研究者業績

福光甘 斎

フクミツ カンサイ  (Kansai Fukumitsu)

基本情報

所属
藤田医科大学 医学部 生理学Ⅱ 助教
(兼任)精神・神経病態解明センター 神経生理学部門 助教
学位
博士(生命科学)(京都大学)

連絡先
kansai.fukumitsufujita-hu.ac.jp
J-GLOBAL ID
201201031940878973
researchmap会員ID
B000222421

外部リンク

受賞

 1

論文

 10
  • Mercedes Hildebrandt, Masanori Koshimizu, Yasuki Asada, Kansai Fukumitsu, Mahito Ohkuma, Na Sang, Takashi Nakano, Toshiaki Kunikata, Kai Okazaki, Noriaki Kawaguchi, Takayuki Yanagida, Linyuan Lian, Jianbing Zhang, Takayuki Yamashita
    International Journal of Molecular Sciences 25(21) 11365-11365 2024年10月22日  査読有り
    When exposed to X-rays, scintillators emit visible luminescence. X-ray-mediated optogenetics employs scintillators for remotely activating light-sensitive proteins in biological tissue through X-ray irradiation. This approach offers advantages over traditional optogenetics, allowing for deeper tissue penetration and wireless control. Here, we assessed the short-term safety and efficacy of candidate scintillator materials for neuronal control. Our analyses revealed that lead-free halide scintillators, such as Cs3Cu2I5, exhibited significant cytotoxicity within 24 h and induced neuroinflammatory effects when injected into the mouse brain. In contrast, cerium-doped gadolinium aluminum gallium garnet (Ce:GAGG) nanoparticles showed no detectable cytotoxicity within the same period, and injection into the mouse brain did not lead to observable neuroinflammation over four weeks. Electrophysiological recordings in the cerebral cortex of awake mice showed that X-ray-induced radioluminescence from Ce:GAGG nanoparticles reliably activated 45% of the neuronal population surrounding the implanted particles, a significantly higher activation rate than europium-doped GAGG (Eu:GAGG) microparticles, which activated only 10% of neurons. Furthermore, we established the cell-type specificity of this technique by using Ce:GAGG nanoparticles to selectively stimulate midbrain dopamine neurons. This technique was applied to freely behaving mice, allowing for wireless modulation of place preference behavior mediated by midbrain dopamine neurons. These findings highlight the unique suitability of Ce:GAGG nanoparticles for X-ray-mediated optogenetics. The deep tissue penetration, short-term safety, wireless neuronal control, and cell-type specificity of this system offer exciting possibilities for diverse neuroscience applications and therapeutic interventions.
  • Kumi O. Kuroda, Kansai Fukumitsu, Takuma Kurachi, Nami Ohmura, Yuko Shiraishi, Chihiro Yoshihara
    Annals of the New York Academy of Sciences 2024年3月  査読有り
    Abstract This review consolidates current knowledge on mammalian parental care, focusing on its neural mechanisms, evolutionary origins, and derivatives. Neurobiological studies have identified specific neurons in the medial preoptic area as crucial for parental care. Unexpectedly, these neurons are characterized by the expression of molecules signaling satiety, such as calcitonin receptor and BRS3, and overlap with neurons involved in the reproductive behaviors of males but not females. A synthesis of comparative ecology and paleontology suggests an evolutionary scenario for mammalian parental care, possibly stemming from male‐biased guarding of offspring in basal vertebrates. The terrestrial transition of tetrapods led to prolonged egg retention in females and the emergence of amniotes, skewing care toward females. The nocturnal adaptation of Mesozoic mammalian ancestors reinforced maternal care for lactation and thermal regulation via endothermy, potentially introducing metabolic gate control in parenting neurons. The established maternal care may have served as the precursor for paternal and cooperative care in mammals and also fostered the development of group living, which may have further contributed to the emergence of empathy and altruism. These evolution‐informed working hypotheses require empirical validation, yet they offer promising avenues to investigate the neural underpinnings of mammalian social behaviors.
  • Kansai Fukumitsu, Kumi O. Kuroda
    Neuroscience Research 194 36-43 2023年9月  査読有り筆頭著者責任著者
  • Kansai Fukumitsu, Kumi O Kuroda
    Brain Nerve 75(3) 263-268 2023年3月  招待有り筆頭著者責任著者
    Prolonged social isolation has been reported to be one of the risk factors for human health, equivalent to smoking cigarettes. Therefore, some developed countries have recognized prolonged social isolation as a social problem and have started to address this problem. Studies on rodent models are essential to fundamentally clarify the impacts of social isolation on human health mentally and physically. In this review, we conduct an overview of the neuromolecular mechanisms of loneliness, perceived social isolation, and the effects of prolonged social isolation. Finally, we consider the evolutionary development of neural bases of loneliness.
  • Kansai Fukumitsu, Arthur J. Huang, Thomas J. McHugh, Kumi O. Kuroda
    Molecular Brain 16(1) 10-10 2023年1月19日  査読有り筆頭著者責任著者
    Abstract Social animals become stressed upon social isolation, proactively engaging in affiliative contacts among conspecifics after resocialization. We have previously reported that calcitonin receptor (Calcr) expressing neurons in the central part of the medial preoptic area (cMPOA) mediate contact-seeking behaviors in female mice. Calcr neurons in the posterodorsal part of the medial amygdala (MeApd) are also activated by resocialization, however their role in social affiliation is still unclear. Here we first investigated the functional characteristics of MeApd Calcr + cells; these neurons are GABAergic and show female-biased Calcr expression. Next, using an adeno-associated virus vector expressing a short hairpin RNA targeting Calcr we aimed to identify its molecular role in the MeApd. Inhibiting Calcr expression in the MeApd increased social contacts during resocialization without affecting locomotor activity, suggesting that the endogenous Calcr signaling in the MeApd suppresses social contacts. These results demonstrate the distinct roles of Calcr in the cMPOA and MeApd for regulating social affiliation.
  • Kansai Fukumitsu, Misato Kaneko, Teppo Maruyama, Chihiro Yoshihara, Arthur J. Huang, Thomas J. McHugh, Shigeyoshi Itohara, Minoru Tanaka, Kumi O. Kuroda
    Nature Communications 13(1) 2022年2月  査読有り筆頭著者責任著者
    Abstract Social animals actively engage in contact with conspecifics and experience stress upon isolation. However, the neural mechanisms coordinating the sensing and seeking of social contacts are unclear. Here we report that amylin-calcitonin receptor (Calcr) signaling in the medial preoptic area (MPOA) mediates affiliative social contacts among adult female mice. Isolation of females from free social interactions first induces active contact-seeking, then depressive-like behavior, concurrent with a loss of Amylin mRNA expression in the MPOA. Reunion with peers induces physical contacts, activates both amylin- and Calcr-expressing neurons, and leads to a recovery of Amylin mRNA expression. Chemogenetic activation of amylin neurons increases and molecular knockdown of either amylin or Calcr attenuates contact-seeking behavior, respectively. Our data provide evidence in support of a previously postulated origin of social affiliation in mammals.
  • Chihiro Yoshihara, Kenichi Tokita, Teppo Maruyama, Misato Kaneko, Yousuke Tsuneoka, Kansai Fukumitsu, Eri Miyazawa, Kazutaka Shinozuka, Arthur J. Huang, Katsuhiko Nishimori, Thomas J. McHugh, Minoru Tanaka, Shigeyoshi Itohara, Kazushige Touhara, Kazunari Miyamichi, Kumi O. Kuroda
    Cell Reports 35(9) 109204-109204 2021年6月  査読有り
    Maternal mammals exhibit heightened motivation to care for offspring, but the underlying neuromolecular mechanisms have yet to be clarified. Here, we report that the calcitonin receptor (Calcr) and its ligand amylin are expressed in distinct neuronal populations in the medial preoptic area (MPOA) and are upregulated in mothers. Calcr+ MPOA neurons activated by parental care project to somatomotor and monoaminergic brainstem nuclei. Retrograde monosynaptic tracing reveals that significant modification of afferents to Calcr+ neurons occurs in mothers. Knockdown of either Calcr or amylin gene expression hampers risk-taking maternal care, and specific silencing of Calcr+ MPOA neurons inhibits nurturing behaviors, while pharmacogenetic activation prevents infanticide in virgin males. These data indicate that Calcr+ MPOA neurons are required for both maternal and allomaternal nurturing behaviors and that upregulation of amylin-Calcr signaling in the MPOA at least partially mediates risk-taking maternal care, possibly via modified connectomics of Calcr+ neurons postpartum.
  • Hatsukano T, Kurisu J, Fukumitsu K, Fujishima K, Kengaku M
    Frontiers in Cellular Neuroscience 11(133) 2017年5月  査読有り
  • Kansai Fukumitsu, Tetsu Hatsukano, Azumi Yoshimura, John Heuser, Kazuto Fujishima, Mineko Kengaku
    MOLECULAR AND CELLULAR NEUROSCIENCE 71 56-65 2016年3月  査読有り筆頭著者
    Mitochondria dynamically change their shape by repeated fission and fusion in response to physiological and pathological conditions. Recent studies have uncovered significant roles of mitochondrial fission and fusion in neuronal functions, such as neurotransmission and spine formation. However, the contribution of mitochondrial fission to the development of dendrites remains controversial. We analyzed the function of the mitochondrial fission GTPase Drp1 in dendritic arborization in cerebellar Purkinje cells. Overexpression of a dominant-negative mutant of Drp1 in postmitotic Purkinje cells enlarged and clustered mitochondria, which failed to exit from the soma into the dendrites. The emerging dendrites lacking mitochondrial transport remained short and unstable in culture and in vivo. The dominant-negative Drp1 affected neither the basal respiratory function of mitochondria nor the survival of Purkinje cells. Enhanced ATP supply by creatine treatment, but not reduced ROS production by antioxidant treatment, restored the hypomorphic dendrites caused by inhibition of Drp1 function. Collectively, our results suggest that Drp1 is required for dendritic distribution of mitochondria and thereby regulates energy supply in growing dendritic branches in developing Purkinje cells. (C) 2015 Elsevier Inc. All rights reserved.
  • Kansai Fukumitsu, Kazuto Fujishima, Azumi Yoshimura, You Kure Wu, John Heuser, Mineko Kengaku
    JOURNAL OF NEUROSCIENCE 35(14) 5707-5723 2015年4月  査読有り筆頭著者
    The distribution of mitochondria within mature, differentiated neurons is clearly adapted to their regional physiological needs and can be perturbed under various pathological conditions, but the function of mitochondria in developing neurons has been less well studied. We have studied mitochondrial distribution within developing mouse cerebellar Purkinje cells and have found that active delivery of mitochondria into their dendrites is a prerequisite for proper dendritic outgrowth. Even when mitochondria in the Purkinje cell bodies are functioning normally, interrupting the transport of mitochondria into their dendrites severely disturbs dendritic growth. Additionally, we find that the growth of atrophic dendrites lacking mitochondria can be rescued by activating ATP-phosphocreatine exchange mediated by creatine kinase (CK). Conversely, inhibiting cytosolic CKs decreases dendritic ATP levels and also disrupts dendrite development. Mechanistically, this energy depletion appears to perturb normal actin dynamics and enhance the aggregation of cofilin within growing dendrites, reminiscent of what occurs in neurons overexpressing the dephosphorylated form of cofilin. These results suggest that local ATP synthesis by dendritic mitochondria and ATP-phosphocreatine exchange act synergistically to sustain the cytoskeletal dynamics necessary for dendritic development.

MISC

 3
  • Kumi Kuroda, Kansai Fukumitsu, Takuma Kurachi, Nami Ohmura, Yuko Shiraishi, Chihiro Yoshihara
    EcoevoRxiv 2023年12月5日  
    Mammalian parental care is highly mother-biased, prompting researchers to presume its connection to female reproductive behavior and physiology, not male. However, recent findings in neurobiological studies suggest the opposite. Considering the evolutionary path of mammalian parental care, the ancestral form of vertebrate parental care appears to be male-biased as in living teleosts (bony fish), and originated from egg guarding as an extension of territorial behavior. Phylogenetic analyses suggest that in basal tetrapods, the harsh reproductive environments have facilitated terrestrial adaptation and extensive parental investment in females, and salamander-like basal amniotes exhibited extended egg retention in female bodies. Molecular and fossil evidence indicates that synapsids that have later evolved into mammals have already performed extensive maternal care including egg/offspring hydration in the Carboniferous period. Then the nocturnal adaptation in Jurassic mammaliaforms promoted endothermy and prolonged maternal care for thermal control and lactation. This situation may have added nutritional gate control to the offspring care circuit to balance parental provisioning with maternal homeostatic needs. Combining these paleontological, comparative ecological, and neuromolecular findings, we propose that the mammalian parenting circuit may be derived from MPOA neurons controlling reproductive behaviors during the terrestrial adaptation in anamniotes, either by divergent or parallel evolution. Next, we discuss another long-postulated hypothesis that complex affiliative sociality among adults, including group living, cooperative infant care, empathy, and altruism, may have emerged primarily for extended support of the offspring growth, utilizing the established maternal care circuit in mammals. These evolution-informed working hypotheses may also help dissect the neural basis of the complex cognitive functions in mammals.
  • 福光甘斎, 黒田公美
    精神科 = Psychiatry / 精神科編集委員会 編 39(5) 546-552 2021年11月  招待有り筆頭著者
  • Kansai Fukumitsu, Kazuto Fujishima, Mineko Kengaku
    Neuroscience Research 71 e96-e96 2011年9月  査読有り

共同研究・競争的資金等の研究課題

 9

メディア報道

 10