• Proceedings of the PSK Conference
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• 2003.10b
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• pp.188.2-188.2
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• 2003

Large-conductance $Ca^{2+}$ activated potassium channels $(BK_{ca})$ are widely distributed and play key roles in various cell functions. In nerve cells, B $K_{ca}$ channels shorten the duration of action potentials and block $Ca^{2+}$ entry thereby repolarizing excitable cells after excitation. $(BK_{ca})$ channel opening has been postulated to confer neuroprotection during stroke and has attracted attention as a means for therapeutic intervention in asthma, hypertension, convulsion, and traumatic brain injury. (omitted)

• Applied Microscopy
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• v.38 no.4
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• pp.375-382
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• 2008

In order to investigate shape of synaptic vesicles of the tooth pulp afferent boutons and their presynaptic endings (p-endings), and the neuroactive substance of the p-endings in the trigeminal nucleus principalis, rat incisor tooth pulp afferents were labeled by the horseradish peroxidase (HRP) and quantitative ultrastructural analysis and postembedding immunogold labeling were performed. Labeled tooth pulp afferent boutons contained clear, spherical synaptic vesicles (diameter: $45{\sim}55\;nm$) and occasionally dense core vesicles(diameter: $80{\sim}120\;nm$). They formed symmetrical synapses with unlabeled axon terminals (p-endings) containing pleomorphic synaptic vesicles. The ratio of short to long diameter (form factor) of synaptic vesicles of pulp afferent boutons was 0.6 to 0.99, whereas that of p-endings was 0.25 to 0.99. In addition, most of the p-endings showed GABA-like immunoreactivity. These results indicate that the shape of synaptic vesicles is quite different between the tooth pulp afferent boutons and p-endings, and the p-endings may contain GABA as a neuroactive substance in the trigeminal nucleus principalis.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.71-78
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• 2001

The current understanding of the neurobiology of anxiety is generally based on experimental animal model, empirical effective psychopharmacological agents, chemical and naturalistic challenge paradigms, and psychoendocinological assessment. This article focuses on reviewing neuroanantomical, neuroendocinological and neurofunctional research of anxiety disorder. In the decade ahead, we anticipate that extension of current research and the new integrated approach promise novel insight into mechanism of anxiety.

• Journal of Korean Neuropsychiatric Association
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• v.57 no.3
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• pp.230-234
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• 2018

A large proportion of patients with schizophrenia show a poor response to first-line antipsychotic drugs, which is termed treatment-resistant schizophrenia. Previous studies found that a different neurobiology might underlie treatment-resistant schizophrenia, which necessitates the development of different therapeutic approaches for treating treatment-resistant schizophrenia. This study reviewed previous studies on the pathophysiology of treatment-resistant schizophrenia and the pharmacological intervention, and forthcoming investigations of treatment-resistant schizophrenia are suggested.

• Animal cells and systems
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• v.1 no.3
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• pp.497-505
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• 1997

Dopamine plays diverse roles in the fetal brain development and differentiation. However, the development of the dopaminergic neurons and its receptors has not been fully understood. In our studies, in situ hybridization and immunohistochemical methods were used to investigate the ontogeny of dopaminergic neurons and its receptor subtypes during the fetal development of the rat. In situ hybridization data showed that dopamine $D_1$ and $D_2$ receptor mRNAs were expressed in the ventricular and subventricular zones of ganglionic eminence, thalamus, hypothalamus, and cortical neuroepithelium on gestational day 13. Expression of dopamine $D_1$ and $D_2$ receptors during gestational days 17 and 19 reached the same or similar level of that in the adult brain. Expression of $D_1$ receptor mRNA preceded that of $D_2$ receptor mRNA in the early developmental stage, although this pattern was reversed with the sharp increase of $D_2$ receptor mRNA soon after. $D_2$ receptor mRNA was expressed in substantia nigra of mesencephalon of the fetal rat brain. However, $D_1$ receptor mRNA was not detected in substantia nigra. Our results indicate that dopamine might function in the fetal brain during the early gestational period.

• Anxiety and mood
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• v.3 no.2
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• pp.91-96
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• 2007

Panic disorder is a common psychiatric illness that causes considerable morbidity. However, the biological basis of panic disorder remains unclear. In this report, we present and summarize the current literature on functional neuroimaging studies related to the neurobiology of panic disorder. The findings were summarized and divided into six groups : (1) known brain structures related to anxiety, especially panic disorder ; (2) structural results ; (3) functional imaging studies at rest ; (4) functional imaging studies with challenge testing ; (5) neuroreceptor studies ; and (6) changes in the treatment of panic disorder. Based on the findings of these neuroimaging studies, it seems as though panic disorder involves the hippocampal and parahippocampal areas, including the amygdala, as well as some cortical regions, such as the temporal and prefrontal cortices. Panic disorder is known to be associated with an imbalance between the right and left hemispheres of the brain at rest or during panic attacks. During a panic attack, patients with panic disorder are likely to experience an increase in local activity in the cingulate, insula, midbrain, and so on. On the other hand, a widespread reduction in the cortical areas has also been reported in most provocation studies. Thus, panic disorder may be related to the excess activation of the fear networks in response to subtle environmental cues and insufficient inhibition from higher cortical control areas ; however ; further studies are recommended in order to fully understand the neurobiology of panic disorder.

• International Journal of Oral Biology
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• v.40 no.4
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• pp.175-182
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• 2015

Previous studies suggested that myelinated axons innervating rat molar pulps undergo morphological changes in their peripheral course. However, little information is available on the morphological feature of the parent axons at the site of origin. We therefore investigated the size of the myelinated parent axons and their morphological features at the proximal sensory root of the trigeminal ganglion by horseradish peroxidase (HRP) injection into rat upper molar pulps and subsequent light and electron microscopy. A total of 248 HRP-labeled myelinated axons investigated were highly variable in the size. Fiber area, fiber diameter, axon area (axoplasm area), axon diameter (axoplasm diameter), and myelin thickness were $11.32{\pm}8.36{\mu}m^2(0.80{\sim}53.17{\mu}m^2)$, $3.99{\pm}1.53{\mu}m(1.08{\sim}9.26{\mu}m)$, $8.70{\pm}6.30{\mu}m^2(0.70{\sim}41.83{\mu}m^2)$, $3.13{\pm}1.13{\mu}m(0.94{\sim}7.20{\mu}m)$ and $0.43{\pm}0.23{\mu}m(0.07{\sim}1.06{\mu}m)$, respectively. The g-ratio (axon diameter / fiber diameter) of the labeled axons was $0.79{\pm}0.05$ (0.61~0.91). Axon diameter was highly correlated with myelin thickness (correlation coefficients, r=0.83) but little correlated with g-ratio (r=-0.33) of individual myelinated parent axons. These results indicate that myelin thickness of the myelinated parent axons innervating rat molar pulps increase with increasing axon diameter, thus maintaining a constant g-ratio.

• International Journal of Oral Biology
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• v.36 no.2
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• pp.83-89
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• 2011

Substantia gelatinosa (SG) neurons receive synaptic inputs from primary afferent $A{\delta}$- and C-fibers, where nociceptive information is integrated and modulated by numerous neurotransmitters or neuromodulators. A number of studies were dedicated to the molecular mechanism underlying the modulation of excitability or synaptic plasticity in SG neurons and revealed that second messengers, such as cAMP and cGMP, play an important role. Recently, cAMP and cGMP were shown to downregulate each other in heart muscle cells. However, involvement of the crosstalk between cAMP and cGMP in neurons is yet to be addressed. Therefore, we investigated whether interaction between cAMP and cGMP modulates synaptic plasticity in SG neurons using slice patchclamp recording from rats. Synaptic activity was measured by excitatory post-synaptic currents (EPSCs) elicited by stimulation onto dorsal root entry zone. Application of 1 mM of 8-bromoadenosine 3,5-cyclic monophosphate (8-Br-cAMP) or 8-bromoguanosine 3,5-cyclic monophosphate (8-Br-cGMP) for 15 minutes increased EPSCs, which were maintained for 30 minutes. However, simultaneous application of 8-BrcAMP and 8-Br-cGMP failed to increase EPSCs, which suggested antagonistic cross-talk between two second messengers. Application of 3-isobutyl-1-methylxanthine (IBMX) that prevents degradation of cAMP and cGMP by blocking phosphodiesterase (PDE) increased EPSCs. Co-application of cAMP/cGMP along with IBMX induced additional increase in EPSCs. These results suggest that second messengers, cAMP and cGMP, might contribute to development of chronic pain through the mutual regulation of the signal transduction.

• International Journal of Oral Biology
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• v.43 no.3
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• pp.155-160
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• 2018

There exists very little information on the ultrastructure of substance P immunopositive (+) fibers in the human dental pulp, which may help in understanding the mechanism for substance P associated pulpal inflammatory pain. To address this issue, we investigated the presence of substance P+ fibers in the human dental pulp by light- and electron-microscopic immunohistochemistry. Light microscopy revealed that substance P+ fibers ran within neurovascular bundles in the radicular pulp and in the core of coronal pulp. They were also frequently present in the peripheral pulp. Substance P+ fibers showed beads like swellings interconnected by thin axonal strand, in a manner similar to bouton en passants and interconnecting axonal strand in the spinal cord. Electron microscopy revealed that almost all the substance P+ axons were unmyelinated. The axonal swellings of the substance P+ contained numerous clear round vesicles (40-50 nm in diameter) and many large dense-cored vesicles (80-110 nm in diameter) as well as many mitochondria. The vesicles and mitochondria were rarely observed in the thin axonal strand interconnecting the swellings. Intimate interrelationship or synaptic structure between the swellings of substance P+ axon and nearby pulpal cells or axons was not found. These findings suggest co-release of substance P and glutamate from the substance P+ pulpal axons and its action on nearby structures in a paracrine manner.

• BMB Reports
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• v.48 no.6
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• pp.348-353
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• 2015

In the present study, we investigated the characteristics of drug efflux transporter expressions following status epilepticus (SE). In the hippocampus and piriform cortex (PC), vasogenic edema peaked 3-4 days after SE. The expression of breast cancer resistance protein (BCRP), multidrug resistance protein-4 (MRP4), and p-glycoprotein (p-GP) were decreased 4 days after SE when vasogenic edema was peaked, but subsequently increased 4 weeks after SE. Multidrug resistance protein-1 (MRP1) expression gradually decreased in endothelial cells until 4 weeks after SE. These findings indicate that SE-induced vasogenic edema formation transiently reduced drug efflux pump expressions in endothelial cells. Subsequently, during recovery of vasogenic edema drug efflux pump expressions were differentially upregulated in astrocytes, neuropils, and endothelial cells. Therefore, we suggest that vasogenic edema formation may be a risk factor in pharmacoresistent epilepsy. [BMB Reports 2015; 48(6): 348-353]