Yi Sul Cho

Kyungpook National University

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Yong Chul Bae

Kyungpook National University

Yun‐Sook Kim

Kyungpook National University

Eunjoon Kim

Korea Advanced Institute of Science and Technology

Dong Kuk Ahn

Kyungpook National University

Sang Kyoo Paik

Kyungpook National University

Hyun Kim

Korea University

Jin Young Bae

Catholic University of Daegu

Sook Kyung Park

Kyungpook National University

Junyeop Daniel Roh

Korea Advanced Institute of Science and Technology

Won Mah

Kyungpook National University

Cooperative Institutions

Korea Advanced Institute of Science and Technology

Kyungpook National University

Seoul National University

Institute for Basic Science

Yonsei University

Korea University

Daegu Gyeongbuk Institute of Science and Technology

Catholic University of Korea

Chonnam National University

Seoul National University Dental Hospital

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Increase of glutamate in satellite glial cells of the trigeminal ganglion in a rat model of craniofacial neuropathic pain

Frontiers in Neuroanatomy (2023)

Yi Sul Cho Won Mah Dong Ho Youn Yu Shin Kim Hyoung‐Gon Ko

Satellite glial cells (SGCs) that envelop the cell bodies of neurons in sensory ganglia have been shown to both release glutamate, and be activated by glutamate in the context of nociceptive signaling. However, little is known about the subpopulations of SGCs that are activated following nerve injury and whether glutamate mechanisms in the SGCs are involved in the pathologic pain.

Trigeminal ganglion

10.3389/fnana.2023.1302373

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Citations (2)

Autistic-like social behaviour in Shank2-mutant mice improved by restoring NMDA receptor function

Nature (2012)

Hyejung Won Hye‐Ryeon Lee Heon Yung Gee Won Mah Jae‐Ick Kim

10.1038/nature11208

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Citations (631)

Expression of Vesicular Glutamate Transporters VGLUT1 and VGLUT2 in the Rat Dental Pulp and Trigeminal Ganglion following Inflammation

PLoS ONE (2014)

Eun Sun Yang Myoung Uk Jin Jae Hyun Hong Yun‐Sook Kim So Young Choi

Background There is increasing evidence that peripheral glutamate signaling mechanism is involved in the nociceptive transmission during pathological conditions. However, little is known about the glutamate signaling mechanism and related specific type of vesicular glutamate transporter (VGLUT) in the dental pulp following inflammation. To address this issue, we investigated expression and protein levels of VGLUT1 and VGLUT2 in the dental pulp and trigeminal ganglion (TG) following complete Freund’s adjuvant (CFA) application to the rat dental pulp by light microscopic immunohistochemistry and Western blot analysis. Results The density of VGLUT2− immunopositive (+) axons in the dental pulp and the number of VGLUT2+ soma in the TG increased significantly in the CFA-treated group, compared to control group. The protein levels of VGLUT2 in the dental pulp and TG were also significantly higher in the CFA-treated group than control group by Western blot analysis. The density of VGLUT1+ axons in the dental pulp and soma in the TG remained unchanged in the CFA-treated group. Conclusions These findings suggest that glutamate signaling that is mediated by VGLUT2 in the pulpal axons may be enhanced in the inflamed dental pulp, which may contribute to pulpal axon sensitization leading to hyperalgesia following inflammation.

Trigeminal ganglion

10.1371/journal.pone.0109723

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SALM4 suppresses excitatory synapse development by cis-inhibiting trans-synaptic SALM3–LAR adhesion

Nature Communications (2016)

Eunkyung Lie Ji Seung Ko Su‐Yeon Choi Junyeop Daniel Roh Yi Sul Cho

Abstract Synaptic adhesion molecules regulate various aspects of synapse development, function and plasticity. These functions mainly involve trans -synaptic interactions and positive regulations, whereas cis -interactions and negative regulation are less understood. Here we report that SALM4, a member of the SALM/Lrfn family of synaptic adhesion molecules, suppresses excitatory synapse development through cis inhibition of SALM3, another SALM family protein with synaptogenic activity. Salm4 -mutant ( Salm4 −/− ) mice show increased excitatory synapse numbers in the hippocampus. SALM4 cis -interacts with SALM3, inhibits trans -synaptic SALM3 interaction with presynaptic LAR family receptor tyrosine phosphatases and suppresses SALM3-dependent presynaptic differentiation. Importantly, deletion of Salm3 in Salm4 −/− mice ( Salm3 −/− ; Salm4 −/− ) normalizes the increased excitatory synapse number. These results suggest that SALM4 negatively regulates excitatory synapses via cis inhibition of the trans -synaptic SALM3–LAR adhesion.

Excitatory synapse

10.1038/ncomms12328

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Citations (31)

Distribution of excitatory and inhibitory axon terminals on the rat hypoglossal motoneurons

IBRO Reports (2019)

Yi Sul Cho Sang Kyoo Paik Hong‐Il Yoo Seung Ki Choi Jin Young Bae

10.1016/j.ibror.2019.07.1712

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Synaptic connectivity of the TRPV1-positive trigeminal afferents in the rat lateral parabrachial nucleus

Frontiers in Cellular Neuroscience (2023)

Su Bin An Yi Sul Cho Sook Kyung Park Yun‐Sook Kim Yong Chul Bae

Recent studies have shown a direct projection of nociceptive trigeminal afferents into the lateral parabrachial nucleus (LPBN). Information about the synaptic connectivity of these afferents may help understand how orofacial nociception is processed in the LPBN, which is known to be involved primarily in the affective aspect of pain. To address this issue, we investigated the synapses of the transient receptor potential vanilloid 1-positive (TRPV1+) trigeminal afferent terminals in the LPBN by immunostaining and serial section electron microscopy. TRPV1 + afferents arising from the ascending trigeminal tract issued axons and terminals (boutons) in the LPBN. TRPV1+ boutons formed synapses of asymmetric type with dendritic shafts and spines. Almost all (98.3%) TRPV1+ boutons formed synapses with one (82.6%) or two postsynaptic dendrites, suggesting that, at a single bouton level, the orofacial nociceptive information is predominantly transmitted to a single postsynaptic neuron with a small degree of synaptic divergence. A small fraction (14.9%) of the TRPV1+ boutons formed synapses with dendritic spines. None of the TRPV1+ boutons were involved in axoaxonic synapses. Conversely, in the trigeminal caudal nucleus (Vc), TRPV1+ boutons often formed synapses with multiple postsynaptic dendrites and were involved in axoaxonic synapses. Number of dendritic spine and total number of postsynaptic dendrites per TRPV1+ bouton were significantly fewer in the LPBN than Vc. Thus, the synaptic connectivity of the TRPV1+ boutons in the LPBN differed significantly from that in the Vc, suggesting that the TRPV1-mediated orofacial nociception is relayed to the LPBN in a distinctively different manner than in the Vc.

Lateral parabrachial nucleus

10.3389/fncel.2023.1162874

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Citations (4)

Spartin Regulates Synaptic Growth and Neuronal Survival by Inhibiting BMP-Mediated Microtubule Stabilization

Neuron (2013)

Minyeop Nahm Min-Jung Lee William Parkinson Mihye Lee Hae Ran Kim

10.1016/j.neuron.2012.12.015

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Citations (97)

Early correction of synaptic long-term depression improves abnormal anxiety-like behavior in adult GluN2B-C456Y-mutant mice

PLoS Biology (2020)

Wangyong Shin Kyungdeok Kim Benjamin Serraz Yi Sul Cho Doyoun Kim

Extensive evidence links Glutamate receptor, ionotropic, NMDA2B (GRIN2B), encoding the GluN2B/NR2B subunit of N-methyl-D-aspartate receptors (NMDARs), with various neurodevelopmental disorders, including autism spectrum disorders (ASDs), but the underlying mechanisms remain unclear. In addition, it remains unknown whether mutations in GluN2B, which starts to be expressed early in development, induces early pathophysiology that can be corrected by early treatments for long-lasting effects. We generated and characterized Grin2b-mutant mice that carry a heterozygous, ASD-risk C456Y mutation (Grin2b+/C456Y). In Grin2b+/C456Y mice, GluN2B protein levels were strongly reduced in association with decreased hippocampal NMDAR currents and NMDAR-dependent long-term depression (LTD) but unaltered long-term potentiation, indicative of mutation-induced protein degradation and LTD sensitivity. Behaviorally, Grin2b+/C456Y mice showed normal social interaction but exhibited abnormal anxiolytic-like behavior. Importantly, early, but not late, treatment of young Grin2b+/C456Y mice with the NMDAR agonist D-cycloserine rescued NMDAR currents and LTD in juvenile mice and improved anxiolytic-like behavior in adult mice. Therefore, GluN2B-C456Y haploinsufficiency decreases GluN2B protein levels, NMDAR-dependent LTD, and anxiety-like behavior, and early activation of NMDAR function has long-lasting effects on adult mouse behavior.

Haploinsufficiency

Long-term depression

10.1371/journal.pbio.3000717

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Citations (45)

Hyung Joon Ahn Sang Kyoo Paik Yong Chul Bae Cheil Moon Yun‐Sook Kim

Collagen fibril

Collagen fiber

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An ultrastructural evidence for the expression of transient receptor potential ankyrin 1 (TRPA1) in astrocytes in the rat trigeminal caudal nucleus