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Search Results: 1 - 10 of 8075 matches for " Bai-Chuang Shyu "
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Short-term synaptic plasticity in the nociceptive thalamic-anterior cingulate pathway
Bai-Chuang Shyu, Brent A Vogt
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-51
Abstract: A single nociceptive electrical stimulus to the sciatic nerve induced a prominent sink current in the layer II/III of the ACC in vivo, while high frequency stimulation potentiated the response of this current. Paired-pulse facilitation by electrical stimulation of midline, mediodorsal and intralaminar thalamic nuclei (MITN) suggesting that the MITN projection to ACC mediates the nociceptive short-term plasticity. The short-term synaptic plasticities were evaluated for different inputs in vitro where the medial thalamic and contralateral corpus callosum afferents were compared. Stimulation of the mediodorsal afferent evoked a stronger short-term synaptic plasticity and effectively transferred the bursting thalamic activity to cingulate cortex that was not true for contralateral stimulation. This short-term enhancement of synaptic transmission was mediated by polysynaptic pathways and NMDA receptors. Layer II/III neurons of the ACC express a short-term plasticity that involves glutamate and presynaptic calcium influx and is an important mechanism of the short-term plasticity.The potentiation of ACC neuronal activity induced by thalamic bursting suggest that short-term synaptic plasticities enable the processing of nociceptive information from the medial thalamus and this temporal response variability is particularly important in pain because temporal maintenance of the response supports cortical integration and memory formation related to noxious events. Moreover, these modifications of cingulate synapses appear to regulate afferent signals that may be important to the transition from acute to chronic pain conditions associated with persistent peripheral noxious stimulation. Enhanced and maintained nociceptive activities in cingulate cortex, therefore, can become adverse and it will be important to learn how to regulate such changes in thalamic firing patterns that transmit nociceptive information to ACC in early stages of chronic pain.The cingulate cortex is one of t
Anterior Cingulate epilepsy: mechanisms and modulation
Wei-Pang Chang,Bai-Chuang Shyu
Frontiers in Integrative Neuroscience , 2014, DOI: 10.3389/fnint.2013.00104
Abstract: Epilepsy is a common neurological disorder, about 1% population worldwide suffered from this disease. In 1989, the International League Against Epilepsy (ILAE) classified anterior cingulate epilepsy as a form of frontal lobe epilepsy (FLE). FLE is the second most common type of epilepsy. Previous clinical studies showed that FLE account an important cause in refractory epilepsy, therefore to find alternative approach to modulate FLE is very important. Basic research using animal models and brain slice have revealed some insights on the epileptogenesis and modulation of seizure in anterior cingulate cortex (ACC). Interneurons play an important role in the synchronization of cingulate epilepsy. Research has shown that the epileptogenesis of seizure originated from mesial frontal lobe might be caused by a selective increase in nicotine-evoked γ-aminobutyric acid (GABA) inhibition, because the application of the GABAA receptor antagonist picrotoxin inhibited epileptic discharges. Gap junctions are also involved in the regulation of cingulate epilepsy. Previous studies have shown that the application of gap junction blockers could attenuate ACC seizures, while gap junction opener could enhance them in an in vitro preparation. μ-Opioid receptors have been shown to be involved in the epileptic synchronization mechanism in ACC seizures in a brain slice preparation. Application of the μ-opioid agonist DAMGO significantly abolished the ictal discharges in a 4-aminopyridine induced electrographic seizure model in ACC. Basic research has also found that thalamic modulation has an inhibitory effect on ACC seizures. Studies have shown that the medial thalamus may be a target for deep brain stimulation to cure ACC seizures.
Anxiety- and depressive-like responses and c-fos activity in preproenkephalin knockout mice: Oversensitivity hypothesis of enkephalin deficit-induced posttraumatic stress disorder
Jen-Chuang Kung, Tsung-Chieh Chen, Bai-Chuang Shyu, Sigmund Hsiao, Andrew Huang
Journal of Biomedical Science , 2010, DOI: 10.1186/1423-0127-17-29
Abstract: Posttraumatic stress disorder (PTSD) shows a variety of symptoms including the exaggerated fear, helplessness, and horror after patients suffer from an extremely stressful traumatic event (an unconditioned stimulus [US]) [1]. For example, the reexperiencing of symptoms of an earlier traumatic event includes panic attack, phobic avoidance of situations that resemble the traumatic event, and psychic numbing [2,3]. Additional symptoms comprise autonomic hyperarousal responses and fear sensitization, such as exaggerated startle responses, hypervigilance, insomnia, irritability, and impaired concentration [4].In addition to the traumatic event US inducing PTSD-like responses, the environmental stimulus (conditioned stimulus [CS]) associated with the traumatic event US is also able to elicit PTSD-like avoidance fear responses [5]. Accordingly, an animal model of PTSD has been developed in which individuals are repeatedly exposed to situational reminders that have been previously associated with a traumatic stress US to elicit the fear response [6,7].The PTSD-like symptoms have been shown to be governed by specific neurotransmitters [8,9]. For example, a recent report has demonstrated that the releasing concentrations of serotonin, norepinephrine, and dopamine in the hippocampus and frontal cortex would be enhanced, and the plasma corticosterone levels in the hypothalamic-pituitary-adrenal axis were increased after acute stress exposure [10]. Moreover, a recent study demonstrated overactivity of norepinephrine and vasopressin systems, and deficits of glucocorticoid and serotonin systems resulted in a cognitive syndrome resembling PTSD [11].Additionally, several lines of evidence suggest that the opioid system is also involved in PTSD. When reencountering a traumatic stressor, PTSD patients exhibit an increased endogenous opioid-mediated and stress-induced analgesic effect [7,12,13]. The pain mechanism is also associated with PTSD-like symptoms, particularly associative fea
Roles of the anterior cingulate cortex and medial thalamus in short-term and long-term aversive information processing
Sin-Chee Chai, Jen-Chuang Kung, Bai-Chuang Shyu
Molecular Pain , 2010, DOI: 10.1186/1744-8069-6-42
Abstract: Behavioral training began 1 week after surgery, in which radiofrequency lesions of the ACC or MT were performed. The retention tests were conducted 30 s (short-term) or 24 h (long-term) after training. Pretraining radiofrequency lesions of the ACC impaired performance in the 30 s, but not 24 h, retention test. Microinfusions of lidocaine into the ACC immediately after training impaired performance in the retention test conducted 10 min later. Pretraining radiofrequency lesions of the MT impaired performance in both the 30 s and 24 h retention tests. However, posttraining, but not pretest, microinfusions of lidocaine into the MT impaired performance in the 24 h retention test.These results suggest that the ACC may play an important role in short-term, but not long-term, nociceptive information processing. In contrast, the MT may be important for the consolidation of nociceptive information storage.In rodents, area 24 of the anterior cingulate cortex (ACC) is a part of the medial prefrontal cortex, together with areas 25 and 32, and is implicated in the cognitive and emotional aspects of nociception [1-3]. Neuroimaging studies in humans have demonstrated ACC activation during noxious stimulation [4]. Behavioral studies in experimental animals have demonstrated that the ACC mediates responses to inflammatory pain [5,6], neuropathic pain [7], pain in the formalin test [8], and formalin-induced conditioned place avoidance [9,10]. These studies support the hypothesis that the ACC is involved in the processing of affective nociceptive information [11-14]. The ACC has been reported to be involved in the processing of both sensory nociceptive information and the anticipation of painful stimuli [1]. Therefore, a link between nociceptive stimuli (unconditioned stimulus, US) and anticipatory stimuli (conditioned stimulus, CS) may occur in this region [15]. Recent studies from our laboratory have explored the functional role of the ACC in nociceptive emotional learning. We found
Differential regulation of morphine antinociceptive effects by endogenous enkephalinergic system in the forebrain of mice
Tsung-Chieh Chen, Ying-Ying Cheng, Wei-Zen Sun, Bai-Chuang Shyu
Molecular Pain , 2008, DOI: 10.1186/1744-8069-4-41
Abstract: The genotypes of bred KO mice were confirmed by PCR. Met-enkephalin immunoreactive neurons were labeled in the caudate-putamen, intermediated part of lateral septum, lateral globus pallidus, intermediated part of lateral septum, hypothalamus, and amygdala of WT mice. Met-enkephalin immunoreactive neurons were not found in the same brain areas in KO mice. Tail withdrawal and von Frey test results did not differ between WT and KO mice. KO mice had shorter latency to start paw licking than WT mice in the hot plate test. The maximal percent effect of morphine treatments (5 mg/kg and 10 mg/kg, i.p.) differed between WT and KO mice in hot plate test. The current source density (CSD) profiles evoked by peripheral noxious stimuli in the primary somatosenstory cortex (S1) and anterior cingulate cortex (ACC) were similar in WT and KO mice. After morphine injection, the amplitude of the laser-evoked sink currents was decreased in S1 while the amplitude of electrical-evoked sink currents was increased in the ACC. These differential morphine effects in S1 and ACC were enhanced in KO mice. Facilitation of synaptic currents in the ACC is mediated by GABA inhibitory interneurons in the local circuitry. Percent increases in opioid receptor binding in S1 and ACC were 5.1% and 5.8%, respectively.The present results indicate that the endogenous enkephalin system is not involved in acute nociceptive transmission in the spinal cord, S1, and ACC. However, morphine preferentially suppressed supraspinal related nociceptive behavior in KO mice. This effect was reflected in the potentiated differential effects of morphine in the S1 and ACC in KO mice. This potentiation may be due to an up-regulation of opioid receptors. Thus these findings strongly suggest an antagonistic interaction between the endogenous enkephalinergic system and exogenous opioid analgesic actions in the supraspinal brain structures.Opioid systems play an important role in numerous functions in the central nervous system (
Network dynamics in nociceptive pathways assessed by the neuronal avalanche model
José Jiun-Shian Wu, Hsi-Chien Shih, Chen-Tung Yen, Bai-Chuang Shyu
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-33
Abstract: Neuronal activity was recorded with a 4 × 8 multichannel electrode array in the primary somatosensory cortex (S1) and anterior cingulate cortex (ACC). Under light anesthesia, peripheral pinch stimulation increased the slope of the α value in both the ACC and S1, whereas brush stimulation increased the α value only in the S1. The increase in α values was blocked in both regions under deep anesthesia. The increase in α values in the ACC induced by peripheral pinch stimulation was blocked by medial thalamic lesion, but the increase in α values in the S1 induced by brush and pinch stimulation was not affected.The neuronal avalanche model shows a critical state in the cortical network for noxious-related signal processing. The α value may provide an index of brain network activity that distinguishes the responses to somatic stimuli from the control state. These network dynamics may be valuable for the evaluation of acute nociceptive processes and may be applied to chronic pathological pain conditions.
Spontaneous inflammatory pain model from a mouse line with N-ethyl-N-nitrosourea mutagenesis
Tsung-Chieh Chen, Jiun-Shian Wu, Wei-Pang Chang, Ping-Ning Hsu, Sung-Tsang Hsieh, Bai-Chuang Shyu
Journal of Biomedical Science , 2012, DOI: 10.1186/1423-0127-19-55
Abstract: We investigated abnormal sensory processing, neuronal peptides, and behavioral responses after the induction of autoinflammatory disease. Single-nucleotide polymorphism (SNP) markers and polymerase chain reaction product sequencing were used to identify the mutation site.All affected mice developed paw inflammation at 4–8?weeks. Histological examinations revealed hyperplasia of the epidermis in the inflamed paws and increased macrophage expression in the spleen and paw tissues. Mechanical and thermal nociceptive response thresholds were reduced in the affected mice. Locomotor activity was decreased in affected mice with inflamed hindpaws, and this reduction was attributable to the avoidance of contact of the affected paw with the floor. Motor strength and daily activity in the home cage in the affected mice did not show any significant changes. Although Fos immunoreactivity was normal in the dorsal horn of affected mice, calcitonin gene-related peptide immunoreactivity significantly increased in the deep layer of the dorsal horn. The number of microglia increased in the spinal cord, hippocampus, and cerebral cortex in affected mice, and the proliferation of microglia was maintained for a couple of months. Two hundred eighty-five SNP markers were used to reveal the affected gene locus, which was found on the distal part of chromosome 18. A point mutation was detected at A to G in exon 8 of the pstpip2 gene, resulting in a conserved tyrosine residue at amino acid 180 replaced by cysteine (Y180 C).The data provide definitive evidence that a mutation in pstpip2 causes autoinflammatory disease in an N-ethyl-N-nitrosourea mutagenesis mouse model. Thus, our pstpip2 mutant mice provide a new model for investigating the potential mechanisms of inflammatory pain.
The Effect of Developing a Tunnel across a Highway on the Water Quality in an Upstream Reservoir Watershed Area—A Case Study of the Hsuehshan Tunnel in Taiwan
Guey-Shin Shyu,Bai-You Cheng,Wei-Ta Fang
International Journal of Environmental Research and Public Health , 2012, DOI: 10.3390/ijerph9093344
Abstract: Cities in Taiwan are so dependent on reservoir water that preservation of the upstream reservoir watershed has become a significant public concern. However, due to the high-density development of land, resulting in rapid urban expansion, the construction of tunnels and elevated highways across reservoirs to better utilize the surrounding land has become a global trend. Based on data from long-term observation of the reservoir, this study verifies the difference in water quality before and after the highway construction. The results indicate that the total phosphorus (TP) increased on average 14 μg/L to 36.5 μg/L per annum, and the water quality is expected to require 10 years to recover. During the highway development, the average TP was more than twice the normal level. During summer, the TP level increases 3.1-fold due to rainfall. As indicated by the results, the large-scale land development will harm the long-term preservation of the reservoir’s water quality, and therefore should be avoided.
Applying Factor Analysis Combined with Kriging and Information Entropy Theory for Mapping and Evaluating the Stability of Groundwater Quality Variation in Taiwan
Guey-Shin Shyu,Bai-You Cheng,Chi-Ting Chiang,Pei-Hsuan Yao,Tsun-Kuo Chang
International Journal of Environmental Research and Public Health , 2011, DOI: 10.3390/ijerph8041084
Abstract: In Taiwan many factors, whether geological parent materials, human activities, and climate change, can affect the groundwater quality and its stability. This work combines factor analysis and kriging with information entropy theory to interpret the stability of groundwater quality variation in Taiwan between 2005 and 2007. Groundwater quality demonstrated apparent differences between the northern and southern areas of Taiwan when divided by the Wu River. Approximately 52% of the monitoring wells in southern Taiwan suffered from progressing seawater intrusion, causing unstable groundwater quality. Industrial and livestock wastewaters also polluted 59.6% of the monitoring wells, resulting in elevated EC and TOC concentrations in the groundwater. In northern Taiwan, domestic wastewaters polluted city groundwater, resulting in higher NH 3-N concentration and groundwater quality instability was apparent among 10.3% of the monitoring wells. The method proposed in this study for analyzing groundwater quality inspects common stability factors, identifies potential areas influenced by common factors, and assists in elevating and reinforcing information in support of an overall groundwater management strategy.
CAI多媒體教學軟體之開發模式 Using an Instructional Design Model for Developing a Multimedia CAI Courseware
Hsin-Yih Shyu
Journal of Educational Media & Library Sciences , 1995,
Abstract: 無 This article outlined a systematic instructional design model for developing a multimedia computer-aided instruction (CAI) courseware. The model illustrated roles and tasks as two dimensions necessary in a CAI production teamwork. Four major components (Analysis, Design, Development, and Revise/Evaluation) following by totally 25 steps are provided. Eight roles with each competent skills were identified. The model will be useful in serving as a framework for developing a mulrimedia CAI courseware for educators, instructional designers and CAI industry developers.
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