The aim of this study was to evaluate the effects of propofol on cortical electroencephalogram (EEG) in seven dogs. Propofol infusion was accomplished from low concentration to high concentration in series, and each concentration was infused for 20 minutes (M0: 0, M0.5: 0.5, M1.0:1.0, and M1.5: 1.5 mg/kg/min of infusion rate). EEG was recorded via needle electrode placed at Cz, which was applied to International 10-20 system. Arterial blood pressure. blood gas analysis and ECG were also measured. Hoemodynamics, Pa$CO_2$, PaO$_2$, heart rate and respiratory rate were variable, but were net significant(p>0.05). The power spectra of EEG in every concentration was compared wish those of control (MO). The powers at a1l frequencies at M1.0 and Ml.5 were decreased. Especially, the powers of the frequencies over 20 Hz were significantly decreased (p<0.O5). Powers at frequencies between 8 and 15Hz at MO.S were significantly increased (p<0.05) in response to the painful stimuli. It was inferred that they may reflect activity of the brain which is consciously processing the external Stimuli. Like the Power spectra, al1 the band powers of He EEG ($\delta$ 1-4, $\theta$4-8, $\alpha$ 8-13, $\beta$L13-21. $\beta$H 21-30, \ulcorner 30-50, and total 1-5OHz) were decreased in proportion to the increase of infusion rate at M1 .0 and M1.5. Especially, decrease of $\beta$H and ${\gamma}$ were significant(p<0.01). At M0.5, $\alpha$ band was significantly increased(p<0.05) among all the bands. Seizure activities which were concide with occurrence of spike wave were shown in all dogs at Ml .0 and M1.5.
Objectives ; This study was undertaken to determine if Salviae Radix herb-acupuncture (SRA) exerts protective effect against alterations in membrane transport function in rabbits with mercury chloride (Hg)-induced acute renal failure. Methods and Results ; The administration of Hg at a subcutaneous single dose of 10mg/kg caused a reduction in GFR to 9.4% of the basal value and an increase in fractional Na+ excretion to 10-fold, indicating generation of acute renal failure. When animals were acupunctured with $0.5m{\ell}$ of SRA extract (0.1%) in both sides of Shinsu(BL23) for 7 days prod to Hg administration, such changes were significantly attenuated. The fractional excretion of glucose and phosphate was increased to approximately 132-fold and 7-fold, respectively, in rabbits treated with Hg alone, but the fractional excretion of glucose was increased to 26-fold and that of phosphate was not different from the basal value in SRA-pretreated rabbits. Uptakes of glucose and phosphate in purified isolated brush-border membrane and $Na^+-K^+$-ATPase activity in microsomal fraction were inhibited in rabbits treated with Hg alone, suggesting that impairment in proximal reabsorption of glucose and phosphate is resulted from a direct damage of membrane transport carriers and disruption of the normal $Na^+$ gradient. Conclusions ; Such changes were prevented by SRA. Uptakes of organic ions, PAH and TEA, in renal cortical slices were inhibited by the administration of Hg, which was prevented by SRA. Pretreatment of an antioxidant DPPD attenuated the increase in the fractional excretion of glucose and phosphate induced by the administration of Hg.
Transcranial direct current stimulation (tDCS) is a neuromodulatory technique that delivers low-intensity direct current to cortical areas, thereby facilitating or inhibiting spontaneous neuronal activity. This study was designed to investigate changes in various sensory functions after tDCS. We conducted a single-center, single-blinded, randomized trial to determine the effect of a single session of tDCS with the current perception threshold (CPT) in 50 healthy volunteers. Nerve conduction studies were performed in relation to the median sensory and motor nerves on the dominant hand to discriminate peripheral nerve lesions. The subjects received anodal tDCS with 1 mA for 15 minutes under two different conditions, with 25 subjects in each groups: the conditions were as follows tDCS on the primary motor cortex (M1) and sham tDCS on M1. We recorded the parameters of the CPT a with Neurometer$^{(R)}$ at frequencies of 2000, 250, and 5 Hz in the dominant index finger to assess the tactile sense, fast pain and slow pain, respectively. In the test to measure CPT values of the M1 in the tDCS group, the values of the distal part of the distal interphalangeal joint of the second finger statistically increased in all of 2000 Hz (p=.000), 250 Hz (p=.002), and 5 Hz (p=.008). However, the values of the sham tDCS group decreased in all of 2000 Hz (p=.285), 250 Hz (p=.552), and 5 Hz (p=.062), and were not statistically significant. These results show that M1 anodal tDCS can modulate sensory perception and pain thresholds in healthy adult volunteers. The study suggests that tDCS may be a useful strategy for treating central neurogenic pain in rehabilitation medicine.
Journal of rehabilitation welfare engineering & assistive technology
/
v.7
no.1
/
pp.45-50
/
2013
Recently, a method for detecting animal tinnitus objectively, gap prepulse inhibition of acoustic startling (GPIAS) were reported. However, the GPIAS method is difficult to be directly applied to human tinnitus research because measuring repeatedly startling responses evoked by more than 110 dB SPL acoustic stimuli for human is not easy. In this paper, the auditory late latency response (ALLR) measurement system which can measure conveniently evoked potentials involving the information about the brain cortical activity related with auditory psychologic phenomena such as a tinnitus has been implemented. By using the implemented system, 8 persons with normal hearing sense have been experimented to measure N1-P2 amplitudes of ALLRs evoked by gap prepulse based acoustic stimuli. Through the experimental results, the prepulse inhibitions of all the participants' N1-P2 responses have been observed and their characteristics were evaluated. And it is verified that our implemented system can be utilized as a device for researching and evaluating the objective tinnitus detection method in the future study.
Lee, Myungook;Ahn, Jong Il;Lee, Ah Ran;Ko, Dong Woo;Yang, Woo Sub;Lee, Gene;Ahn, Ji Yeon;Lim, Jeong Mook
Molecules and Cells
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v.40
no.8
/
pp.558-566
/
2017
Regular monitoring on experimental animal management found the fluctuation of ART outcome, which showed a necessity to explore whether superovulation treatment is responsible for such unexpected outcome. This study was subsequently conducted to examine whether superovulation treatment can preserve ultrastructural integrity and developmental competence of oocytes following oocyte activation and embryo culture. A randomized study using mouse model was designed and in vitro development (experiment 1), ultrastructural morphology (experiment 2) and functional integrity of the oocytes (experiment 3) retrieved after PMSG/hCG injection (superovulation group) or not (natural ovulation; control group) were evaluated. In experiment 1, more oocytes were retrieved following superovulation than following natural ovulation, but natural ovulation yielded higher (p < 0.0563) maturation rate than superovulation. The capacity of mature oocytes to form pronucleus and to develop into blastocysts in vitro was similar. In experiment 2, a notable (p < 0.0186) increase in mitochondrial deformity, characterized by the formation of vacuolated mitochondria, was detected in the superovulation group. Multivesicular body formation was also increased, whereas early endosome formation was significantly decreased. No obvious changes in other microorganelles, however, were detected, which included the formation and distribution of mitochondria, cortical granules, microvilli, and smooth and rough endoplasmic reticulum. In experiment 3, significant decreases in mitochondrial activity, ATP production and dextran uptake were detected in the superovulation group. In conclusion, superovulation treatment may change both maturational status and functional and ultrastuctural integrity of oocytes. Superovulation effect on preimplantation development can be discussed.
Kim, Byung-Kon;Choi, In-Sun;Cho, Jin-Hwa;Jang, Il-Sung;Lee, Maan-Gee;Choi, Byung-Ju
The Korean Journal of Physiology and Pharmacology
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v.10
no.5
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pp.235-242
/
2006
Cortical malformation-associated epileptic seizures are resistant to conventional anticonvulsant drugs. Relatively little research has been conducted on the effects of antiepileptic drugs (AEDs) on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate (MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of ethosuximide (ETX) in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed and age-matched vehicle-injected control animals. Field potential recordings were used to monitor the amplitude and number of population spikes, and paired pulse inhibition in response to stimulation of the commissural pathway. Pharmaco-resistance was tested by measuring seizure latencies after pilocarpine administration (320 mg/kg, Lp.) with and without pre-treatment with ETX. Pre-treatment with 300 mg of ETX significantly prolonged the latency to the status epilepticus (SE) in both control and MAM-treated groups. Pre-treatment with ETX 100mg and ETX 200 mg had little effect in MAMexposed rats. However, ETX 200 mg prolonged the latency to the SE in control groups. Spontaneous field potential and secondary after-discharges were higher for MAM-treated rat in comparison with control rats injects with ETX. The main findings of this study are that acute seizures initiated in MAM-exposed rats are relatively resistant to standard ETX assessed in vivo. These data suggest that ETX do not prolong seizure latencies in MAM-rats exposed to pilocarpine.
Kim, Moo-Seong;Kim, Kyoung-Ryong;Ahn, Do-Whan;Park, Yang-Saeng
The Korean Journal of Physiology and Pharmacology
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v.4
no.1
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pp.63-72
/
2000
Chronic exposure to cadmium (Cd) results in an inhibition of protein endocytosis in the renal proximal tubule, leading to proteinuria. In order to gain insight into the mechanism by which Cd impairs the protein endocytosis, we investigated the effect of Cd on the acidification of renal cortical endocytotic vesicles (endosomes). The endosomal acidification was assessed by measuring the pH gradient-dependent fluorescence change, using acridine orange or FITC-dextran as a probe. In renal endosomes isolated from Cd-intoxicated rats, the $V_{max}$ of ATP-driven fluorescence quenching ($H^+-ATPase$ dependent intravesicular acidification) was significantly attenuated with no substantial changes in the apparent $K_m,$ indicating that the capacity of acidification was reduced. When endosomes from normal animals were directly exposed to free Cd in vitro, the $V_{max}$ was slightly reduced, whereas the $K_m$ was markedly increased, implying that the biochemical property of the $H^+-ATPase$ was altered by Cd. In endosomes exposed to free Cd in vitro, the rate of dissipation of the transmembrane pH gradient after $H^+-ATPase$ inhibition appeared to be significantly faster compared to that in normal endosomes, indicating that the $H^+-conductance$ of the membrane was increased by Cd. These results suggest that in long-term Cd-exposed animals, free Cd ions liberated in the proximal tubular cytoplasm by lysosomal degradation of cadmium-metallothionein complex (CdMT) may impair endosomal acidification 1) by reducing the $H^+-ATPase$ density in the endosomal membrane, 2) by suppressing the intrinsic $H^+-ATPase$ activity, and 3) possibly by increasing the membrane conductance to $H^+$ ion. Such effects of Cd could be responsible for the alterations of proximal tubular endocytotic activities, protein reabsorption and various transporter distributions observed in Cd-exposed cells and animals.
Glutamate toxicity-mediated mitochondrial dysfunction and neuronal cell death are involved in the pathogenesis of several neurodegenerative diseases as well as acute brain ischemia/stroke. In this study, we investigated the neuroprotective mechanism of dieckol (DEK), one of the phlorotannins isolated from the marine brown alga Ecklonia cava, against glutamate toxicity. Primary cortical neurons ($100{\mu}M$, 24 h) and HT22 neurons (5 mM, 12 h) were stimulated with glutamate to induce glutamate toxic condition. The results demonstrated that DEK treatment significantly increased cell viability in a dose-dependent manner ($1-50{\mu}M$) and recovered morphological deterioration in glutamate-stimulated neurons. In addition, DEK strongly attenuated intracellular reactive oxygen species (ROS) levels, mitochondrial overload of $Ca^{2+}$ and ROS, mitochondrial membrane potential (${\Delta}{\Psi}_m$) disruption, adenine triphosphate depletion. DEK showed free radical scavenging activity in the cell-free system. Furthermore, DEK enhanced protein expression of heme oxygenase-1 (HO-1), an important anti-oxidant enzyme, via the nuclear translocation of nuclear factor-like 2 (Nrf2). Taken together, we conclude that DEK exerts neuroprotective activities against glutamate toxicity through its direct free radical scavenging property and the Nrf-2/HO-1 pathway activation.
Journal of The Korean Society of Integrative Medicine
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v.7
no.3
/
pp.171-180
/
2019
Purpose : The purpose of this study was to investigate the difference in motor cortical excitability during mental practice and action observation in subjects with forward head posture. Methods : This study was performed in two groups, a forward head posture group (n=17) and a normal posture group (n=17). Electroencephalography (EEG) was conducted to investigate cerebral cortex activity, and six electrodes were attached to Fp1, Fp2, C1, C2, C3, and C4 to measure the relative alpha power, relative beta power, relative gamma power, and mu rhythms. The subjects were requested to perform the four different conditions, which were eye opening, eye closing, mental practice, and action observation for 300 seconds. Results : The results showed that the relative alpha waves showed a significant difference between the normal and forward head posture groups in the C1, C2, C3, and C4 regions with the eyes open (p<.05). The relative beta waves also showed a significant difference between the two groups in the Fp1 and Fp2 regions during action observation (p<.05). The relative gamma waves were significantly different between the normal and forward head posture groups in the Fp1 and Fp2 regions during action observation (p<.05) in C1, C2, and C3 with eyes closed (p<.05) and in C1, C2, C3, and C4 with eyes open (p<.05). Conclusion : The results of this study showed that EEG change in the forward head posture group was different from that in the normal control group in action observation rather than in mental practice. Therefore, we are expected to provide a neurophysiological basis for applying action observation to motor skill learning during exercise for correcting forward head posture.
Minji Bang;Seung Jin Yang;TaeJin Ahn;Seol-Heui Han;Chan Young Shin;Kyoung Ja Kwon
Biomolecules & Therapeutics
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v.31
no.1
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pp.116-126
/
2023
Mainly due to the slanted focus on the mechanism and regulation of neuronal aging, research on astrocyte aging and its modulation during brain aging is scarce. In this study, we established aged astrocyte culture model by long-term culturing. Cellular senescence was confirmed through SA-β-gal staining as well as through the examination of morphological, molecular, and functional markers. RNA sequencing and functional analysis of astrocytes were performed to further investigate the detailed characteristics of the aged astrocyte model. Along with aged phenotypes, decreased astrocytic proliferation, migration, mitochondrial energetic function and support for neuronal survival and differentiation has been observed in aged astrocytes. In addition, increased expression of cytokines and chemokine-related factors including plasminogen activator inhibitor -1 (PAI-1) was observed in aged astrocytes. Using the RNA sequencing results, we searched potential drugs that can normalize the dysregulated gene expression pattern observed in long-term cultured aged astrocytes. Among several candidates, minoxidil, a pyrimidine-derived anti-hypertensive and anti-pattern hair loss drug, normalized the increased number of SA-β-gal positive cells and nuclear size in aged astrocytes. In addition, minoxidil restored up-regulated activity of PAI-1 and increased mitochondrial superoxide production in aged astrocytes. We concluded that long term culture of astrocytes can be used as a reliable model for the study of astrocyte senescence and minoxidil can be a plausible candidate for the regulation of brain aging.
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