Curriculum Vitaes

Etsuko SUZUKI

  (鈴木 江津子)

Profile Information

Affiliation
Faculty of Human Sciences Department of Psychology, Sophia University
Degree
博士(心理学)(専修大学)

ORCID ID
 https://orcid.org/0000-0001-5806-1162
J-GLOBAL ID
201201076798399446
researchmap Member ID
B000225883

External link

Research History

 6

Committee Memberships

 2

Awards

 1

Papers

 12
  • Ken Miya, Etsuko Suzuki, Kazuko Keino-Masu, Takuya Okada, Kenta Kobayashi, Toshihiko Momiyama, Masayuki Masu
    eneuro, ENEURO.0088-25.2025, Dec 11, 2025  Peer-reviewedLead author
    Sulf1 is an extracellular sulfatase that regulates cell signaling by removing 6- O -sulfates from heparan sulfate. Although the roles of Sulf1 in neural development have been studied extensively, its functions in the adult brain remain largely unknown. Here, we report the effects of Sulf1 disruption on the neuronal properties of the medium spiny neurons (MSNs) in the nucleus accumbens (NAc) shell, one of the regions highly expressing Sulf1 . We separately labeled MSNs expressing dopamine D1 receptors (D1-MSNs) or D2 receptors (D2-MSNs) by injecting adult male Drd1-Cre and Drd2-Cre mice with a Cre-dependent AAV vector expressing a red fluorescent protein, mCherry, and examined their electrophysiological properties by means of whole-cell patch-clamp recording. In the D2-MSNs, Sulf1 disruption led to drastic changes in neural firing responses to depolarizing current injections: in the Sulf1 knockout mice, the rheobase was smaller than in the wild-type mice, but the number of action potentials elicited by depolarization did not increase at larger current injections. In the D1-MSNs, Sulf1 disruption resulted in more depolarized resting membrane potentials and increase in the AMPA/NMDA ratio. These results suggest that Sulf1 is essential for regulation of neuronal excitability and glutamatergic transmission of NAc MSNs in adult mice and implicate the potential roles of Sulf1 in NAc circuit activity, reward-aversion behaviors, and psychiatric disorders such as schizophrenia and drug addiction. Significance Statement Heparan sulfate plays critical roles in neural differentiation, axon guidance, synaptogenesis, and neurotransmission. Sulf1 is an extracellular sulfatase that removes 6- O -sulfate from heparan sulfate, thereby regulating various cellular functions. Although its roles during development have been studied extensively, its functions in the adult brain remain largely unknown. Here, we examined the electrophysiological properties of medium spiny neurons in the nucleus accumbens shell of adult mice by means of whole-cell patch-clamp recording. We found that Sulf1 disruption led to changes in neuronal excitability and glutamatergic transmission in medium spiny neurons. This study demonstrates the roles of the Sulf1 gene in neuronal activities at the cellular level, providing an important clue toward understanding the functions of Sulf1 in the adult brain.
  • Toshihiko Momiyama, Takuma Nishijo, Etsuko Suzuki, Kunio Kitamura
    European Journal of Neuroscience, 60(8) 6015-6029, Oct 16, 2024  Peer-reviewed
  • Masami Arai, Etsuko Suzuki, Satoshi Kitamura, Momoyo Otaki, Kaori Kanai, Miwako Yamasaki, Masahiko Watanabe, Yuki Kambe, Koshi Murata, Yuuki Takada, Tetsu Arisawa, Kenta Kobayashi, Rei Tajika, Tomoyuki Miyazaki, Masahiro Yamaguchi, Michael Lazarus, Yu Hayashi, Shigeyoshi Itohara, Alban de Kerchove d'Exaerde, Hiroyuki Nawa, Ryang Kim, Haruhiko Bito, Toshihiko Momiyama, Daiki Masukawa, Yoshio Goshima
    The Journal of Neuroscience, Jan 29, 2024  Peer-reviewed
    <jats:p>Dopamine neurons play crucial roles in pleasure, reward, memory, learning, and fine motor skills and their dysfunction is associated with various neuropsychiatric diseases. Dopamine receptors are the main target of treatment for neurologic and psychiatric disorders. Antipsychotics that antagonize the dopamine D2 receptor (DRD2) are used to alleviate the symptoms of these disorders, but may also sometimes cause disabling side effects such as parkinsonism (catalepsy in rodents). Here we show that GPR143, a G-protein-coupled receptor for L-3,4-dihydroxyphenylalanine (L-DOPA), expressed in striatal cholinergic interneurons enhances the DRD2-mediated side effects of haloperidol, an antipsychotic agent. Haloperidol-induced catalepsy was attenuated in male<jats:italic>Gpr143 gene</jats:italic>-deficient (<jats:italic>Gpr143<jats:sup>−/y</jats:sup></jats:italic>) mice compared with wild-type (Wt) mice. Reducing the endogenous release of L-DOPA and preventing interactions between GPR143 and DRD2 suppressed the haloperidol-induced catalepsy in Wt mice but not<jats:italic>Gpr143<jats:sup>−/y</jats:sup></jats:italic>mice. The phenotypic defect in<jats:italic>Gpr143<jats:sup>−/y</jats:sup></jats:italic>mice was mimicked in cholinergic interneuron-specific<jats:italic>Gpr143<jats:sup>−/y</jats:sup></jats:italic>(<jats:italic>Chat-cre;Gpr143<jats:sup>flox/y</jats:sup></jats:italic>) mice. Administration of haloperidol increased the phosphorylation of ribosomal protein S6 at Ser<jats:sup>240/244</jats:sup>in the dorsolateral striatum of Wt mice but not<jats:italic>Chat-cre;Gpr143<jats:sup>flox/y</jats:sup></jats:italic>mice. In Chinese hamster ovary cells stably expressing DRD2, co-expression of GPR143 increased cell surface expression level of DRD2, and L-DOPA application further enhanced the DRD2 surface expression. Shorter pauses in cholinergic interneuron firing activity were observed after intrastriatal stimulation in striatal slice preparations from<jats:italic>Chat-cre;Gpr143<jats:sup>flox/y</jats:sup></jats:italic>mice compared with those from Wt mice. Together, these findings provide evidence that GPR143 regulates DRD2 function in cholinergic interneurons and may be involved in parkinsonism induced by antipsychotic drugs.</jats:p><jats:p><jats:bold>Significance Statement</jats:bold>Dopamine neuron systems play crucial roles in the control of multiple functions including cognition, fine motor skills and behavioral flexibility, and are involved in neurologic and psychiatric disorders. Antipsychotics are used to alleviate the positive symptoms of schizophrenia and other psychiatric disorders. The therapeutic efficacy of these drugs is related to their antagonistic activities against D2 receptors (DRD2), but disabling side effects may also be caused by DRD2 blockade in multiple dopaminergic pathways. L-DOPA receptor GPR143 when coupled with DRD2 potentiates DRD2-mediated signaling. The neuronal pathways is involved in the GPR143 function, however, have not yet been identified. Here, we identified cholinergic interneurons as the neural circuits in which DRD2 coupled with the L-DOPA receptor GPR143 mediates haloperidol-induced catalepsy.</jats:p>
  • Takuma Nishijo, Etsuko Suzuki, Toshihiko Momiyama
    The Journal of Physiology, 600(13) 3149-3167, Jul, 2022  Peer-reviewedLead author
  • Etsuko Suzuki, Toshihiko Momiyama
    European Journal of Neuroscience, 53(3) 796-813, Feb, 2021  Peer-reviewedLead author
  • Shunta Hashiguchi, Hiroshi Doi, Misako Kunii, Yukihiro Nakamura, Misa Shimuta, Etsuko Suzuki, Shigeru Koyano, Masaki Okubo, Hitaru Kishida, Masaaki Shiina, Kazuhiro Ogata, Fumiko Hirashima, Yukichi Inoue, Shun Kubota, Noriko Hayashi, Haruko Nakamura, Keita Takahashi, Atsuko Katsumoto, Mikiko Tada, Kenichi Tanaka, Toshikuni Sasaoka, Satoko Miyatake, Noriko Miyake, Hirotomo Saitsu, Nozomu Sato, Kokoro Ozaki, Kiyobumi Ohta, Takanori Yokota, Hidehiro Mizusawa, Jun Mitsui, Hiroyuki Ishiura, Jun Yoshimura, Shinichi Morishita, Shoji Tsuji, Hideyuki Takeuchi, Kinya Ishikawa, Naomichi Matsumoto, Taro Ishikawa, Fumiaki Tanaka
    Neurobiology of disease, 130 104516-104516, Oct, 2019  
    Spinocerebellar ataxia 42 (SCA42) is a neurodegenerative disorder recently shown to be caused by c.5144G > A (p.Arg1715His) mutation in CACNA1G, which encodes the T-type voltage-gated calcium channel CaV3.1. Here, we describe a large Japanese family with SCA42. Postmortem pathological examination revealed severe cerebellar degeneration with prominent Purkinje cell loss without ubiquitin accumulation in an SCA42 patient. To determine whether this mutation causes ataxic symptoms and neurodegeneration, we generated knock-in mice harboring c.5168G > A (p.Arg1723His) mutation in Cacna1g, corresponding to the mutation identified in the SCA42 family. Both heterozygous and homozygous mutants developed an ataxic phenotype from the age of 11-20 weeks and showed Purkinje cell loss at 50 weeks old. Degenerative change of Purkinje cells and atrophic thinning of the molecular layer were conspicuous in homozygous knock-in mice. Electrophysiological analysis of Purkinje cells using acute cerebellar slices from young mice showed that the point mutation altered the voltage dependence of CaV3.1 channel activation and reduced the rebound action potentials after hyperpolarization, although it did not significantly affect the basic properties of synaptic transmission onto Purkinje cells. Finally, we revealed that the resonance of membrane potential of neurons in the inferior olivary nucleus was decreased in knock-in mice, which indicates that p.Arg1723His CaV3.1 mutation affects climbing fiber signaling to Purkinje cells. Altogether, our study shows not only that a point mutation in CACNA1G causes an ataxic phenotype and Purkinje cell degeneration in a mouse model, but also that the electrophysiological abnormalities at an early stage of SCA42 precede Purkinje cell loss.
  • Etsuko Suzuki, Haruyuki Kamiya
    NEUROSCIENCE RESEARCH, 107 14-19, Jun, 2016  Peer-reviewedLead author
  • Etsuko Suzuki, Makiko Sato, Ryota Takezawa, Toyonobu Usuki, Takashi Okada
    JOURNAL OF PHYSIOLOGICAL SCIENCES, 61(5) 421-427, Sep, 2011  Peer-reviewedLead author
  • Etsuko Suzuki, Takashi Okada
    BRAIN RESEARCH, 1313 45-52, Feb, 2010  Peer-reviewedLead author
  • Etsuko Suzuki, Takashi Okada
    BRAIN RESEARCH, 1247 21-27, Jan, 2009  Peer-reviewedLead author
  • Etsuko Suzuki, Takashi Okada
    NEUROSCIENCE RESEARCH, 59(2) 183-190, Oct, 2007  Peer-reviewedLead author

Misc.

 28

Books and Other Publications

 2

Presentations

 2

Teaching Experience

 10

Professional Memberships

 6

Research Projects

 9