• The Korean Journal of Physiology and Pharmacology
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• v.6 no.6
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• pp.287-291
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• 2002

Intrinsic excitabilities of acutely isolated medial vestibular nucleus (MVN) neurons of rats with normal labyrinth and with undergoing vestibular compensation from 30 min to 24 h after unilateral vestibular deafferentation (UVD) were compared. In control rats, proportions of type A and B cells were 30 and 70%, respectively, however, the proportion of type A cells increased following UVD. Bursting discharge and irregular firing patterns were recorded from 2 to 12 h post UVD. The spontaneous discharge rate of neurons in the ipsilesional MVN increased significantly at 2 h post-UVD and remained high until 12 h post-UVD in both type A and type B cells. After-hyperpolarization (AHP) of the MVN neurons decreased significantly from 2 h post-UVD in both types of cells. These results suggest that the early stage of vestibular compensation after peripheral neurectomy is associated with an increase in intrinsic excitability due to reduction of AHP in MVN neurons.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.3
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• pp.169-175
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• 2000

To learn the developmental changes in intrinsic electrophysiological properties of the second order taste neurons, whole cell recordings from the developing nucleus of the solitary tract neurons were done in brainstem slices of postnatal rats. Rats aged from postnatal 0 to 21 days (P0-P21) were used, being divided into 3 age groups: postnatal first week (P0-P7 days), second week (P8-P14 days), and third week (P15-P21 days). Slices containing gustatory NTS were cut horizontally in the thickness of $300\;{\mu}m.$ Whole cell recordings were obtained from neurons in response to a series of hyperpolarizing and depolarizing current pulses. The intrinsic electrophysiological properties of the rostral NTS (rNTS) neurons were compared among the age groups. Depolarizing current pulses evoked a train of action potentials in all neurons of all age groups. The resting membrane potential and input resistance of the neurons did not show any significant differences during the postnatal 3 weeks. The time constant, however, decreased during the development. Duration of action potential measured at half maximum amplitude was longer in younger age groups. Both the maximum rate of rise and the maximum rate of fall in the action potential increased during the first 3 weeks postnatal. Electrophysiologically more than half neurons were type III. In summary, it is suggested that developmental changes in electrophysiological properties in rNTS occur during the first three weeks in rats.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.3
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• pp.169-174
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• 2003

${\gamma}$-Aminobutyric acid (GABA) has been reported to enhance exocrine secretion evoked not only by secretagogues but also by intrinsic neuronal excitation in the pancreas. The pancreas contains cholinergic neurons abundantly that exert a stimulatory role in exocrine secretion. This study was undertaken to examine effects of GABA on an action of cholinergic neurons in exocrine secretion of the pancreas. Intrinsic neurons were excited by electrical field stimulation (EFS; 15 V, 2 msec, 8 Hz, 45 min) in the isolated, perfused rat pancreas. Tetrodotoxin or atropine was used to block neuronal or cholinergic action. Acetylcholine was infused to mimic cholinergic excitation. GABA $(30{\mu}M)$ and muscimol $(10{\mu}M)$, given intra-arterially, did not change spontaneous secretion but enhanced cholecystokinin (CCK; 10 pM)-induced secretions of fluid and amylase. GABA (3, 10, $30{\mu}M$) further elevated EFS-evoked secretions of fluid and amylase dose-dependently. GABA (10, 30, $100{\mu}M$) also further increased acetylcholine $(5{\mu}M)$-induced secretions of fluid and amylase in a dose-dependent manner. Bicuculline $(10{\mu}M)$ effectively blocked the enhancing effects of GABA $(30{\mu}M)$ on the pancreatic secretions evoked by either EFS or CCK. Both atropine $(2{\mu}M)$ and tetrodotoxin $(1{\mu}M)$ markedly reduced the GABA $(10{\mu}M)$-enhanced EFS- or CCK-induced pancreatic secretions. The results indicate that GABA enhances intrinsic cholinergic neuronal action on exocrine secretion via the $GABA_A$ receptors in the rat pancreas.

• BMB Reports
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• v.42 no.5
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• pp.245-259
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• 2009

The process by which adult neural stem cells generate new and functionally integrated neurons in the adult mammalian brain has been intensely studied, but much more remains to be discovered. It is known that neural progenitors progress through distinct stages to become mature neurons, and this progression is tightly controlled by cell-cell interactions and signals in the neurogenic niche. However, less is known about the cell-intrinsic signaling required for proper progression through stages of adult neurogenesis. Techniques have recently been developed to manipulate genes specifically in adult neural stem cells and progenitors in vivo, such as the use of inducible transgenic mice and viral-mediated gene transduction. A critical mass of publications utilizing these techniques has been reached, making it timely to review which molecules are now known to play a cell-intrinsic role in regulating adult neurogenesis in vivo. By drawing attention to these isolated molecules (e.g. Notch), we hope to stimulate a broad effort to understand the complex and compelling cascades of intrinsic signaling molecules important to adult neurogenesis. Understanding this process opens the possibility of understanding brain functions subserved by neurogenesis, such as memory, and also of harnessing neural stem cells for repair of the diseased and injured brain.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.1
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• pp.1-8
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• 2000

To investigate the contributions of intrinsic membrane properties to the spontaneous activity of medial vestibular nucleus (MVN) neurons, we assessed the effects of blocking large and small calcium-activated potassium channels by means of patch clamp recordings. Almost all the MVN neurons recorded in neonatal $(P13{\sim}P17)$ rat were shown to have either a single deep after-hyperpolarization (AHP; type A cells), or an early fast and a delayed slow AHP (type B cells). Among the recorded MVN cells, immature action potential shapes were found. Immature type A cell showed single uniform AHP and immature B cell showed a lack of the early fast AHP, and the delayed AHP was separated from the repolarization phase of the spike by a period of isopotentiality. Application of apamin and charybdotoxin (CTX), which selectively block the small and large calcium-activated potassium channels, respectively, resulted in significant changes in spontaneous firings. In both type A and type B cells, CTX (20 nM) resulted in a significant increase in spike frequency but did not induce bursting activity. By contrast, apamin (300 nM) selectively abolished the delayed slow AHP and induced bursting activity in type B cells. Apamin had no effect on the spike frequency of type A cells. These data suggest that there are differential roles of apamin and CTX sensitive potassium conductances in spontaneous firing patterns of MVN neurons, and these conductances are important in regulating the intrinsic rhythmicity and excitability.

• The Korean Journal of Zoology
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• v.38 no.1
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• pp.66-73
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• 1995

Putative gamma aminobu%sic acid (GABA)-ersic elements in the basilar pontine nuclei were examined in the dos using an antiserum against GABA-glutaraldehvde-protein conjusBtes and the peroxidase-antiperoxidase method. GABA-immunoreactive neuronal somata in the basilar Pons exhibited various morphology with the majority being spindle-shaped or multipolar, while some were spheroidal. The size of GABA-orgic neuronal somata was relatively small (approximately $10-20\mum)$ in diameter. GABA-immunoreactive neurons were scattered throughout the pontine nuclei, but the midline region of the medial nucleus at the rostral pons, the lateral nucleus at mid-pontine levels, and the ventral nucleus at the caudal pons exhibited a relatively greater concentration of cell bodies. A sparse number of GABA-ergic neurons were observed within the cerebral peduncle and along the ventral borders of the basilar pons adjacent to the middle cerebellar peduncle at the rostrocaudal levels of the pontine nuclei. These obsenrations provide anatomic evidence of how this inhibitory neural element performs its function in the cortico-prontocerbellar circuitry.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.27 no.2
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• pp.73-77
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• 2016

Laryngopharyngeal reflux disease (LPRD) is different with gastroesophageal reflux disease (GERD). The lower esophageal sphincter (LES) possesses an intrinsic nervous plexus that allows the LES to have a considerable degree of independent neural control. Sympathetic control of the LES and stomach stems from cholinergic preganglionic neurons in the intermediolateral column of the thoracic spinal cord (T6 through T9 divisions), which impinge on postganglionic neurons in the celiac ganglion, of which the catecholaminergic neurons provide the LES and stomach with most of its sympathetic supply. Sympathetic regulation of motility primarily involves inhibitory presynaptic modulation of vagal cholinergic input to postganglionic neurons in the enteric plexus. The magnitude of sympathetic inhibition of motility is directly proportional to the level of background vagal efferent input. Recognizing that the LES is under the dual control of the sympathetic and parasympathetic nervous systems, we refer the reader to other comprehensive reviews on the role of the sympathetic and parasympatetic control of LES and gastric function. The present review focuses on the functionally dominant parasympathetic control of the LES and stomach via the dorsal motor nucleus of the vagus.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.355-366
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• 1997

Although cerebellar Purkinje cells display spontaneous electrical activity in vivo and in slice experiments, the mechanism of the spontaneous activity generation has not been clearly understood. The aim of this study was to investigate whether cerebellar Purkinje cells of postnatal rats generate spontaneous electrical activity without synaptic inputs. Dissociated cerebellar Purkinje cells were used for reducing synaptic inputs in the present study. Cerebellar Purkinje cells with dendrites were dissociated from postnatal rats using enzymatic treatment followed by mechanical trituration. Spontaneous electrical activities were recorded from dissociated cells without any stimulus using whole-cell patch clamp configuration. Two types, spontaneously firing or quiescent, of dissociated Purkinje cells were observed in postnatal rats. Both types of cells were identified as Purkinje cells using immunocytochemical staining technique with anti-calbindin after recording. Spontaneously active cells displayed two patterns of firing, repetitive and burst firings. Two thirds of dissociated Purkinje cells displayed repetitive firing and the rest of them did burst firing under same recording condition. Repetitive firing activities were maintained even after further isolation using either physical or pharmacological techniques. Neither high magnessium solution nor excitatory synaptic blockers, AP-5 and DNQX, block the spontaneous activity. These results demonstrate that spontaneous electrical activity of isolated cerebellar Purkinje cells in postnatal rats is generated by intrinsic membrane properties rather than synaptic inputs.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.2
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• pp.135-141
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• 2014

The downregulation of A-type $K^+$ channels ($I_A$ channels) accompanying enhanced somatic excitability can mediate epileptogenic conditions in mammalian central nervous system. As $I_A$ channels are dominantly targeted by dendritic and postsynaptic processings during synaptic plasticity, it is presumable that they may act as cellular linkers between synaptic responses and somatic processings under various excitable conditions. In the present study, we electrophysiologically tested if the downregulation of somatic $I_A$ channels was sensitive to synaptic activities in young hippocampal neurons. In primarily cultured hippocampal neurons (DIV 6~9), the peak of $I_A$ recorded by a whole-cell patch was significantly reduced by high KCl or exogenous glutamate treatment to enhance synaptic activities. However, the pretreatment of MK801 to block synaptic NMDA receptors abolished the glutamate-induced reduction of the $I_A$ peak, indicating the necessity of synaptic activation for the reduction of somatic $I_A$. This was again confirmed by glycine treatment, showing a significant reduction of the somatic $I_A$ peak. Additionally, the gating property of $I_A$ channels was also sensitive to the activation of synaptic NMDA receptors, showing the hyperpolarizing shift in inactivation kinetics. These results suggest that synaptic LTP possibly potentiates somatic excitability via downregulating $I_A$ channels in expression and gating kinetics. The consequential changes of somatic excitability following the activity-dependent modulation of synaptic responses may be a series of processings for neuronal functions to determine outputs in memory mechanisms or pathogenic conditions.

• Molecules and Cells
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• v.45 no.11
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• pp.855-867
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• 2022

For proper function of proteins, their subcellular localization needs to be monitored and regulated in response to the changes in cellular demands. In this regard, dysregulation in the nucleocytoplasmic transport (NCT) of proteins is closely associated with the pathogenesis of various neurodegenerative diseases. However, it remains unclear whether there exists an intrinsic regulatory pathway(s) that controls NCT of proteins either in a commonly shared manner or in a target-selectively different manner. To dissect between these possibilities, in the current study, we investigated the molecular mechanism regulating NCT of truncated ataxin-3 (ATXN3) proteins of which genetic mutation leads to a type of polyglutamine (polyQ) diseases, in comparison with that of TDP-43. In Drosophila dendritic arborization (da) neurons, we observed dynamic changes in the subcellular localization of truncated ATXN3 proteins between the nucleus and the cytosol during development. Moreover, ectopic neuronal toxicity was induced by truncated ATXN3 proteins upon their nuclear accumulation. Consistent with a previous study showing intracellular calcium-dependent NCT of TDP-43, NCT of ATXN3 was also regulated by intracellular calcium level and involves Importin α3 (Imp α3). Interestingly, NCT of ATXN3, but not TDP-43, was primarily mediated by CBP. We further showed that acetyltransferase activity of CBP is important for NCT of ATXN3, which may acetylate Imp α3 to regulate NCT of ATXN3. These findings demonstrate that CBP-dependent acetylation of Imp α3 is crucial for intracellular calcium-dependent NCT of ATXN3 proteins, different from that of TDP-43, in Drosophila neurons.