Evidence map›Paper›PMID 38877480›Full record

ArticleMolecular brain2024

Chemogenetic activation of histamine neurons promotes retrieval of apparently lost memories.

Yuto Yokoi, Ayame Kubo, Kyoka Nishimura, Yuki Takamura, Yoshikazu Morishita, Masabumi Minami, Hiroshi Nomura

Abstract read
In one paragraph

Article in Molecular brain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Histamine HMolecular brain · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yuto Yokoi *Endowed Department of Cognitive Function and Pathology, Institute of Brain Science, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Ayame Kubo *Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Kyoka NishimuraDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Yuki TakamuraEndowed Department of Cognitive Function and Pathology, Institute of Brain Science, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Yoshikazu MorishitaEndowed Department of Cognitive Function and Pathology, Institute of Brain Science, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Masabumi MinamiDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Hiroshi NomuraEndowed Department of Cognitive Function and Pathology, Institute of Brain Science, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan. hnomura@med.nagoya-cu.ac.jp.ORCID 0000-0002-6172-4788

Funding

Fusion Oriented REsearch for disruptive Science and Technology JPMJFR204AJapan Society for the Promotion of Science 21H00296Japan Society for the Promotion of Science 22H05080Japan Society for the Promotion of Science 22K19482Japan Society for the Promotion of Science 23H02787
6 · The paper itself

Abstract

Memory retrieval can become difficult over time, but it is important to note that memories that appear to be forgotten might still be stored in the brain, as shown by their occasional spontaneous retrieval. Histamine in the central nervous system is a promising target for facilitating the recovery of memory retrieval. Our previous study demonstrated that histamine H3 receptor (H3R) inverse agonists/antagonists, activating histamine synthesis and release, enhance activity in the perirhinal cortex and help in retrieving forgotten long-term object recognition memories. However, it is unclear whether enhancing histaminergic activity alone is enough for the recovery of memory retrieval, considering that H3Rs are also located in other neuron types and affect the release of multiple neurotransmitters. In this study, we employed a chemogenetic method to determine whether specifically activating histamine neurons in the tuberomammillary nucleus facilitates memory retrieval. In the novel object recognition test, control mice did not show a preference for objects based on memory 1 week after training, but chemogenetic activation of histamine neurons before testing improved memory retrieval. This selective activation did not affect the locomotor activity or anxiety-related behavior. Administering an H2R antagonist directly into the perirhinal cortex inhibited the recovery of memory retrieval induced by the activation of histamine neurons. Furthermore, we utilized the Barnes maze test to investigate whether chemogenetic activation of histamine neurons influences the retrieval of forgotten spatial memories. Control mice explored all the holes in the maze equally 1 week after training, whereas mice with chemogenetically activated histamine neurons spent more time around the target hole. These findings indicate that chemogenetic activation of histamine neurons in the tuberomammillary nucleus can promote retrieval of seemingly forgotten object recognition and spatial memories.

Indexed as

HistamineNeuronsAnimalsAnxietyHistamine H2 AntagonistsHypothalamic Area, LateralMaleMemoryMental RecallMiceMice, Inbred C57BLRecognition, PsychologyHistamineHistamine H2 AntagonistsChemogeneticsHistamineMemoryPerirhinal cortexRetrievalTuberomammillary nucleus

Identifiers

PMID38877480
PMCPMC11179205

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.