• Electronics and Telecommunications Trends
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• v.33 no.6
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• pp.69-80
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• 2018

Sensory devices have been developed to help people with disabled or weakened sensory functions. Such devices play a role in collecting and transferring data for the five senses (vision, sound, smell, taste, and tactility) and also stimulating nerves. To provide brain or prosthesis devices with more sophisticated senses, hyper sensory devices with a high resolution comparable to or even better than the human system based on individual neuron cells are essential. As for data collecting components, technologies for sensors with higher resolution and sensitivity, and the conversion of algorithms from physical sensing data to human neuron signals, are needed. Converted data can be transferred to neurons that are responsible for human senses through communication with high security, and neural interfaces with high resolution. When communication deals with human data, security is the most important consideration, and intra-body communication is expected to be a candidate with high priority. To generate sophisticated human senses by modulating neurons, neural interfaces should modulate individual neurons, and therefore a high resolution compared to human neurons (~ several tens of um) with a large area covering neuron cells for human senses (~ several tens of mm) should be developed. The technological challenges for developing sensory devices with human and even beyond-human capabilities have been tackled by various research groups, the details of which are described in this paper.

• Anatomy and Cell Biology
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• v.51 no.4
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• pp.266-273
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• 2018

The ganglion cardiacum or juxtaductal body is situated along the left recurrent laryngeal nerve in the aortic window and is an extremely large component of the cardiac nerve plexus. This study was performed to describe the morphologies of the ganglion cardiacum or juxtaductal body in human fetuses and to compare characteristics with intracardiac ganglion. Ganglia were immunostained in specimens from five fetuses of gestational age 12-16 weeks and seven fetuses of gestational age 28-34 weeks. Many ganglion cells in the ganglia were positive for tyrosine hydroxylase (TH; sympathetic nerve marker) and chromogranin A, while a few neurons were positive for neuronal nitric oxide synthase (NOS; parasympathetic nerve marker) or calretinin. Another ganglion at the base of the ascending aorta carried almost the same neuronal populations, whereas a ganglion along the left common cardinal vein contained neurons positive for chromogranin A and NOS but no or few TH-positive neurons, suggesting a site-dependent difference in composite neurons. Mixtures of sympathetic and parasympathetic neurons within a single ganglion are consistent with the morphology of the cranial base and pelvic ganglia. Most of the intracardiac neurons are likely to have a non-adrenergic non-cholinergic phenotype, whereas fewer neurons have a dual cholinergic/noradrenergic phenotype. However, there was no evidence showing that chromogranin A- and/or calretinin-positive cardiac neurons corresponded to these specific phenotypes. The present study suggested that the ganglion cardiacum was composed of a mixture of sympathetic and parasympathetic neurons, which were characterized the site-dependent differences in and near the heart.

• Journal of Integrative Natural Science
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• v.6 no.3
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• pp.143-150
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• 2013

Prevailing role of intracellular amyloid ${\beta}$ ($iA{\beta}$) in Alzheimer's disease (AD) initiation and progression attracts more and more attention in recent years. To address whether $iA{\beta}$ induces early alterations of electrophysiological properties in cultured human primary neurons, we delivered $iA{\beta}$ with adenovirus and measured the electrophysiological properties of infected neurons with whole-cell recordings. Our results show that $iA{\beta}$ induces an increase in neuronal resting membrane potentials, a decrease in $K^+$ currents and a hyperpolarizing shift in voltage-dependent activation of $K^+$ currents. These results suggest the electrophysiological impairments induced by $iA{\beta}$ may be responsible for its neuronal toxicity.

• Development and Reproduction
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• v.14 no.3
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• pp.171-177
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• 2010

A recent report demonstrated that in human aging brain after menopause/andropause luteinizing hormone (LH) is localized in the cytoplasm of pyramidal neurons of hippocampus and a significant increase of LH is also detected in the cytoplasm of pyramidal neurons and neurofibrillary tangles of Alzheimer's disease brain compared to age-matched control brain. It was suggested that the decreased steroid hormone production and the resulting LH expression in the neurons vulnerable to Alzheimer's disease pathology may have some relevance to the development of Alzheimer's disease. It is, however, unclear whether the presence of LH in neurons of human aging and Alzheimer's disease brain is due to intracellular LH expression or to LH uptake from extracellular sources, since gonadotropins are known to cross the blood brain barrier. Moreover, there is no report by using the brain of experimental animal that LH is expressed in such neurons as found in the human brain. In the present study, we found that LH immunoreactivity is localized in the pyramidal neurons of cerebral cortex and hippocampus of 12 and 18 months old rats but can not detect any immunoreactivity for LH in the young adult (3-5 months old) rats. To confirm that these LH immunoreactivity results from de novo synthesis in the brain but not the uptake from extracellular space, we performed RT-PCR and found that mRNA for LH is detected in several regions of brain including cerebral cortex and hippocampus. These findings suggest us that LH expression in old rat brain may play an important role in aging process of rat brain.

• Clinical and Experimental Pediatrics
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• v.53 no.9
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• pp.845-851
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• 2010

Purpose: Recombinant human growth hormone (rhGH) has been widely used to treat short stature. However, there are some concerns that growth hormone treatment may induce skeletal maturation and early onset of puberty. In this study, we investigated whether rhGH can directly affect the neuronal activities of of gonadotropin-releasing hormone (GnRH). Methods: We performed brain slice gramicidin-perforated current clamp recording to examine the direct membrane effects of rhGH on GnRH neurons, and a whole-cell voltage-clamp recording to examine the effects of rhGH on spontaneous postsynaptic events and holding currents in immature (postnatal days 13-21) and adult (postnatal days 42-73) mice. Results: In immature mice, all 5 GnRH neurons recorded in gramicidin-perforated current clamp mode showed no membrane potential changes on application of rhGH (0.4, $1{\mu}g/mL$). In adult GnRH neurons, 7 (78%) of 9 neurons tested showed no response to rhGH ($0.2-1{\mu}g/mL$) and 2 neurons showed slight depolarization. In 9 (90%) of 10 immature neurons tested, rhGH did not induce any membrane holding current changes or spontaneous postsynaptic currents (sPSCs). There was no change in sPSCs and holding current in 4 of 5 adult GnRH neurons. Conclusion: These findings demonstrate that rhGH does not directly affect the GnRH neuronal activities in our experimental model.

• Molecules and Cells
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• v.45 no.4
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• pp.169-176
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• 2022

A primary cilium, a hair-like protrusion of the plasma membrane, is a pivotal organelle for sensing external environmental signals and transducing intracellular signaling. An interesting linkage between cilia and obesity has been revealed by studies of the human genetic ciliopathies Bardet-Biedl syndrome and Alström syndrome, in which obesity is a principal manifestation. Mouse models of cell type-specific cilia dysgenesis have subsequently demonstrated that ciliary defects restricted to specific hypothalamic neurons are sufficient to induce obesity and hyperphagia. A potential mechanism underlying hypothalamic neuron cilia-related obesity is impaired ciliary localization of G protein-coupled receptors involved in the regulation of appetite and energy metabolism. A well-studied example of this is melanocortin 4 receptor (MC4R), mutations in which are the most common cause of human monogenic obesity. In the paraventricular hypothalamus neurons, a blockade of ciliary trafficking of MC4R as well as its downstream ciliary signaling leads to hyperphagia and weight gain. Another potential mechanism is reduced leptin signaling in hypothalamic neurons with defective cilia. Leptin receptors traffic to the periciliary area upon leptin stimulation. Moreover, defects in cilia formation hamper leptin signaling and actions in both developing and differentiated hypothalamic neurons. The list of obesity-linked ciliary proteins is expending and this supports a tight association between cilia and obesity. This article provides a brief review on the mechanism of how ciliary defects in hypothalamic neurons facilitate obesity.

• Toxicological Research
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• v.17
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• pp.11-16
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• 2001

The development of the central nervous system is a continuous process during the embryonic and fetal periods. For a better understanding of congenital anomalies of central nervous system, three major events of normal development, i.e., neurulation (3 to 4 weeks), brain vesicle formation (4 to 7 weeks) and mantle formation (over 8 weeks) should be kept in mind. The first category of anomalies is neural tube defect. Neural tube defects encompass all the anomalies arise in completion of neurulation. The second category of central nervous system anomalies is disorders of brain vesicle formation. This is anomaly that applies for "the face predicts the brain". Holoprosencephaly covers a spectrum of anomalies of intracranial and midfacial development which result from incomplete development and septation of midline structures within the forebrain or prosencephalon. The last category of central nervous system malformation is disorders involving the process of mantle formation. In the human, neurons are generated in two bursts, the first from 8 to 10 weeks and next from 12 to 14 weeks. By 16 weeks, most of the neurons have been generated and have started their migration into the cortex. Mechanism of migration disorders are multifactorial. Abnormal migration into the cortex, abnormal neurons, faulty neural growth within the cortex, unstable pial-glial border, degeneration of neurons, neural death by exogenous factors are some of the proposed mechanism. Agyria-pachygyria are characterized by a four-layerd cortex. Polymicrogyria is gyri that are too numerous and too small, and is morphologically heterogeneous. Cortical dysplasia is characterized by the presence Q[ abnormal neurons and glia arranged abnormally in focal areas of the cerebral cortex. Neuroglial malformative lesions associated with medically intractable epilepsy are hamartia or hamartoma, focal cortical dysplasia and microdysgenesis.ysgenesis.

• Korean Journal of Acupuncture
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• v.32 no.3
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• pp.136-143
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• 2015

This study was performed to comparative investigate the distribution of primary sensory and motor neurons associated with Cheonji(PC1) acupoint by using neural tracing technique. A total 4 SD rats were used in the present study. After anesthesia, the rats received microinjection of $6{\mu}l$ of cholera toxin B subunit(CTB) into the corresponding sites of the acupoints Cheonji(PC1) in the human body for observing the distribution of the related primary sensory neurons in dorsal root ganglia(DRGs) and motor neurons in the spinal cord(C3~T4) and sympathetic ganglia. Three days after the microinjection, the rats were anesthetized and transcardially perfused saline and 4% paraformaldehyde, followed by routine section of the DRGs, sympathetic chain ganglia(SCGs) and spinal cord. Labeled neurons and nerve fibers were detected by immunohistochemical method and observed by light microscope equipped with a digital camera. The labeled neurons were recorded and counted. From this research, the distribution of primary sensory and motor neurons associated with Cheonji(PC1) acupoints were concluded as follows. Muscle meridian related Cheonji(PC1) are controlled by spinal segments of C5~T1, C6~T4, respectively.

• Biomolecules & Therapeutics
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• v.31 no.3
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• pp.264-275
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• 2023

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by tremors, bradykinesia, and rigidity. PD is caused by loss of dopaminergic (DA) neurons in the midbrain substantia nigra (SN) and therefore, replenishment of DA neurons via stem cell-based therapy is a potential treatment option. Astrocytes are the most abundant non-neuronal cells in the central nervous system and are promising candidates for reprogramming into neuronal cells because they share a common origin with neurons. The ability of neural progenitor cells (NPCs) to proliferate and differentiate may overcome the limitations of the reduced viability and function of transplanted cells after cell replacement therapy. Achaete-scute complex homolog-like 1 (Ascl1) is a well-known neuronal-specific factor that induces various cell types such as human and mouse astrocytes and fibroblasts to differentiate into neurons. Nurr1 is involved in the differentiation and maintenance of DA neurons, and decreased Nurr1 expression is known to be a major risk factor for PD. Previous studies have shown that direct conversion of astrocytes into DA neurons and NPCs can be induced by overexpression of Ascl1 and Nurr1 and additional transcription factors genes such as superoxide dismutase 1 and SRY-box 2. Here, we demonstrate that astrocytes isolated from the ventral midbrain, the origin of SN DA neurons, can be effectively converted into DA neurons and NPCs with enhanced viability. In addition, when these NPCs are inducted to differentiate, they exhibit key characteristics of DA neurons. Thus, direct conversion of midbrain astrocytes is a possible cell therapy strategy to treat neurodegenerative diseases.

• The Journal of the Korea institute of electronic communication sciences
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• v.19 no.3
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• pp.583-588
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• 2024

With the emergence of Brain-Computer Interface (BCI) technology, analyzing mirror neurons has become more feasible. However, evaluating the accuracy of BCI systems that rely on human thoughts poses challenges due to their qualitative nature. To harness the potential of BCI, we propose a new approach to measure accuracy based on the characteristics of mirror neurons in the human brain that are influenced by speech speed, depending on the ultimate goal of movement. In Chapter 2 of this paper, we introduce mirror neurons and provide an explanation of human posture estimation for mirror neurons. In Chapter 3, we present a powerful pose estimation method suitable for real-time dynamic environments using the technique of human posture estimation. Furthermore, we propose a method to analyze the accuracy of BCI using this robotic environment.