Katalin Tóth
- Cellular and Molecular Neuroscience top 0.5%
- Cognitive Neuroscience top 1%
- Molecular Biology top 10%
- Neurology top 2%
- Developmental Neuroscience top 2%
- Co-authors
- Richard MilesTamás F. FreundAttila I. GulyásChris J. McBainNorbert HájosZsolt BorhegyiSimon ChamberlandAlesya Evstratova
- Topics
- Neuroscience and Neuropharmacology Research (29 papers)Photoreceptor and optogenetics research (13 papers)Neural dynamics and brain function (11 papers)
- Partner nations
- CanadaUnited StatesHungary
In The Last Decade
Katalin Tóth
40 papers receiving 3.8k citations
Hit Papers
Peers
Comparison fields: 5 of 102
- Cellular and Molecular Neuroscience 3.2k
- Cognitive Neuroscience 2.2k
- Molecular Biology 1.2k
- Neurology 409
- Developmental Neuroscience 291
Countries citing papers authored by Katalin Tóth
This map shows the geographic impact of Katalin Tóth'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 Katalin Tóth with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Katalin Tóth more than expected).
Fields of papers citing papers by Katalin Tóth
This network shows the impact of papers produced by Katalin Tóth. 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 Katalin Tóth. The network helps show where Katalin Tóth may publish in the future.
Co-authorship network of co-authors of Katalin Tóth
This figure shows the co-authorship network connecting the top 25 collaborators of Katalin Tóth. A scholar is included among the top collaborators of Katalin Tóth based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Katalin Tóth. Katalin Tóth is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 5 | |
| 2 | 7 | |
| 3 | 18 | |
| 4 | 11 | |
| 5 | 220 | |
| 6 | 24 | |
| 7 | 17 | |
| 8 | 6 | |
| 9 | 34 | |
| 10 | 35 | |
| 11 | 14 | |
| 12 | 123 | |
| 13 | 15 | |
| 14 | 31 | |
| 15 | 5 | |
| 16 | 83 | |
| 17 | 42 | |
| 18 | Differences between Somatic and Dendritic Inhibition in the Hippocampusbreakdown → | 765 |
| 19 | 285 | |
| 20 | 81 |
About Katalin Tóth
Katalin Tóth is a scholar working on Cellular and Molecular Neuroscience, Cognitive Neuroscience and Neurology, having authored 40 papers that have together received 3.9k indexed citations. Recurring topics across this work include Neuroscience and Neuropharmacology Research (29 papers), Photoreceptor and optogenetics research (13 papers) and Neural dynamics and brain function (11 papers). The work is most often cited by research in Cellular and Molecular Neuroscience (3.2k citations), Cognitive Neuroscience (2.2k citations) and Developmental Neuroscience (291 citations). Katalin Tóth has collaborated with scholars based in Canada, United States and Hungary. Frequent co-authors include Richard Miles, Tamás F. Freund, Attila I. Gulyás, Chris J. McBain, Norbert Hájos, Zsolt Borhegyi, Simon Chamberland, Alesya Evstratova, Gianmaria Maccaferri and Attila Sı́k. Their work appears in journals such as Nature, Science and Cell.
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.