Sam A. Booker

1.5k total citations
41 papers, 862 citations indexed

About

Sam A. Booker is a scholar working on Cellular and Molecular Neuroscience, Cognitive Neuroscience and Molecular Biology. According to data from OpenAlex, Sam A. Booker has authored 41 papers receiving a total of 862 indexed citations (citations by other indexed papers that have themselves been cited), including 32 papers in Cellular and Molecular Neuroscience, 20 papers in Cognitive Neuroscience and 17 papers in Molecular Biology. Recurrent topics in Sam A. Booker's work include Neuroscience and Neuropharmacology Research (31 papers), Neural dynamics and brain function (12 papers) and Neuroinflammation and Neurodegeneration Mechanisms (10 papers). Sam A. Booker is often cited by papers focused on Neuroscience and Neuropharmacology Research (31 papers), Neural dynamics and brain function (12 papers) and Neuroinflammation and Neurodegeneration Mechanisms (10 papers). Sam A. Booker collaborates with scholars based in United Kingdom, Germany and India. Sam A. Booker's co-authors include Imre Vida, David J. A. Wyllie, Peter C. Kind, Ákos Kulik, Marlene Bartos, Claudio Elgueta, Thomas Meyer, Shakuntala Savanthrapadian, John Isaac and Masahiko Watanabe and has published in prestigious journals such as Nature Communications, Journal of Neuroscience and The Journal of Physiology.

In The Last Decade

Sam A. Booker

38 papers receiving 850 citations

Peers

Sam A. Booker
Gisella Vetere Italy
Shannon Farris United States
Vivek Mahadevan Canada
Isabel del Pino Spain
Jayms D. Peterson United States
Giada Spigolon Sweden
Amy A. Arguello United States
António Pinto‐Duarte United States
Brent Asrican United States
Gisella Vetere Italy
Sam A. Booker
Citations per year, relative to Sam A. Booker Sam A. Booker (= 1×) peers Gisella Vetere

Countries citing papers authored by Sam A. Booker

Since Specialization
Citations

This map shows the geographic impact of Sam A. Booker'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 Sam A. Booker with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sam A. Booker more than expected).

Fields of papers citing papers by Sam A. Booker

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Sam A. Booker. 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 Sam A. Booker. The network helps show where Sam A. Booker may publish in the future.

Co-authorship network of co-authors of Sam A. Booker

This figure shows the co-authorship network connecting the top 25 collaborators of Sam A. Booker. A scholar is included among the top collaborators of Sam A. Booker 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 Sam A. Booker. Sam A. Booker is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Meftah, S., Robert I. McGeachan, Christopher J. A. Cowie, et al.. (2025). Phylogenetic divergence of GABAB receptor signaling in neocortical networks over adult life. Nature Communications. 16(1). 4194–4194.
2.
McGeachan, Robert I., S. Meftah, James H. Catterson, et al.. (2025). Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures. Nature Communications. 16(1). 3753–3753. 2 indexed citations
3.
McGeachan, Robert I., S. Meftah, Jamie Rose, et al.. (2024). p-tau Ser356 is associated with Alzheimer’s disease pathology and is lowered in brain slice cultures using the NUAK inhibitor WZ4003. Acta Neuropathologica. 147(1). 7–7. 15 indexed citations
4.
5.
Watson, Thomas C. & Sam A. Booker. (2024). Somatostatin Interneurons Recruit Pre- and Postsynaptic GABABReceptors in the Adult Mouse Dentate Gyrus. eNeuro. 11(8). ENEURO.0115–24.2024. 2 indexed citations
6.
Vida, Imre, et al.. (2024). Postsynaptic GABAB‐receptor mediated currents in diverse dentate gyrus interneuron types. Hippocampus. 34(10). 551–562. 1 indexed citations
7.
O’Leary, Heather, Elizabeth C. Davenport, Paul Baxter, et al.. (2024). Enhanced hippocampal LTP but normal NMDA receptor and AMPA receptor function in a rat model of CDKL5 deficiency disorder. Molecular Autism. 15(1). 28–28. 4 indexed citations
8.
Levenstein, Daniel, et al.. (2024). Hyperpolarization-activated currents drive neuronal activation sequences in sleep. Current Biology. 34(14). 3043–3054.e8. 3 indexed citations
9.
Yang, Yifei, Sam A. Booker, Owen Dando, et al.. (2023). Identifying foetal forebrain interneurons as a target for monogenic autism risk factors and the polygenic 16p11.2 microdeletion. BMC Neuroscience. 24(1). 5–5. 3 indexed citations
10.
Alusi, Ghassan, Elizabeth Berry‐Kravis, David L. Nelson, Lauren L. Orefice, & Sam A. Booker. (2022). Emerging Therapeutic Strategies for Fragile X Syndrome: Q&A. ACS Chemical Neuroscience. 13(24). 3544–3546. 1 indexed citations
11.
Zoupi, Lida, Sam A. Booker, Dimitri Eigel, et al.. (2021). Selective vulnerability of inhibitory networks in multiple sclerosis. Acta Neuropathologica. 141(3). 415–429. 40 indexed citations
12.
Booker, Sam A. & David J. A. Wyllie. (2021). NMDA receptor function in inhibitory neurons. Neuropharmacology. 196. 108609–108609. 23 indexed citations
13.
Booker, Sam A., Owen Dando, Adam D. Jackson, et al.. (2020). Input-Output Relationship of CA1 Pyramidal Neurons Reveals Intact Homeostatic Mechanisms in a Mouse Model of Fragile X Syndrome. Cell Reports. 32(6). 107988–107988. 37 indexed citations
14.
Booker, Sam A., Owen Dando, Adam D. Jackson, et al.. (2019). Altered dendritic spine function and integration in a mouse model of fragile X syndrome. Nature Communications. 10(1). 4813–4813. 45 indexed citations
15.
Booker, Sam A., et al.. (2019). Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex. Nature Communications. 10(1). 4814–4814. 32 indexed citations
16.
Booker, Sam A., Desirée Loreth, Masahiko Watanabe, et al.. (2018). Postsynaptic GABABRs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons. Cell Reports. 22(1). 36–43. 36 indexed citations
17.
Booker, Sam A. & Imre Vida. (2018). Morphological diversity and connectivity of hippocampal interneurons. Cell and Tissue Research. 373(3). 619–641. 127 indexed citations
18.
Booker, Sam A., Nuno Pires, Stuart Cobb, Patrício Soares‐da‐Silva, & Imre Vida. (2015). Carbamazepine and oxcarbazepine, but not eslicarbazepine, enhance excitatory synaptic transmission onto hippocampal CA1 pyramidal cells through an antagonist action at adenosine A1 receptors. Neuropharmacology. 93. 103–115. 23 indexed citations
19.
Booker, Sam A., Jie Song, & Imre Vida. (2014). Whole-cell Patch-clamp Recordings from Morphologically- and Neurochemically-identified Hippocampal Interneurons. Journal of Visualized Experiments. e51706–e51706. 30 indexed citations
20.
Booker, Sam A., Anna Gross, Daniel Althof, et al.. (2013). Differential GABAB-Receptor-Mediated Effects in Perisomatic- and Dendrite-Targeting Parvalbumin Interneurons. Journal of Neuroscience. 33(18). 7961–7974. 46 indexed citations

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.

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