Raymond T. Kado
- Aging top 10%
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- Neuroscience and Neuropharmacology Research 7
- Photoreceptor and optogenetics research 5
- Neurobiology and Insect Physiology Research 5
- Neurology top 10%
- Vestibular and auditory disorders 3
- Physiology top 5%
- Sensory Systems top 5%
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- Neural dynamics and brain function 5
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- Lipid Membrane Structure and Behavior 4
- Ion channel regulation and function 4
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- Physiological and biochemical adaptations 3
Raymond T. Kado
26 papers receiving 864 citations
Peers
Comparison fields: 5 of 101
- Aging 31
- Cellular and Molecular Neuroscience 314
- Neurology 121
- Physiology 64
- Sensory Systems 67
Countries citing papers authored by Raymond T. Kado
This map shows the geographic impact of Raymond T. Kado's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Raymond T. Kado with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Raymond T. Kado more than expected).
Fields of papers citing papers by Raymond T. Kado
This network shows the impact of papers produced by Raymond T. Kado. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Raymond T. Kado. The network helps show where Raymond T. Kado may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Raymond T. Kado, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | Increased calbindin-D28K immunoreactivity in rat cerebellar Purkinje cell with excitatory amino acids agonists is not dependent on protein synthesis. | 2004 | 2 |
| 2 | Synaptic long-term depression (LTD) in vivo recorded on the rat cerebellar cortex. | 2002 | 2 |
| 3 | 2000 | 3 | |
| 4 | 1999 | 10 | |
| 5 | 1997 | 21 | |
| 6 | 1995 | 10 | |
| 7 | 1994 | 126 | |
| 8 | 1991 | 25 | |
| 9 | 1991 | 23 | |
| 10 | 1990 | 128 | |
| 11 | 1989 | 8 | |
| 12 | 1988 | 22 | |
| 13 | 1987 | 74 | |
| 14 | 1986 | 23 | |
| 15 | 1982 | 1 | |
| 16 | 1981 | 61 | |
| 17 | 1967 | 37 | |
| 18 | 1967 | 17 | |
| 19 | 1959 | 69 | |
| 20 | 1958 | 22 |
About Raymond T. Kado
Raymond T. Kado is a scholar working on Cellular and Molecular Neuroscience, Physiology and Neurology, having authored 26 papers that have together received 917 indexed citations. Recurring topics across this work include Neuroscience and Neuropharmacology Research (7 papers), Photoreceptor and optogenetics research (5 papers), Neural dynamics and brain function (5 papers), Neurobiology and Insect Physiology Research (5 papers), Lipid Membrane Structure and Behavior (4 papers), Ion channel regulation and function (4 papers), Physiological and biochemical adaptations (3 papers) and Vestibular and auditory disorders (3 papers). The work is most often cited by research in Aging (31 citations), Cellular and Molecular Neuroscience (314 citations) and Neurology (121 citations). Raymond T. Kado has collaborated with scholars based in France, United States and Japan. Frequent co-authors include Laurinda A. Jaffe, Masao Ito, Alexander Kolin, Kazuyoshi Chiba, Laddawan Karachot, Douglas Kline, Susumu Hagiwara, W. R. Adey, René Ozon and Rainer Hedrich. Their work appears in journals such as Nature, Science and Proceedings of the National Academy of Sciences.
Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.