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\n \n\n \n \n \n \n \n \n Meta-analysis of the comparative efficacy of benzodiazepines and antidepressants for psychic versus somatic symptoms of generalized anxiety disorder.\n \n \n \n \n\n\n \n Beyer, C.; Currin, C. B.; Williams, T.; and Stein, D. J.\n\n\n \n\n\n\n Comprehensive Psychiatry,152479. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Meta-analysis$ Paper\n \n \n \n $\"Meta-analysis$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{beyer_meta-analysis_2024,\n\ttitle = {Meta-analysis of the comparative efficacy of benzodiazepines and antidepressants for psychic versus somatic symptoms of generalized anxiety disorder},\n\tcopyright = {All rights reserved},\n\tissn = {0010-440X},\n\turl = {https://www.sciencedirect.com/science/article/pii/S0010440X24000300},\n\tdoi = {10.1016/j.comppsych.2024.152479},\n\tabstract = {Background\nBenzodiazepines and antidepressants are effective agents for the treatment of generalized anxiety disorder (GAD), with the HAM-A frequently used as a primary outcome measure. The GAD literature is inconsistent regarding which medications are more effective for somatic versus psychic symptoms of GAD, and treatment guidelines do not advocate for prescribing based on subtype. This meta-analysis aimed to determine whether benzodiazepines and antidepressants have a differential impact on the somatic versus psychic subscales of the HAM-A in GAD.\nMethods\nAn electronic search was undertaken for randomized controlled trials of either benzodiazepines or antidepressants for GAD that reported treatment response using the HAM-A subscales. Data were extracted by independent reviewers. A random effects assessment of weighted mean difference with 95\\% confidence intervals and subgroup difference was applied. All analysis was done on SPSS 26. An assessment of bias, and of quality of evidence was performed.\nResults\n24 randomized controlled trials met the inclusion criteria: 18 antidepressant trials, 5 benzodiazepine trials and 1 of both. 14 studies were assessed as having between some and high risk of bias, while 10 were assessed as having low risk of bias. Benzodiazepines (WMD of 1.81 [CI 1.03, 2.58]) were significantly more effective than antidepressants (WMD of 0.83 [CI 0.64, 1.02]) for reducing somatic symptoms of GAD (Chi2 = 5.81, p = 0.02), and were also more effective (WMD of 2.46 [CI 1.83, 3.09]) in reducing psychic symptoms than antidepressants (WMD of 1.83 [CI 1.55, 2.10]), although this comparison did not reach statistical significance (Chi2 = 3.31, p = 0.07).\nConclusion\nThe finding that benzodiazepines were significantly more effective than antidepressants for somatic symptoms needs to be weighed up against potential benefits of antidepressants over benzodiazepines. It may be useful for future treatment guidelines for GAD to explicitly consider symptom subtype.},\n\turldate = {2024-03-29},\n\tjournal = {Comprehensive Psychiatry},\n\tauthor = {Beyer, Chad and Currin, Christopher B. and Williams, Taryn and Stein, Dan J.},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {152479},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/MPR9P6HP/file/view}\n}\n\n\n\n

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\n Background Benzodiazepines and antidepressants are effective agents for the treatment of generalized anxiety disorder (GAD), with the HAM-A frequently used as a primary outcome measure. The GAD literature is inconsistent regarding which medications are more effective for somatic versus psychic symptoms of GAD, and treatment guidelines do not advocate for prescribing based on subtype. This meta-analysis aimed to determine whether benzodiazepines and antidepressants have a differential impact on the somatic versus psychic subscales of the HAM-A in GAD. Methods An electronic search was undertaken for randomized controlled trials of either benzodiazepines or antidepressants for GAD that reported treatment response using the HAM-A subscales. Data were extracted by independent reviewers. A random effects assessment of weighted mean difference with 95% confidence intervals and subgroup difference was applied. All analysis was done on SPSS 26. An assessment of bias, and of quality of evidence was performed. Results 24 randomized controlled trials met the inclusion criteria: 18 antidepressant trials, 5 benzodiazepine trials and 1 of both. 14 studies were assessed as having between some and high risk of bias, while 10 were assessed as having low risk of bias. Benzodiazepines (WMD of 1.81 [CI 1.03, 2.58]) were significantly more effective than antidepressants (WMD of 0.83 [CI 0.64, 1.02]) for reducing somatic symptoms of GAD (Chi2 = 5.81, p = 0.02), and were also more effective (WMD of 2.46 [CI 1.83, 3.09]) in reducing psychic symptoms than antidepressants (WMD of 1.83 [CI 1.55, 2.10]), although this comparison did not reach statistical significance (Chi2 = 3.31, p = 0.07). Conclusion The finding that benzodiazepines were significantly more effective than antidepressants for somatic symptoms needs to be weighed up against potential benefits of antidepressants over benzodiazepines. It may be useful for future treatment guidelines for GAD to explicitly consider symptom subtype.\n

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\n \n\n \n \n \n \n \n \n Ten simple rules for pushing boundaries of inclusion at academic events.\n \n \n \n \n\n\n \n Hall, S. M.; Kochin, D.; Carne, C.; Herterich, P.; Lewers, K. L.; Abdelhack, M.; Ramasubramanian, A.; Alphonse, J. F. M.; Ung, V.; El-Gebali, S.; Currin, C. B.; Plomp, E.; Thompson, R.; and Sharan, M.\n\n\n \n\n\n\n PLOS Computational Biology, 20(3): e1011797. March 2024.\n Publisher: Public Library of Science\n\n\n\n
\n\n\n\n \n \n $\"Ten$ Paper\n \n \n \n $\"Ten$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hall_ten_2024,\n\ttitle = {Ten simple rules for pushing boundaries of inclusion at academic events},\n\tvolume = {20},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\tissn = {1553-7358},\n\turl = {https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1011797},\n\tdoi = {10.1371/journal.pcbi.1011797},\n\tabstract = {Inclusion at academic events is facing increased scrutiny as the communities these events serve raise their expectations for who can practically attend. Active efforts in recent years to bring more diversity to academic events have brought progress and created momentum. However, we must reflect on these efforts and determine which underrepresented groups are being disadvantaged. Inclusion at academic events is important to ensure diversity of discourse and opinion, to help build networks, and to avoid academic siloing. All of these contribute to the development of a robust and resilient academic field. We have developed these Ten Simple Rules both to amplify the voices that have been speaking out and to celebrate the progress of many Equity, Diversity, and Inclusivity practices that continue to drive the organisation of academic events. The Rules aim to raise awareness as well as provide actionable suggestions and tools to support these initiatives further. This aims to support academic organisations such as the Deep Learning Indaba, Neuromatch Academy, the IBRO-Simons Computational Neuroscience Imbizo, Biodiversity Information Standards (TDWG), Arabs in Neuroscience, FAIRPoints, and OLS (formerly Open Life Science). This article is a call to action for organisers to reevaluate the impact and reach of their inclusive practices.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2024-03-04},\n\tjournal = {PLOS Computational Biology},\n\tauthor = {Hall, Siobhan Mackenzie and Kochin, Daniel and Carne, Carmel and Herterich, Patricia and Lewers, Kristen Lenay and Abdelhack, Mohamed and Ramasubramanian, Arun and Alphonse, Juno Felecia Michael and Ung, Visotheary and El-Gebali, Sara and Currin, Christopher Brian and Plomp, Esther and Thompson, Rachel and Sharan, Malvika},\n\tmonth = mar,\n\tyear = {2024},\n\tnote = {Publisher: Public Library of Science},\n\tpages = {e1011797},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/M2NMV974/file/view}\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A structurally precise mechanism links an epilepsy-associated KCNC2 potassium channel mutation to interneuron dysfunction.\n \n \n \n \n\n\n \n Clatot, J.; Currin, C. B.; Liang, Q.; Pipatpolkai, T.; Massey, S. L.; Helbig, I.; Delemotte, L.; Vogels, T. P.; Covarrubias, M.; and Goldberg, E. M.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 121(3): e2307776121. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n \n $\"A$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{clatot_structurally_2024,\n\ttitle = {A structurally precise mechanism links an epilepsy-associated \\textit{{KCNC2}} potassium channel mutation to interneuron dysfunction},\n\tvolume = {121},\n\tcopyright = {All rights reserved},\n\tissn = {0027-8424, 1091-6490},\n\turl = {https://pnas.org/doi/10.1073/pnas.2307776121},\n\tdoi = {10.1073/pnas.2307776121},\n\tabstract = {De novo heterozygous variants in\n              KCNC2\n              encoding the voltage-gated potassium (K\n              +\n              ) channel subunit Kv3.2 are a recently described cause of developmental and epileptic encephalopathy (DEE). A de novo variant in\n              KCNC2\n              c.374G {\\textgreater} A (p.Cys125Tyr) was identified via exome sequencing in a patient with DEE. Relative to wild-type Kv3.2, Kv3.2-p.Cys125Tyr induces K\n              +\n              currents exhibiting a large hyperpolarizing shift in the voltage dependence of activation, accelerated activation, and delayed deactivation consistent with a relative stabilization of the open conformation, along with increased current density. Leveraging the cryogenic electron microscopy (cryo-EM) structure of Kv3.1, molecular dynamic simulations suggest that a strong π-π stacking interaction between the variant Tyr125 and Tyr156 in the α-6 helix of the T1 domain promotes a relative stabilization of the open conformation of the channel, which underlies the observed gain of function. A multicompartment computational model of a Kv3-expressing parvalbumin-positive cerebral cortex fast-spiking γ-aminobutyric acidergic (GABAergic) interneuron (PV-IN) demonstrates how the Kv3.2-Cys125Tyr variant impairs neuronal excitability and dysregulates inhibition in cerebral cortex circuits to explain the resulting epilepsy.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2024-01-10},\n\tjournal = {Proceedings of the National Academy of Sciences},\n\tauthor = {Clatot, Jerome and Currin, Christopher B. and Liang, Qiansheng and Pipatpolkai, Tanadet and Massey, Shavonne L. and Helbig, Ingo and Delemotte, Lucie and Vogels, Tim P. and Covarrubias, Manuel and Goldberg, Ethan M.},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {e2307776121},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/T9SKK786/file/view}\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Altered childhood brain development in autism and epilepsy.\n \n \n \n \n\n\n \n Currin, C. B.; and Beyer, C.\n\n\n \n\n\n\n In Halpern-Felsher, B., editor(s), Encyclopedia of Child and Adolescent Health (First Edition), pages 86–98. Academic Press, Oxford, January 2023.\n \n\n\n\n
\n\n\n\n \n \n $\"Altered$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@incollection{currin_altered_2023,\n\taddress = {Oxford},\n\ttitle = {Altered childhood brain development in autism and epilepsy},\n\tcopyright = {All rights reserved},\n\tisbn = {978-0-12-818873-6},\n\turl = {https://www.sciencedirect.com/science/article/pii/B9780128188729001291},\n\tabstract = {Autism spectrum disorder (ASD) and epilepsy are frequently comorbid neurodevelopmental disorders. Extensive research has demonstrated shared pathological pathways, etiologies, and phenotypes. Many risk factors for these disorders, like genetic mutations and environmental pressures, are linked to changes in childhood brain development, which is a critical period for their manifestation. Decades of research have yielded many signatures for ASD and epilepsy, some shared and others unique or opposing. The anatomical, physiological, and behavioral correlates of these disorders are discussed in this chapter in the context of understanding shared pathological pathways. We end with important takeaways on the presentation, prevention, intervention, and policy changes for ASD and epilepsy. This chapter aims to explore the complexity of these disorders, both in etiology and phenotypes, with the further goal of appreciating the expanse of unknowns still to explore about the brain.},\n\turldate = {2023-12-16},\n\tbooktitle = {Encyclopedia of {Child} and {Adolescent} {Health} ({First} {Edition})},\n\tpublisher = {Academic Press},\n\tauthor = {Currin, Christopher Brian and Beyer, Chad},\n\teditor = {Halpern-Felsher, Bonnie},\n\tmonth = jan,\n\tyear = {2023},\n\tdoi = {10.1016/B978-0-12-818872-9.00129-1},\n\tpages = {86--98},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A Framework for Grassroots Research Collaboration in Machine Learning and Global Health.\n \n \n \n \n\n\n \n Currin, C. B.; Asiedu, M. N.; Fourie, C.; Rosman, B.; Turki, H.; Siam, M.; Tonja, A. L.; Abbott, J.; Ajala, M.; Adedayo, S. A.; Emezue, C. C.; and Machangara, D.\n\n\n \n\n\n\n In International Conference on Learning Representations 2023, 2023. \n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n \n $\"A$ paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@inproceedings{currin_framework_2023,\n\ttitle = {A {Framework} for {Grassroots} {Research} {Collaboration} in {Machine} {Learning} and {Global} {Health}},\n\tcopyright = {Creative Commons Attribution-ShareAlike 4.0 International License (CC-BY-SA)},\n\turl = {https://openreview.net/forum?id=jHY_G91R880},\n\tabstract = {Traditional top-down approaches for global health have historically failed to achieve social progress (Hoffman et al., 2015; Hoffman \\& Røttingen, 2015). However, recently, a more holistic, multi-level approach, One Health (OH) (Osterhaus et al., 2020), is being adopted. Several challenges have been identified for the implementation of OH (dos S. Ribeiro et al., 2019), including policy and funding, education and training, and multi-actor, multi-domain, and multi-level collaborations. This is despite the increasing accessibility to knowledge and digital research tools through the internet. To address some of these challenges, we propose a general framework for grassroots community-based means of participatory research. Additionally, we present a specific roadmap to create a Machine Learning for Global Health community in Africa. The proposed framework aims to enable any small group of individuals with scarce resources to build and sustain an online community within approximately two years. We provide a discussion of the potential impact of the proposed framework on global health research collaborations.},\n\tlanguage = {en},\n\tbooktitle = {International {Conference} on {Learning} {Representations} 2023},\n\tauthor = {Currin, Christopher Brian and Asiedu, Mercy Nyamewaa and Fourie, Chris and Rosman, Benjamin and Turki, Houcemeddine and Siam, Mennatullah and Tonja, Atnafu Lambebo and Abbott, Jade and Ajala, Marvellous and Adedayo, Sadiq Adewale and Emezue, Chris Chinenye and Machangara, Daphne},\n\tyear = {2023},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/EP4ETULP/file/view}\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Machine Learning for Healthcare: A Bibliometric Study of Contributions from Africa.\n \n \n \n \n\n\n \n Turki, H.; Pouris, A.; Ifeanyichukwu, F. M.; Namayega, C.; Taieb, M. A. H.; Adedayo, S. A.; Fourie, C.; Currin, C. B.; Asiedu, M. N.; Tonja, A. L.; Owodunni, A. T.; Dere, A.; Emezue, C. C.; Muhammad, S. H.; Isa, M. M.; and Aouicha, M. B.\n\n\n \n\n\n\n February 2023.\n \n\n\n\n
\n\n\n\n \n \n $\"Machine$ Paper\n \n \n \n $\"Machine$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@misc{turki_machine_2023,\n\ttitle = {Machine {Learning} for {Healthcare}: {A} {Bibliometric} {Study} of {Contributions} from {Africa}},\n\tcopyright = {All rights reserved},\n\tshorttitle = {Machine {Learning} for {Healthcare}},\n\turl = {https://www.preprints.org/manuscript/202302.0010/v1},\n\tdoi = {10.20944/preprints202302.0010.v1},\n\tabstract = {Machine learning has seen enormous growth in the last decade, with healthcare being a prime application for advanced diagnostics and improved patient care. The application of machine learning for healthcare is particularly pertinent in Africa, where many countries are resource-scarce. However, it is unclear how much research on this topic is arising from African institutes themselves, which is a crucial aspect for applications of machine learning to unique contexts and challenges on the continent. Here, we conduct a bibliometric study of African contributions to research publications related to machine learning for healthcare, as indexed in Scopus, between 1993 and 2022. We identified 3,772 research outputs, with most of these published since 2020. North African countries currently lead the way with 64.5\\% of publications for the reported period, yet Sub-Saharan Africa is rapidly increasing its output. We found that international support in the form of funding and collaborations is correlated with research output generally for the continent, with local support garnering less attention. Understanding African research contributions to machine learning for healthcare is a crucial first step in surveying the broader academic landscape, forming stronger research communities, and providing advanced and contextually aware biomedical access to Africa.},\n\tlanguage = {en},\n\turldate = {2023-03-03},\n\tpublisher = {Preprints},\n\tauthor = {Turki, Houcemeddine and Pouris, Anastassios and Ifeanyichukwu, Francis-Alfred Michaelangelo and Namayega, Catherine and Taieb, Mohamed Ali Hadj and Adedayo, Sadiq Adewale and Fourie, Chris and Currin, Christopher Brian and Asiedu, Mercy Nyamewaa and Tonja, Atnafu Lambebo and Owodunni, Abraham Toluwase and Dere, Abdulhameed and Emezue, Chris Chinenye and Muhammad, Shamsuddeen Hassan and Isa, Muhammad Musa and Aouicha, Mohamed Ben},\n\tmonth = feb,\n\tyear = {2023},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/XPGFC3VY/file/view}\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability.\n \n \n \n \n\n\n \n Currin, C. B.; and Raimondo, J. V.\n\n\n \n\n\n\n PLOS Computational Biology, 18(9): e1010534. September 2022.\n Publisher: Public Library of Science\n\n\n\n
\n\n\n\n \n \n $\"Computational$ Paper\n \n \n \n $\"Computational$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{currin_computational_2022,\n\ttitle = {Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability},\n\tvolume = {18},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\tissn = {1553-7358},\n\turl = {https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1010534},\n\tdoi = {10.1371/journal.pcbi.1010534},\n\tabstract = {Many neurons in the mammalian central nervous system have complex dendritic arborisations and active dendritic conductances that enable these cells to perform sophisticated computations. How dendritically targeted inhibition affects local dendritic excitability is not fully understood. Here we use computational models of branched dendrites to investigate where GABAergic synapses should be placed to minimise dendritic excitability over time. To do so, we formulate a metric we term the “Inhibitory Level” (IL), which quantifies the effectiveness of synaptic inhibition for reducing the depolarising effect of nearby excitatory input. GABAergic synaptic inhibition is dependent on the reversal potential for GABAA receptors (EGABA), which is primarily set by the transmembrane chloride ion (Cl-) concentration gradient. We, therefore, investigated how variable EGABA and dynamic chloride affects dendritic inhibition. We found that the inhibitory effectiveness of dendritic GABAergic synapses combines at an encircled branch junction. The extent of this inhibitory accumulation is dependent on the number of branches and location of synapses but is independent of EGABA. This inhibitory accumulation occurs even for very distally placed inhibitory synapses when they are hyperpolarising–but not when they are shunting. When accounting for Cl- fluxes and dynamics in Cl- concentration, we observed that Cl- loading is detrimental to inhibitory effectiveness. This enabled us to determine the most inhibitory distribution of GABAergic synapses which is close to–but not at–a shared branch junction. This distribution balances a trade-off between a stronger combined inhibitory influence when synapses closely encircle a branch junction with the deleterious effects of increased Cl- by loading that occurs when inhibitory synapses are co-located.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2023-01-28},\n\tjournal = {PLOS Computational Biology},\n\tauthor = {Currin, Christopher Brian and Raimondo, Joseph Valentino},\n\tmonth = sep,\n\tyear = {2022},\n\tnote = {Publisher: Public Library of Science},\n\tpages = {e1010534},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/DQDDD7IV/file/view}\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Altered childhood brain development in Autism and Epilepsy.\n \n \n \n \n\n\n \n Currin, C. B.; and Beyer, C.\n\n\n \n\n\n\n In Reference Module in Biomedical Sciences, pages B9780128188729001291. Elsevier, 2022.\n \n\n\n\n
\n\n\n\n \n \n $\"Altered$ Paper\n \n \n \n $\"Altered$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@incollection{currin_altered_2022,\n\ttitle = {Altered childhood brain development in {Autism} and {Epilepsy}},\n\tcopyright = {All rights reserved},\n\tisbn = {978-0-12-801238-3},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/B9780128188729001291},\n\tlanguage = {en},\n\turldate = {2023-01-19},\n\tbooktitle = {Reference {Module} in {Biomedical} {Sciences}},\n\tpublisher = {Elsevier},\n\tauthor = {Currin, Christopher Brian and Beyer, Chad},\n\tyear = {2022},\n\tdoi = {10.1016/B978-0-12-818872-9.00129-1},\n\tpages = {B9780128188729001291},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/MIVBBVFA/file/view}\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Depolarization of echo chambers by random dynamical nudge.\n \n \n \n \n\n\n \n Currin, C. B.; Vera, S. V.; and Khaledi-Nasab, A.\n\n\n \n\n\n\n Scientific Reports, 12(1): 9234. June 2022.\n Number: 1 Publisher: Nature Publishing Group\n\n\n\n
\n\n\n\n \n \n $\"Depolarization$ Paper\n \n \n \n $\"Depolarization$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{currin_depolarization_2022,\n\ttitle = {Depolarization of echo chambers by random dynamical nudge},\n\tvolume = {12},\n\tcopyright = {2022 The Author(s)},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-022-12494-w},\n\tdoi = {10.1038/s41598-022-12494-w},\n\tabstract = {In social networks, users often engage with like-minded peers. This selective exposure to opinions might result in echo chambers, i.e., political fragmentation and social polarization of user interactions. When echo chambers form, opinions have a bimodal distribution with two peaks on opposite sides. In certain issues, where either extreme positions contain a degree of misinformation, neutral consensus is preferable for promoting discourse. In this paper, we use an opinion dynamics model that naturally forms echo chambers in order to find a feedback mechanism that bridges these communities and leads to a neutral consensus. We introduce the random dynamical nudge (RDN), which presents each agent with input from a random selection of other agents’ opinions and does not require surveillance of every person’s opinions. Our computational results in two different models suggest that the RDN leads to a unimodal distribution of opinions centered around the neutral consensus. Furthermore, the RDN is effective both for preventing the formation of echo chambers and also for depolarizing existing echo chambers. Due to the simple and robust nature of the RDN, social media networks might be able to implement a version of this self-feedback mechanism, when appropriate, to prevent the segregation of online communities on complex social issues.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2022-08-28},\n\tjournal = {Scientific Reports},\n\tauthor = {Currin, Christopher Brian and Vera, Sebastián Vallejo and Khaledi-Nasab, Ali},\n\tmonth = jun,\n\tyear = {2022},\n\tnote = {Number: 1\nPublisher: Nature Publishing Group},\n\tpages = {9234},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/H7BDD2PD/file/view}\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Developmentally regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of Dravet syndrome.\n \n \n \n \n\n\n \n Kaneko, K.; Currin, C. B.; Goff, K. M.; Wengert, E. R.; Somarowthu, A.; Vogels, T. P.; and Goldberg, E. M.\n\n\n \n\n\n\n Cell Reports, 38(13): 110580. March 2022.\n Publisher: Cell Press\n\n\n\n
\n\n\n\n \n \n $\"Developmentally$ Paper\n \n \n \n $\"Developmentally$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kaneko_developmentally_2022,\n\ttitle = {Developmentally regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of {Dravet} syndrome},\n\tvolume = {38},\n\tcopyright = {All rights reserved},\n\tissn = {22111247},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2211124722003242},\n\tdoi = {10.1016/j.celrep.2022.110580},\n\tabstract = {Dravet syndrome is a neurodevelopmental disorder characterized by epilepsy, intellectual disability, and sudden death due to pathogenic variants in SCN1A with loss of function of the sodium channel subunit Nav1.1. Nav1.1-expressing parvalbumin GABAergic interneurons (PV-INs) from young Scn1a+/− mice show impaired action potential generation. An approach assessing PV-IN function in the same mice at two time points shows impaired spike generation in all Scn1a+/− mice at postnatal days (P) 16–21, whether deceased prior or surviving to P35, with normalization by P35 in surviving mice. However, PV-IN synaptic transmission is dysfunctional in young Scn1a+/− mice that did not survive and in Scn1a+/− mice ≥ P35. Modeling confirms that PV-IN axonal propagation is more sensitive to decreased sodium conductance than spike generation. These results demonstrate dynamic dysfunction in Dravet syndrome: combined abnormalities of PV-IN spike generation and propagation drives early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology.},\n\tnumber = {13},\n\turldate = {2022-03-30},\n\tjournal = {Cell Reports},\n\tauthor = {Kaneko, Keisuke and Currin, Christopher B. and Goff, Kevin M. and Wengert, Eric R. and Somarowthu, Ala and Vogels, Tim P. and Goldberg, Ethan M.},\n\tmonth = mar,\n\tyear = {2022},\n\tnote = {Publisher: Cell Press},\n\tpages = {110580},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/IHNZ48PJ/file/view}\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n 2021\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability.\n \n \n \n \n\n\n \n Currin, C. B.; and Raimondo, J. V.\n\n\n \n\n\n\n bioRxiv,1–29. 2021.\n \n\n\n\n
\n\n\n\n \n \n $\"Computational$ Paper\n \n \n \n $\"Computational$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{currin_computational_2021,\n\ttitle = {Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\turl = {https://www.biorxiv.org/content/10.1101/2021.12.07.471404v1},\n\tdoi = {10.1101/2021.12.07.471404v1},\n\tabstract = {Many neurons in the mammalian central nervous system have complex dendritic arborisations and active dendritic conductances that enable these cells to perform sophisticated computations. How dendritically targeted inhibition affects local dendritic excitability is not fully understood. Here we use computational models of branched dendrites to investigate where GABAergic synapses should be placed to minimise dendritic excitability over time. To do so, we formulate a metric we term the “Inhibitory Level” (IL), which quantifies the effectiveness of synaptic inhibition for reducing the depolarising effect of nearby excitatory input. GABAergic synaptic inhibition is dependent on the reversal potential for GABAA receptors (EGABA), which is primarily set by the transmembrane chloride ion (Cl-) concentration gradient. We, therefore, investigated how variable EGABA and dynamic chloride affects dendritic inhibition. We found that the inhibitory effectiveness of dendritic GABAergic synapses accumulates at an encircled branch junction. The extent of inhibitory accumulation is dependent on the number of branches and location of synapses but is independent of EGABA. This accumulation occurs even for very distally placed inhibitory synapses when they are hyperpolarising – but not when they are shunting. When accounting for Cl- fluxes and dynamics in Cl- concentration, we observed that Cl- loading is detrimental to inhibitory effectiveness. This enabled us to determine the most inhibitory distribution of GABAergic synapses which is close to – but not at – a shared branch junction. This distribution balances a trade-off between a stronger combined inhibitory influence when synapses closely encircle a branch junction with the deleterious effects of increased Cl- loading that occurs when inhibitory synapses are co-located.},\n\tjournal = {bioRxiv},\n\tauthor = {Currin, Christopher Brian and Raimondo, Joseph Valentino},\n\tyear = {2021},\n\tpages = {1--29},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/DLTDEBUJ/file/view}\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Depolarization of echo chambers by random dynamical nudge.\n \n \n \n \n\n\n \n Currin, C. B.; Vera, S. V.; and Khaledi-Nasab, A.\n\n\n \n\n\n\n arXiv. January 2021.\n arXiv: 2101.04079\n\n\n\n
\n\n\n\n \n \n $\"Depolarization$ Paper\n \n \n \n $\"Depolarization$ paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{currin_depolarization_2021,\n\ttitle = {Depolarization of echo chambers by random dynamical nudge},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\turl = {http://arxiv.org/abs/2101.04079},\n\tabstract = {Interactions among individuals in social networks lead to echo chambers where the distribution of opinions follows a bimodal distribution with two peaks at the opposite extremes. In issues with clear answers, such as global warming, one of the echo chambers reflects an inaccurate judgment, potentially from misinformation. However, in issues without clear answers such as elections, the neutral consensus is preferable for promoting discourse. In this letter, we use an opinion dynamics model to study the effect of a random dynamical nudge where we present random input to each agent from the other individuals in the network. We show that random dynamical nudge disallows the formation of echo chambers and leads to a normal distribution of opinions centered around the neutral consensus. The random dynamical nudge relies on the collective dynamics and it does not require surveillance of every person's opinions. Social media networks could implement a version of this self-feedback mechanism to prevent the formation of segregated online communities on pressing issues such as elections.},\n\turldate = {2021-07-19},\n\tjournal = {arXiv},\n\tauthor = {Currin, Christopher Brian and Vera, Sebastian Vallejo and Khaledi-Nasab, Ali},\n\tmonth = jan,\n\tyear = {2021},\n\tnote = {arXiv: 2101.04079},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/IT25JTDC/file/view}\n}\n\n\n\n

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\n \n 2020\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Chloride dynamics alter the input-output properties of neurons.\n \n \n \n \n\n\n \n Currin, C. B.; Trevelyan, A. J.; Akerman, C. J.; and Raimondo, J. V.\n\n\n \n\n\n\n PLoS Computational Biology, 16(5): e1007932. May 2020.\n Publisher: Public Library of Science\n\n\n\n
\n\n\n\n \n \n $\"Chloride$ Paper\n \n \n \n $\"Chloride$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 13 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{currin_chloride_2020,\n\ttitle = {Chloride dynamics alter the input-output properties of neurons},\n\tvolume = {16},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\tissn = {1553-7358},\n\turl = {https://dx.plos.org/10.1371/journal.pcbi.1007932},\n\tdoi = {10.1371/journal.pcbi.1007932},\n\tabstract = {Fast synaptic inhibition is a critical determinant of neuronal output, with subcellular targeting of synaptic inhibition able to exert different transformations of the neuronal input-output function. At the receptor level, synaptic inhibition is primarily mediated by chloride-permeable Type A GABA receptors. Consequently, dynamics in the neuronal chloride concentration can alter the functional properties of inhibitory synapses. How differences in the spatial targeting of inhibitory synapses interact with intracellular chloride dynamics to modulate the input-output function of neurons is not well understood. To address this, we developed computational models of multi-compartment neurons that incorporate experimentally parametrised mechanisms to account for neuronal chloride influx, diffusion, and extrusion. We found that synaptic input (either excitatory, inhibitory, or both) can lead to subcellular variations in chloride concentration, despite a uniform distribution of chloride extrusion mechanisms. Accounting for chloride changes resulted in substantial alterations in the neuronal input-output function. This was particularly the case for peripherally targeted dendritic inhibition where dynamic chloride compromised the ability of inhibition to offset neuronal input-output curves. Our simulations revealed that progressive changes in chloride concentration mean that the neuronal input-output function is not static but varies significantly as a function of the duration of synaptic drive. Finally, we found that the observed effects of dynamic chloride on neuronal output were mediated by changes in the dendritic reversal potential for GABA. Our findings provide a framework for understanding the computational effects of chloride dynamics on dendritically targeted synaptic inhibition.},\n\tnumber = {5},\n\turldate = {2020-06-09},\n\tjournal = {PLoS Computational Biology},\n\tauthor = {Currin, Christopher B. and Trevelyan, Andrew J. and Akerman, Colin J. and Raimondo, Joseph V.},\n\teditor = {Berry, Hugues},\n\tmonth = may,\n\tyear = {2020},\n\tnote = {Publisher: Public Library of Science},\n\tpages = {e1007932},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/EJSF7UMI/file/view}\n}\n\n\n\n\n\n\n\n

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\n \n 2019\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Chloride dynamics alter the input-output properties of neurons.\n \n \n \n \n\n\n \n Currin, C. B.; Trevelyan, A. J.; Akerman, C. J.; and Raimondo, J. V.\n\n\n \n\n\n\n bioRxiv,710277. July 2019.\n Publisher: Cold Spring Harbor Laboratory\n\n\n\n
\n\n\n\n \n \n $\"Chloride$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{currin_chloride_2019,\n\ttitle = {Chloride dynamics alter the input-output properties of neurons},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\tdoi = {10.1101/710277},\n\tabstract = {Fast synaptic inhibition is a critical determinant of neuronal output, with subcellular targeting of synaptic inhibition able to exert different transformations of the neuronal input-output function. At the receptor level, synaptic inhibition is primarily mediated by chloride-permeable Type A GABA receptors. Consequently, dynamics in the neuronal chloride concentration can alter the functional properties of inhibitory synapses. How differences in the spatial targeting of inhibitory synapses interact with intracellular chloride dynamics to modulate the input-output function of neurons is not well understood. To address this, we developed computational models of multi-compartment neurons that incorporate experimentally parametrised mechanisms to account for neuronal chloride influx, diffusion, and extrusion. We found that synaptic input (either excitatory, inhibitory, or both) can lead to subcellular variations in chloride concentration, despite a uniform distribution of chloride extrusion mechanisms. Accounting for chloride changes resulted in substantial alterations in the neuronal input-output function. This was particularly the case for peripherally targeted dendritic inhibition where dynamic chloride compromised the ability of inhibition to offset neuronal input-output curves. Our simulations revealed that progressive changes in chloride concentration mean that the neuronal input-output function is not static but varies significantly as a function of the duration of synaptic drive. Finally, we found that the observed effects of dynamic chloride on neuronal output were entirely mediated by changes in the dendritic reversal potential for GABA. Our findings provide a framework for understanding the computational effects of chloride dynamics on dendritically targeted synaptic inhibition.\n\nAuthor Summary The fundamental unit of computation in the brain is the neuron, whose output reflects information within the brain. A determining factor in the transfer and processing of information in the brain is the modulation of activity by inhibitory synaptic inputs. Fast synaptic inhibition is mediated by the neurotransmitter GABA binding to GABAA receptors, which are permeable to chloride ions. How changes in chloride ion concentration affect neuronal output is an important consideration for information flow in the brain that is currently not being thoroughly investigated. In this research, we used multi-compartmental models of neurons to link the deleterious effects that accumulation of chloride ions can have on inhibitory signalling with changes in neuronal ouput. Together, our results highlight the importance of accounting for changes in chloride concentration in theoretical and computer-based models that seek to explore the computational properties of inhibition.},\n\turldate = {2019-12-08},\n\tjournal = {bioRxiv},\n\tauthor = {Currin, Christopher B. and Trevelyan, Andrew J. and Akerman, Colin J. and Raimondo, Joseph V.},\n\tmonth = jul,\n\tyear = {2019},\n\tnote = {Publisher: Cold Spring Harbor Laboratory},\n\tpages = {710277},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/E62V9IRC/file/view}\n}\n\n\n\n

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\n Fast synaptic inhibition is a critical determinant of neuronal output, with subcellular targeting of synaptic inhibition able to exert different transformations of the neuronal input-output function. At the receptor level, synaptic inhibition is primarily mediated by chloride-permeable Type A GABA receptors. Consequently, dynamics in the neuronal chloride concentration can alter the functional properties of inhibitory synapses. How differences in the spatial targeting of inhibitory synapses interact with intracellular chloride dynamics to modulate the input-output function of neurons is not well understood. To address this, we developed computational models of multi-compartment neurons that incorporate experimentally parametrised mechanisms to account for neuronal chloride influx, diffusion, and extrusion. We found that synaptic input (either excitatory, inhibitory, or both) can lead to subcellular variations in chloride concentration, despite a uniform distribution of chloride extrusion mechanisms. Accounting for chloride changes resulted in substantial alterations in the neuronal input-output function. This was particularly the case for peripherally targeted dendritic inhibition where dynamic chloride compromised the ability of inhibition to offset neuronal input-output curves. Our simulations revealed that progressive changes in chloride concentration mean that the neuronal input-output function is not static but varies significantly as a function of the duration of synaptic drive. Finally, we found that the observed effects of dynamic chloride on neuronal output were entirely mediated by changes in the dendritic reversal potential for GABA. Our findings provide a framework for understanding the computational effects of chloride dynamics on dendritically targeted synaptic inhibition. Author Summary The fundamental unit of computation in the brain is the neuron, whose output reflects information within the brain. A determining factor in the transfer and processing of information in the brain is the modulation of activity by inhibitory synaptic inputs. Fast synaptic inhibition is mediated by the neurotransmitter GABA binding to GABAA receptors, which are permeable to chloride ions. How changes in chloride ion concentration affect neuronal output is an important consideration for information flow in the brain that is currently not being thoroughly investigated. In this research, we used multi-compartmental models of neurons to link the deleterious effects that accumulation of chloride ions can have on inhibitory signalling with changes in neuronal ouput. Together, our results highlight the importance of accounting for changes in chloride concentration in theoretical and computer-based models that seek to explore the computational properties of inhibition.\n

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\n \n\n \n \n \n \n \n \n Think: Theory for Africa.\n \n \n \n \n\n\n \n Currin, C. B.; Khoza, P. N.; Antrobus, A. D.; Latham, P. E.; Vogels, T. P.; and Raimondo, J. V.\n\n\n \n\n\n\n PLoS Computational Biology, 15(7): e1007049. July 2019.\n Publisher: Public Library of Science\n\n\n\n
\n\n\n\n \n \n $\"Think:$ Paper\n \n \n \n $\"Think:$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n \n \n 3 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{Currin2019a,\n\ttitle = {Think: {Theory} for {Africa}},\n\tvolume = {15},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\turl = {http://dx.plos.org/10.1371/journal.pcbi.1007049},\n\tdoi = {10.1371/journal.pcbi.1007049},\n\tnumber = {7},\n\turldate = {2019-07-18},\n\tjournal = {PLoS Computational Biology},\n\tauthor = {Currin, Christopher B. and Khoza, Phumlani N. and Antrobus, Alexander D. and Latham, Peter E. and Vogels, Tim P. and Raimondo, Joseph V.},\n\teditor = {Isik, Leyla},\n\tmonth = jul,\n\tyear = {2019},\n\tnote = {Publisher: Public Library of Science},\n\tpages = {e1007049},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/YGURPQ4D/file/view}\n}\n\n\n\n

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\n \n 2018\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Biophysical models reveal the relative importance of transporter proteins and impermeant anions in chloride homeostasis.\n \n \n \n \n\n\n \n Düsterwald, K. M; Currin, C. B; Burman, R. J; Akerman, C. J; Kay, A. R; and Raimondo, J. V\n\n\n \n\n\n\n eLife, 7. September 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Biophysical$ Paper\n \n \n \n $\"Biophysical$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{Dusterwald2018,\n\ttitle = {Biophysical models reveal the relative importance of transporter proteins and impermeant anions in chloride homeostasis},\n\tvolume = {7},\n\tcopyright = {Creative Commons Attribution 4.0 International License (CC-BY)},\n\tissn = {2050-084X},\n\turl = {https://elifesciences.org/articles/39575},\n\tdoi = {10.7554/eLife.39575},\n\tabstract = {Fast synaptic inhibition in the nervous system depends on the transmembrane flux of Cl- ions based on the neuronal Cl- driving force. Established theories regarding the determinants of Cl- driving force have recently been questioned. Here, we present biophysical models of Cl- homeostasis using the pump-leak model. Using numerical and novel analytic solutions, we demonstrate that the Na+/K+-ATPase, ion conductances, impermeant anions, electrodiffusion, water fluxes and cation-chloride cotransporters (CCCs) play roles in setting the Cl- driving force. Our models, together with experimental validation, show that while impermeant anions can contribute to setting [Cl-]i in neurons, they have a negligible effect on the driving force for Cl- locally and cell-wide. In contrast, we demonstrate that CCCs are well-suited for modulating Cl- driving force and hence inhibitory signaling in neurons. Our findings reconcile recent experimental findings and provide a framework for understanding the interplay of different chloride regulatory processes in neurons.},\n\turldate = {2018-10-27},\n\tjournal = {eLife},\n\tauthor = {Düsterwald, Kira M and Currin, Christopher B and Burman, Richard J and Akerman, Colin J and Kay, Alan R and Raimondo, Joseph V},\n\tmonth = sep,\n\tyear = {2018},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/AY6CCR8T/file/view}\n}\n\n\n\n

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\n \n 2017\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Early ethanol exposure and vinpocetine treatment alter learning- and memory-related proteins in the rat hippocampus and prefrontal cortex.\n \n \n \n \n\n\n \n Swart, P. C.; Currin, C. B.; Russell, V. A.; and Dimatelis, J. J.\n\n\n \n\n\n\n Journal of Neuroscience Research, 95(5): 1204–1215. 2017.\n ISBN: 1097-4547 (Electronic) 0360-4012 (Linking)\n\n\n\n
\n\n\n\n \n \n $\"Early$ paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{swart_early_2017,\n\ttitle = {Early ethanol exposure and vinpocetine treatment alter learning- and memory-related proteins in the rat hippocampus and prefrontal cortex},\n\tvolume = {95},\n\tcopyright = {All rights reserved},\n\tissn = {10974547 03604012},\n\tdoi = {10.1002/jnr.23894},\n\tabstract = {? 2016 Wiley Periodicals, Inc.This study investigates the effects of early exposure to ethanol on cognitive function and neural plasticity-related proteins in the rat brain. Sprague-Dawley rats were administered 12\\% ethanol solution (4g/kg/day i.p.) or saline from P4 to P9. Vinpocetine, a phosphodiesterase type 1 inhibitor, was tested to determine whether it could reverse any changes induced by early ethanol exposure. Hence, from P25 to P31, ethanol-exposed male rats were injected with vinpocetine (20mg/kg/day i.p.) or vehicle (DMSO) prior to undergoing behavioral testing in the open field and Morris water maze (MWM) tests. Ethanol exposure did not adversely affect spatial memory in the MWM. A key finding in this study was a significant ethanol-induced change in the function of the phosphorylated extracellular signal-related kinase (P-ERK) signaling pathway in the prefrontal cortex (PFC) and dorsal hippocampus (DH) of rats that did not display overt behavioral deficits. The P-ERK/ERK ratio was decreased in the PFC and increased in the DH of ethanol-exposed rats compared with controls. Rats that received vinpocetine in addition to ethanol did not display any behavioral changes but did show alterations in neural plasticity-related proteins. Mitogen-activated protein kinase phosphatase was increased, whereas brain-derived neurotrophic factor was decreased, in the PFC of vinpocetine-treated ethanol-exposed rats, and phosphorylated-glycogen synthase kinase ? and synaptophysin were increased in the DH of these rats. This study provides insight into the long-term effects of early ethanol exposure and its interaction with vinpocetine in the rat brain.},\n\tnumber = {5},\n\tjournal = {Journal of Neuroscience Research},\n\tauthor = {Swart, Patricia C. and Currin, Christopher B. and Russell, Vivienne A. and Dimatelis, Jacqueline J.},\n\tyear = {2017},\n\tpmid = {27614144},\n\tnote = {ISBN: 1097-4547 (Electronic) 0360-4012 (Linking)},\n\tpages = {1204--1215},\n\turl_paper={https://api.zotero.org/users/8810803/publications/items/NHC7CXGK/file/view}\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n Biophysical models reveal the relative importance of transporter proteins and impermeant anions in chloride homeostasis.\n \n \n \n\n\n \n Düsterwald, K. M; Currin, C. B.; Burman, R. J; Akerman, C. J; Kay, A. R; and Raimondo, J. V\n\n\n \n\n\n\n bioRxiv,216150. November 2017.\n Publisher: Cold Spring Harbor Laboratory\n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dusterwald_biophysical_2017,\n\ttitle = {Biophysical models reveal the relative importance of transporter proteins and impermeant anions in chloride homeostasis},\n\tcopyright = {All rights reserved},\n\tdoi = {10.1101/216150},\n\tabstract = {Fast synaptic inhibition in the nervous system depends on the transmembrane flux of   REF \\_Ref515376767  ions based on the neuronal   REF \\_Ref515376767  driving force. Established theories regarding the determinants of   REF \\_Ref515376767  driving force have recently been questioned. Here we present biophysical models of   REF \\_Ref515376767  homeostasis using the pump-leak model. Using novel numerical and analytic solutions, we demonstrate that the Na+/K+ ATPase, ion conductances, impermeant anions, electrodiffusion, water fluxes and cation-chloride cotransporters (CCCs) play roles in setting the   REF \\_Ref515376767  driving force. We show that impermeant anions have a negligible effect on the driving force for   REF \\_Ref515376767  either locally or cell-wide. While impermeant anions can contribute to setting the intracellular   REF \\_Ref515376767  concentration in neurons, they can only affect   REF \\_Ref515376767  driving force by modifying the activity of active transport mechanisms (i.e. the Na+/K+ ATPase). In contrast, we demonstrate that CCCs are well-suited for modulating   REF \\_Ref515376767  driving force and hence inhibitory signaling in neurons.},\n\tjournal = {bioRxiv},\n\tauthor = {Düsterwald, Kira M and Currin, Christopher Brian and Burman, Richard J and Akerman, Colin J and Kay, Alan R and Raimondo, Joseph V},\n\tmonth = nov,\n\tyear = {2017},\n\tnote = {Publisher: Cold Spring Harbor Laboratory},\n\tpages = {216150},\n}\n

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