimulus movie clip or a fear-inducing movie clip. Results : In 16 healthy adults, theta activity decreased significantly after the fear stimulus as compared to the normal stimulus. However the participants showed no differences in heart rate variability or skin temperature between the fear and normal control stimulus situations. Conclusion : In the limbic area, theta activity corresponds with information processing, integration into previous memories and long-term potentiation. In this study, we suggest decreased theta activity represents amygdalo-hippocampal activity, associated with fear, short-term memory, and memory extinction in the healthy adults. Further studies are needed to evaluate the interaction of fear, memory, and the pathophysiology of anxiety disorder in patient with anxiety disorders.

• 대한한의학회지
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• 제25권4호
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• pp.51-60
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• 2004

Objective : The effect Saenggitang (GT), which has been used for amnesia, in Oriental Medicine, on memory and learning ability, was investigated. Methods : Hot water extracts (HWE) of SGT were used for the studies. In passive avoidance performances (step through test), active avoidance performances (lever press test), Motor activity, pentobarbital-induced sleep, 20 and 50 mg/100g of SGT-HWE ameliorated the memory retrieval deficit induced by 40% ethanol. Results : The SGT-HWE did not affect the ambulatory activity of normal mice in normal condition. 20 and 50 mg/100g of SGT-HWE enhanced contextual fear memory, but not cued fear memory in a fear conditioning task, which requires the activation of the NMDA (N-methyl-D-aspartase) receptor. SGT-HWE did not affect the motor activity measured by the titling type ambulometer test performed immediately and 24 hr after the administration. SGT-HWE prolonged the sleeping time induced by 50 mg/kg pentobarbital in mice and decreased SMA (spontaneous motor activity) in active avoidance performances (lever press test). Conclusion : These results indicate that the SGT-HWE have an improving effect on the memory retrieval disability induced by ethanol and may act as a stimulating factor for activating the NMDA receptor. and the SGT-HWE has a tranquilizing and anti-anxiety action.

• Journal of Ginseng Research
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• 제40권1호
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• pp.55-61
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• 2016

Background: A number of neurological and neurodegenerative diseases share impaired cognition as a common symptom. Therefore, the development of clinically applicable therapies to enhance cognition has yielded significant interest. Previously, we have shown that activation of lysophosphatidic acid receptors (LPARs) via gintonin application potentiates synaptic transmission by the blockade of $K^+$ channels in the mature hippocampus. However, whether gintonin may exert any beneficial impact directly on cognition at the neural circuitry level and the behavioral level has not been investigated. Methods: In the current study, we took advantage of gintonin, a novel LPAR agonist, to investigate the effect of gintonin-mediated LPAR activation on cognitive performances. Hippocampus-dependent fear memory test, synaptic plasticity in the hippocampal brain slices, and quantitative analysis on synaptic plasticity-related proteins were used. Results: Daily oral administration of gintonin for 1 wk significantly improved fear memory retention in the contextual fear-conditioning test in mice.We also found that oral administration of gintonin for 1 wk increased the expression of learning and memory-related proteins such as phosphorylated cyclic adenosine monophosphate-response element binding (CREB) protein and brain-derived neurotrophic factor (BDNF). In addition, prolonged gintonin administration enhanced long-term potentiation in the hippocampus. Conclusion: Our observations suggest that the systemic gintonin administration could successfully improve contextual memory formation at the molecular and synaptic levels as well as the behavioral level. Therefore, oral administration of gintonin may serve as an effective noninvasive, nonsurgical method of enhancing cognitive functions.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2008년도 Proceedings of the Convention
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• pp.33-45
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• 2008

Auditory fear memory is thought to be maintained by fear conditioning-induced potentiation of synaptic efficacy. The conditioning-induced potentiation has been shown to be maintained, at least in part, by enhanced expression of surface AMPA receptor (AMPAR) at excitatory synapses in the lateral amygdala (LA). Depotentiation, reversal of conditioning-induced potentiation, has been proposed as a cellular mechanism for fear extinction. However, a direct link between depotentiation and extinction has not yet been tested. To address this, we applied both ex vivo and in vivo approaches to rats in which fear memory had been consolidated. We found a novel form of ex vivo depotentiation; the depotentiation reversed conditioning-induced potentiation at thalamic input synapses onto the LA (T-LA synapses) ex vivo, and it could be induced only when both NMDA and metabotropic glutamate receptors were co-activated. Extinction returned the enhanced T-LA synaptic efficacy observed in conditioned rats to baseline and occluded the depotentiation. Consistently, extinction reversed conditioning-induced enhancement of surface expression of AMPAR subunits in LA synaptosomal preparations. A GluR2-derived peptide that blocks regulated AMPAR endocytosis inhibited depotentiation, and microinjection of a cell-permeable form of the peptide into the LA attenuated extinction. Our results are consistent with the use of depotentiation to weaken potentiated synaptic inputs onto the LA during extinction, and they provide strong evidence that AMPAR removal at excitatory synapses in the LA underlies extinction. The results described here are in line with previous findings. Neural activity in the LA has been shown to decrease after extinction in the rat and human. The NMDAR dependency of the depotentiation fits nicely with a large body of evidence that fear extinction depends upon amygdala NMDARs. Similarly, blockade of metabotropic glutamate recepotrs in the LA has recently been shown to attenuate fear extinction.

• BMB Reports
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• 제49권1호
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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]

• Molecules and Cells
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• 제23권3호
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• pp.259-271
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• 2007

Investigation of molecular and cellular mechanisms of synaptic plasticity is the major focus of many neuroscientists. There are two major reasons for searching new genes and molecules contributing to central plasticity: first, it provides basic neural mechanism for learning and memory, a key function of the brain; second, it provides new targets for treating brain-related disease. Long-term potentiation (LTP), mostly intensely studies in the hippocampus and amygdala, is proposed to be a cellular model for learning and memory. Although it remains difficult to understand the roles of LTP in hippocampus-related memory, a role of LTP in fear, a simplified form of memory, has been established. Here, I will review recent cellular studies of LTP in the anterior cingulate cortex (ACC) and then compare studies in vivo and in vitro LTP by genetic/pharmacological approaches. I propose that ACC LTP may serve as a cellular model for studying central sensitization that related to chronic pain, as well as pain-related cognitive emotional disorders. Understanding signaling pathways related to ACC LTP may help us to identify novel drug target for various mental disorders.

• 대한약리학회:학술대회논문집
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• 대한약리학회 2006년도 The 6th Congress of the Federation of Asian and Oceanian Physiological Societies
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• pp.105.2-105.2
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• 2006

• 대한약리학회:학술대회논문집
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• 대한약리학회 2006년도 The 6th Congress of the Federation of Asian and Oceanian Physiological Societies
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• pp.83.2-83.2
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• 2006