Nagoya City University

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Nagoya City University Nagoya City University official page. Under these slogans, NCU has matured as a university where every citizen feels a sense of pride and affinity.

Nagoya City University (NCU), a municipal university corporation, is located in the geographically central area of Nagoya City, one of the metropolis in Japan. NCU is an urban-type university holding over 4,000 students, over 140 international students and over 1,600 faculty members. Among the prefectural and municipal university corporations in Japan, only NCU has three medical faculties – “Medical School,” “Faculty of Pharmaceutical Sciences,” and “School of Nursing.” In addition, NCU has “Faculty of Economics,” “School of Humanities and Social Sciences,” “School of Design and Architecture” and “Graduate School of Natural Sciences” on four campuses in Nagoya City. NCU has produced a large number of leaders in many regions, and thus contributed to the development of regional society. In addition, NCU has approached a wide range of institutions at home and abroad, and thus globally active in contributing to regional society and the international community. On each NCU campus three slogans are promoted namely:
“Draw individual potential,” “Study the past to create new things” and “Call up your courage to take on a challenge,” are widespread. NCU takes pride in providing an environment in which all enrolled individual students and faculty members can draw their potencials, cultivate their spirit in studying the old and creating the new, and being courageous when taking on new challenges.

A neural brake on adult glioma progressionNeuron study shows that inhibitory brain circuits suppress tumor calcium activ...
08/09/2026

A neural brake on adult glioma progression
Neuron study shows that inhibitory brain circuits suppress tumor calcium activity and downstream oncogenic programs

Summary Text
Researchers at Nagoya City University and collaborators found that inhibitory neurons can restrain adult glioma progression. The study, published in Neuron, shows that GABAergic input suppresses calcium activity in tumor cells and reduces YAP1/mTOR-associated oncogenic programs, revealing a circuit-based mechanism that slows brain tumor growth.

Full Text
This study was led by Daisuke Kawauchi of Nagoya City University, Naofumi Uesaka of Institute of Science Tokyo, and Reo Maruyama of the Japanese Foundation for Cancer Research, in collaboration with their respective research teams and institutions.

News release
Brain tumors do not grow in isolation. They develop within the highly active environment of the brain, where neurons continuously exchange electrical and chemical signals. While previous studies have shown that neuronal activity can promote glioma growth, a new study published in Neuron reveals that some brain circuits can have the opposite effect: they can act as a brake on tumor progression.

A research team led by Professor Daisuke Kawauchi at Nagoya City University, in close collaboration with Professor Naofumi Uesaka, Dr. Reo Maruyama and colleagues, has found that inhibitory neurons suppress the growth of adult gliomas by reducing calcium activity inside tumor cells. The findings identify a tumor-suppressive role for GABAergic inhibitory circuits and suggest that the balance of neural activity in the tumor microenvironment can shape how brain cancers progress.

Gliomas are aggressive brain tumors that interact closely with surrounding neurons. Much attention has focused on excitatory neuronal activity, which can drive tumor growth through neuron–glioma communication. However, the role of inhibitory neurons, which normally help regulate brain activity by limiting excessive excitation, has remained unclear.

In the new study, the researchers used mouse models of adult glioma and patient-derived tumor models to investigate whether inhibitory neurons communicate with glioma cells and influence their behavior. They found that inhibitory neurons form synaptic contacts with tumor cells and that increasing inhibitory tone reduced tumor cell proliferation and prolonged survival in preclinical models.

The team further discovered that this effect was linked to calcium dynamics within tumor cells. Glioma cells showed active calcium transients during proliferative phases, but activation of inhibitory circuits suppressed these tumor calcium signals. Conversely, restoring calcium activity in tumor cells weakened the anti-proliferative effect of inhibitory circuit activation, indicating that tumor calcium dynamics are a key mediator of this circuit-based control.

Downstream analyses revealed that inhibitory circuit activation reduced YAP1- and mTOR-associated oncogenic programs, two signaling pathways linked to tumor growth and survival. Together, the results suggest that inhibitory input from the surrounding brain microenvironment can restrain adult glioma progression by suppressing calcium-driven growth programs within tumor cells.

“Our study shows that the brain is not simply a permissive environment for tumor growth,” said Professor Kawauchi. “In adult glioma, inhibitory circuits can function as a tumor-suppressive force by quieting tumor calcium activity and downstream oncogenic signaling.”

Professor Uesaka added, “This project required a close integration of neuroscience and cancer biology. By combining circuit-level approaches, electrophysiology, imaging, and tumor models, we were able to show that inhibitory neuron–glioma communication has a functional impact on tumor progression.”

The findings add an important layer to the emerging field of cancer neuroscience, which explores how neural activity and tumor biology interact. They also highlight the importance of considering glioma not only as a disease of cancer cells, but as a disease shaped by the broader brain ecosystem.

Although the study was performed in preclinical models, the work raises the possibility that strengthening inhibitory tone or suppressing tumor calcium activity could inspire new therapeutic strategies for adult gliomas. Further research will be needed to determine how these mechanisms operate across different glioma subtypes and whether they can be safely targeted in patients.

Reference
Journal：Neuron
DOI：10.1016/j.neuron.2026.08.008

Author
Daisuke Kawauchi

Nagoya City University

Stored but inaccessible: brain histamine neurons gate moment-to-moment memory accessMemories can be stored yet temporari...
15/06/2026

Stored but inaccessible: brain histamine neurons gate moment-to-moment memory access
Memories can be stored yet temporarily unreachable. A study in mice published in Neuron shows that slow fluctuations in hypothalamic histamine neurons act as a dynamic gate, making stored memories more or less accessible when a cue arrives.

Summary Text
Why does a stored memory sometimes feel out of reach? A study in mice from Nagoya City University, published in Neuron, shows that slow fluctuations in brain histamine neurons shape whether learned memories become accessible when a memory cue is presented. The work suggests that memory access depends not only on stored memory traces, but also on moment-to-moment brain states.

Full Text
The same memory can feel vivid and accessible one moment, yet stubbornly out of reach the next — even when the memory itself remains intact. A research team led by Professor Hiroshi Nomura at the Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, has identified a neural mechanism that may explain this variability.
The study shows that slow spontaneous fluctuations in brain histamine neurons help control moment-to-moment memory accessibility. When histamine neuron activity was high just before a memory cue, mice were more likely to express a learned memory. When histamine neuron activity was low, the same cue was less effective.
“Our findings suggest that failure to recall is not always due to loss of the memory itself,” said Hiroshi Nomura, senior author of the study. “Instead, the brain may sometimes be in a state in which a stored memory is difficult to access.”
Histamine neurons are located in the tuberomammillary nucleus of the hypothalamus and are best known for regulating wakefulness. They also project widely to memory-related brain regions, including the cortex, hippocampus and amygdala. However, whether their activity during wakefulness shapes access to stored memories has remained unclear.
The team recorded histamine neuron activity in awake mice and found that their activity rose and fell slowly over tens of seconds. These slow fluctuations were accompanied by changes in cortical activity, pupil size, and facial movement, indicating that histamine activity reflected a broader brain and body state.
The researchers then trained mice to associate a sound with a sugar-water reward. After learning, mice licked in response to the sound, indicating that the sound cue elicited a learned reward-related response. Histamine neuron activity was higher before trials in which mice showed strong memory-guided licking than before trials in which they showed no licking, suggesting that histamine activity helps prepare the brain before the cue appears.
To go beyond this correlation, the researchers used a real-time system that monitored histamine neuron activity and delivered a memory cue during either high- or low-activity states. Memory-guided licking responses were about 40% higher when the cue was presented during a high-histamine state than during a low-histamine state.
The researchers further tested causality by manipulating these neurons using optogenetics. Suppressing histamine neurons immediately before the sound cue reduced memory-guided licking, whereas activating them increased it. These manipulations did not alter general licking behavior, responses to the reward itself, auditory responses, or pupil size, suggesting that the effects were not readily explained by broad changes in arousal, sensory responses, or movement.
The study also identified a downstream mechanism in the basolateral amygdala, a brain region important for learned reward associations. Calcium imaging showed that, when mice strongly expressed the learned memory, populations of amygdala neurons more reliably reproduced the activity pattern associated with the learned cue. When histamine neurons were suppressed before the cue, this memory-related amygdala pattern became weaker and less reliable.
Together, the findings support a “priming-state” model: spontaneous fluctuations in histamine neuron activity prepare memory circuits in advance, making it more or less likely that an incoming cue will trigger the appropriate memory-related neural pattern.
“This work provides a new way to think about memory retrieval,” Nomura said. “Rather than viewing recall simply as reading out a stored trace, we show that internal brain state can gate whether that trace becomes accessible at a given moment.”
Because the study used a reward memory task in mice, further research will be needed to determine whether histamine-dependent brain states shape other forms of memory, such as fear, spatial, and social memory, and whether similar fluctuations contribute to everyday memory variability in humans. The findings may also provide a framework for studying conditions in which cognition fluctuates over time, such as aging and dementia.

Reference
Journal：Neuron
DOI：10.1016/j.neuron.2026.05.019

Author
Hiroshi Nomura

Nagoya City University

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1, Kawasumi, Mizuho-ku
Nagoya-shi, Aichi
467-8601

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