Boris Mlinar
- Cellular and Molecular Neuroscience top 2%
- Molecular Biology
- Social Psychology top 10%
- Cardiology and Cardiovascular Medicine
- Cognitive Neuroscience top 10%
- Co-authors
- John J. EnyeartRenato CorradettiB. A. BiagiJudith A. EnyeartCornelius T. GrossAlberto MontalbanoEnrica AuderoKlaus‐Peter Lesch
- Topics
- Neuroscience and Neuropharmacology Research (24 papers)Neurotransmitter Receptor Influence on Behavior (15 papers)Ion channel regulation and function (14 papers)
- Partner nations
- ItalyUnited StatesGermany
In The Last Decade
Boris Mlinar
34 papers receiving 1.2k citations
Peers
Comparison fields: 5 of 93
- Cellular and Molecular Neuroscience 738
- Molecular Biology 669
- Social Psychology 151
- Cardiology and Cardiovascular Medicine 139
- Cognitive Neuroscience 135
Countries citing papers authored by Boris Mlinar
This map shows the geographic impact of Boris Mlinar'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 Boris Mlinar with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Boris Mlinar more than expected).
Fields of papers citing papers by Boris Mlinar
This network shows the impact of papers produced by Boris Mlinar. 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 Boris Mlinar. The network helps show where Boris Mlinar may publish in the future.
Co-authorship network of co-authors of Boris Mlinar
This figure shows the co-authorship network connecting the top 25 collaborators of Boris Mlinar. A scholar is included among the top collaborators of Boris Mlinar 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 Boris Mlinar. Boris Mlinar is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 16 | |
| 2 | 23 | |
| 3 | 25 | |
| 4 | 12 | |
| 5 | 39 | |
| 6 | 21 | |
| 7 | 28 | |
| 8 | 79 | |
| 9 | 8 | |
| 10 | 15 | |
| 11 | 11 | |
| 12 | 30 | |
| 13 | 18 | |
| 14 | 11 | |
| 15 | 35 | |
| 16 | 31 | |
| 17 | 12 | |
| 18 | 51 | |
| 19 | 34 | |
| 20 | 103 |
About Boris Mlinar
Boris Mlinar is a scholar working on Cellular and Molecular Neuroscience, Behavioral Neuroscience and Molecular Biology, having authored 34 papers that have together received 1.2k indexed citations. Recurring topics across this work include Neuroscience and Neuropharmacology Research (24 papers), Neurotransmitter Receptor Influence on Behavior (15 papers) and Ion channel regulation and function (14 papers). The work is most often cited by research in Cellular and Molecular Neuroscience (738 citations), Behavioral Neuroscience (94 citations) and Biological Psychiatry (47 citations). Boris Mlinar has collaborated with scholars based in Italy, United States and Germany. Frequent co-authors include John J. Enyeart, Renato Corradetti, B. A. Biagi, Judith A. Enyeart, Cornelius T. Gross, Alberto Montalbano, Enrica Audero, Klaus‐Peter Lesch, Raffaella Morini and Naozumi Araragi. Their work appears in journals such as Science, Journal of Biological Chemistry and Journal of Neuroscience.
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.