Optogenetically‐induced sustained hypothalamic hyperexcitability impairs memory via thalamic spread
Excessive neural excitation, specifically propagating from the lateral hypothalamus to the mediodorsal thalamus during encoding, alters physiological neural activity and transiently impairs working memory. This study clarifies the pathophysiological mechanism underlying cognitive disabilities associated with working memory impairment in HH-related epileptic encephalopathy.
Authors
- Isao Hasegawa (ORCID: https://orcid.org/0000-0002-8633-2502)
- Eishi Asano (ORCID: https://orcid.org/0000-0001-8391-4067)
- Tetsuya Yamamoto (ORCID: https://orcid.org/0000-0001-9977-9373)
- Masaki Sonoda (ORCID: https://orcid.org/0000-0002-4612-5728)
- Shinobu Hirai (ORCID: https://orcid.org/0000-0002-2354-3759)
- Keisuke Kawasaki (ORCID: https://orcid.org/0000-0002-3378-816X)
- Haruo Okado (ORCID: https://orcid.org/0000-0001-5674-420X)
- Reiko Meguro
- Haruo Toda (ORCID: https://orcid.org/0000-0001-9188-1058)
- Masao Horie
- Shigeki Kameyama
- Hisao Aimi
Institutions
- Wayne State University (US)
- Detroit Medical Center (US)
- Niigata College of Nursing (JP)
- Tokyo Metropolitan Institute of Medical Science (JP)
- Children's Hospital of Michigan (US)
- Obihiro National Hospital (JP)
- Niigata University of Health and Welfare (JP)
- Niigata University (JP)
- Yokohama City University (JP)
Publication Details
- Journal
- Epilepsia
- Published
- 2025-03-11
- DOI
- https://doi.org/10.1111/epi.18321
- Primary Topic
- Photoreceptor and optogenetics research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Japan Agency for Medical Research and Development
- Japan Society for the Promotion of Science
- National Institute for Physiological Sciences