Jorge J. Palop-Esteban, PhD

Title(s)Associate Professor, Neurology
SchoolSchool of Medicine
Address35 Medical Center Way, #1038
San Francisco CA 94143
ORCID ORCID Icon0000-0001-6086-1070 Additional info
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    Title(s)UCSF Weill Institute for Neurosciences

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    Mechanisms of Network and Interneuron Dysfunction in Alzheimer’s Disease

    Our laboratory seeks to understand the neuronal processes underlying cognitive impairments in neurodegenerative disorders, such as Alzheimer’s disease (AD), and in neuropsychiatric conditions associated with abnormal synchronization of neuronal networks, such as schizophrenia, autism, and epilepsy. We aim to identify molecular, circuit, and network mechanisms of cognitive dysfunction and to develop novel therapeutic approaches to restore brain functions in AD and related disorders. We are particularly focused on understanding the role of impaired inhibitory interneurons in network hypersynchrony, altered oscillatory brain rhythms, and cognitive dysfunction in AD.

    To study these complex diseases, my laboratory primarily uses mouse models that recapitulate key aspects of the cognitive dysfunction and pathology of these conditions to dissect network and circuits mechanisms of brain dysfunction in mouse models of AD. We use electroencephalography (EEG), local field potentials (LFP), and single-unit recordings to assess neuron activity in vivo, optogenetic approaches to modulate interneuron function in vivo, genetic and pharmacological manipulations to manipulate specific pathways in vivo, and behavioral assessment to determine the cognitive consequences of our mechanistic interventions.

    Areas de investigation

    Network hypersynchrony in AD and related mouse models: We discovered that mouse models of AD (hAPP mice) develop aberrant patterns of neuronal network activity, including epileptiform activity and non-convulsive seizures, that result in profound anatomical and physiological alterations in learning and memory centers (e.g., calbindin depletions). These unexpected findings may be related to the epileptic phenotype of many pedigrees of patients with early-onset familial AD and to the hyperactivation of neuronal networks in patients with sporadic AD and amyloid-positive nondemented subjects. Thus, network abnormalities leading to, or induced by, A accumulation appear to be a relatively early pathogenic event in AD. These results prompted the field to reexamine the effects of abnormal patterns of network activity on cognitive dysfunction in AD. We are investigating mechanisms of network hypersynchronization in AD and testing novel therapies to prevent such deficits.

    Altered interneuron dysfunction and oscillatory rhythms in cognitive disorders: Inhibitory interneurons regulate oscillatory rhythms and network synchrony that are required for cognitive functions and disrupted in AD. We are currently focused on understanding the role of inhibitory interneurons and oscillatory brain rhythms in cognitive functions in health and disease. We discovered that impaired inhibitory interneurons lead to altered oscillatory activity, network hypersynchrony, and cognitive deficits in mouse models of AD. Importantly, cognitive performance in AD mouse models was improved when interneuron-dependent oscillatory brain activity was enhanced by restoration of Nav1.1 levels in endogenous inhibitory interneurons. We are currently profiling inhibitory interneuron cell types in mouse models of AD to identify potential molecular mechanisms of interneuron dysfunction and potential targets of intervention. We are also dissecting the circuit and neuron alterations in behaving mouse models of AD using single-unit recordings and optogenetic approaches. Thus, we are identifying molecular and circuit mechanisms of brain dysfunction and exploring the therapeutic implications of enhancing inhibitory functions and/or restoring oscillatory rhythms in brain disorders associated with abnormal synchronization of neuronal networks, such as AD, schizophrenia, autism, or epilepsy.

    Interneuron cell-based therapy in AD and related models: During brain development, embryonic interneuron precursors are generated in the medial ganglionic eminence (MGE) and retain a remarkable capacity for migration and integration in adult host brains, where they fully mature into functional inhibitory interneurons. Thus, MGE, or MGE-like, precursors provide a great opportunity for cell-based therapy in animal models of neurological disorders linked to impaired inhibitory function. We discovered that transplanting Nav1.1-overexpressing, but not wildtype, MGE-derived interneurons enhanced behavior-related modulation of gamma oscillatory activity, reduced network hypersynchrony, and improved cognitive function in hAPP mice. Interestingly, Nav1.1-deficient interneuron transplants were sufficient to cause behavioral abnormalities in wild-type mice, indicating the key functional role of interneurons and Nav1.1 for cognitive functions. These findings highlight the potential of Nav1.1 and inhibitory interneurons as a therapeutic target in AD and that disease-specific molecular optimization of cell transplants may be required to ensure therapeutic benefits in different conditions.

    Translational focus: We hope to translate our basic research to develop novel treatments. We are evaluating the therapeutic potential of interneuron-based interventions by using cell-based therapy and pharmacology. We established formal partnerships with major pharmaceutical and biotechnology companies to develop compounds or identify targets that enhance interneuron function or restore brain rhythms in models of AD and epilepsy. We are currently developing small molecule Nav1.1 activators that increase Nav1.1 currents and interneuron-dependent gamma oscillations in vitro and in vivo to develop novel therapies for conditions with impaired interneuron function, including AD and Dravet syndrome.

    Our current short- and long-term research questions include:
    • Does epileptiform activity or network hypersynchrony contribute to AD pathology and cognitive dysfunction in AD and related mouse models?
    • Do impaired inhibitory interneurons contribute to altered oscillatory activity and network hypersynchrony?
    • Can we identify small-molecule Nav1.1 activators to enhance gamma oscillations in vivo?
    • Do inhibitory interneuron cell types have altered molecular profile in AD and related mouse models?
    • What are the functional alterations of principal and interneuron cell types in vivo at the single-cell level in mouse models of AD?
    • Are synaptic depression and aberrant excitatory neuronal activity mechanistically related?
    • What are the molecular mechanisms of hAPP/A-induced epileptiform activity and interneuron dysfunction?
    • Is hAPP/A part of a homeostatic mechanism controlling neuronal activity, and is it dysregulated in AD?
    • Can we restore cognitive function in AD by enhancing interneuron function?

    Collapse Research 
    Collapse Research Activities and Funding
    Optogenetic dissection of cellular and circuit mechanisms of network dysfunction and amyloid deposition in mouse models of Alzheimer's disease in vivo
    NIH-NIA R01AG062234Sep 1, 2018 - Aug 23, 2023
    Role: Principal Investigator
    Restoring Brain Functions in Alzheimer Models with Interneuron Transplants
    NIH/NIA R01AG047313May 15, 2014 - Apr 30, 2019
    Role: Principal Investigator

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    Collapse Publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help. to make corrections and additions.
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    Altmetrics Details PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
    1. GluN2A NMDA Receptor Enhancement Improves Brain Oscillations, Synchrony, and Cognitive Functions in Dravet Syndrome and Alzheimer's Disease Models. Cell Rep. 2020 01 14; 30(2):381-396.e4. Hanson JE, Ma K, Elstrott J, Weber M, Saillet S, Khan AS, Simms J, Liu B, Kim TA, Yu GQ, Chen Y, Wang TM, Jiang Z, Liederer BM, Deshmukh G, Solanoy H, Chan C, Sellers BD, Volgraf M, Schwarz JB, Hackos DH, Weimer RM, Sheng M, Gill TM, Scearce-Levie K, Palop JJ. PMID: 31940483; PMCID: PMC7017907.
      View in: PubMed   Mentions: 34     Fields:    Translation:HumansAnimalsCells
    2. What electrophysiology tells us about Alzheimer's disease: a window into the synchronization and connectivity of brain neurons. Neurobiol Aging. 2020 01; 85:58-73. Babiloni C, Blinowska K, Bonanni L, Cichocki A, De Haan W, Del Percio C, Dubois B, Escudero J, Fernández A, Frisoni G, Guntekin B, Hajos M, Hampel H, Ifeachor E, Kilborn K, Kumar S, Johnsen K, Johannsson M, Jeong J, LeBeau F, Lizio R, Lopes da Silva F, Maestú F, McGeown WJ, McKeith I, Moretti DV, Nobili F, Olichney J, Onofrj M, Palop JJ, Rowan M, Stocchi F, Struzik ZM, Tanila H, Teipel S, Taylor JP, Weiergräber M, Yener G, Young-Pearse T, Drinkenburg WH, Randall F. PMID: 31739167.
      View in: PubMed   Mentions: 73     Fields:    Translation:HumansAnimals
    3. Ovarian Cycle Stages Modulate Alzheimer-Related Cognitive and Brain Network Alterations in Female Mice. eNeuro. 2018 Nov-Dec; 5(6). Broestl L, Worden K, Moreno AJ, Davis EJ, Wang D, Garay B, Singh T, Verret L, Palop JJ, Dubal DB. PMID: 30627643; PMCID: PMC6325547.
      View in: PubMed   Mentions: 19     Fields:    Translation:HumansAnimals
    4. Nav1.1-Overexpressing Interneuron Transplants Restore Brain Rhythms and Cognition in a Mouse Model of Alzheimer's Disease. Neuron. 2018 04 04; 98(1):75-89.e5. Martinez-Losa M, Tracy TE, Ma K, Verret L, Clemente-Perez A, Khan AS, Cobos I, Ho K, Gan L, Mucke L, Alvarez-Dolado M, Palop JJ. PMID: 29551491; PMCID: PMC5886814.
      View in: PubMed   Mentions: 94     Fields:    Translation:HumansAnimalsCells
    5. Epilepsy as a Network Disorder (2): What can we learn from other network disorders such as dementia and schizophrenia, and what are the implications for translational research? Epilepsy Behav. 2018 01; 78:302-312. Scharfman HE, Kanner AM, Friedman A, Blümcke I, Crocker CE, Cendes F, Diaz-Arrastia R, Förstl H, Fenton AA, Grace AA, Palop J, Morrison J, Nehlig A, Prasad A, Wilcox KS, Jette N, Pohlmann-Eden B. PMID: 29097123; PMCID: PMC5756681.
      View in: PubMed   Mentions: 10     Fields:    Translation:Humans
    6. Ketogenic diet or BHB improves epileptiform spikes, memory, survival in Alzheimer's model. bioRxiv, 136226. 2017. Newman JC , Kroll F , Ulrich S, Palop JJ, Verdin E.
    7. Network abnormalities and interneuron dysfunction in Alzheimer disease. Nat Rev Neurosci. 2016 12; 17(12):777-792. Palop JJ, Mucke L. PMID: 27829687; PMCID: PMC8162106.
      View in: PubMed   Mentions: 388     Fields:    Translation:HumansAnimalsCells
    8. Nuclear pore complex remodeling by p75(NTR) cleavage controls TGF-β signaling and astrocyte functions. Nat Neurosci. 2015 Aug; 18(8):1077-80. Schachtrup C, Ryu JK, Mammadzada K, Khan AS, Carlton PM, Perez A, Christian F, Le Moan N, Vagena E, Baeza-Raja B, Rafalski V, Chan JP, Nitschke R, Houslay MD, Ellisman MH, Wyss-Coray T, Palop JJ, Akassoglou K. PMID: 26120963; PMCID: PMC4878404.
      View in: PubMed   Mentions: 23     Fields:    Translation:HumansAnimalsCells
    9. Lamin B1 mediates cell-autonomous neuropathology in a leukodystrophy mouse model. J Clin Invest. 2013 Jun; 123(6):2719-29. Heng MY, Lin ST, Verret L, Huang Y, Kamiya S, Padiath QS, Tong Y, Palop JJ, Huang EJ, Ptácek LJ, Fu YH. PMID: 23676464; PMCID: PMC3668844.
      View in: PubMed   Mentions: 44     Fields:    Translation:HumansAnimalsCells
    10. Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model. Proc Natl Acad Sci U S A. 2012 Oct 16; 109(42):E2895-903. Sanchez PE, Zhu L, Verret L, Vossel KA, Orr AG, Cirrito JR, Devidze N, Ho K, Yu GQ, Palop JJ, Mucke L. PMID: 22869752; PMCID: PMC3479491.
      View in: PubMed   Mentions: 292     Fields:    Translation:HumansAnimalsCells
    11. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell. 2012 Apr 27; 149(3):708-21. Verret L, Mann EO, Hang GB, Barth AM, Cobos I, Ho K, Devidze N, Masliah E, Kreitzer AC, Mody I, Mucke L, Palop JJ. PMID: 22541439; PMCID: PMC3375906.
      View in: PubMed   Mentions: 548     Fields:    Translation:HumansAnimalsCells
    12. Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease. J Neurosci. 2011 Jan 12; 31(2):700-11. Roberson ED, Halabisky B, Yoo JW, Yao J, Chin J, Yan F, Wu T, Hamto P, Devidze N, Yu GQ, Palop JJ, Noebels JL, Mucke L. PMID: 21228179; PMCID: PMC3325794.
      View in: PubMed   Mentions: 366     Fields:    Translation:AnimalsCells
    13. Step-by-step in situ hybridization method for localizing gene expression changes in the brain. Methods Mol Biol. 2011; 670:207-30. Palop JJ, Roberson ED, Cobos I. PMID: 20967593.
      View in: PubMed   Mentions: 14     Fields:    Translation:Animals
    14. Quantifying biomarkers of cognitive dysfunction and neuronal network hyperexcitability in mouse models of Alzheimer's disease: depletion of calcium-dependent proteins and inhibitory hippocampal remodeling. Methods Mol Biol. 2011; 670:245-62. Palop JJ, Mucke L, Roberson ED. PMID: 20967595; PMCID: PMC8153735.
      View in: PubMed   Mentions: 37     Fields:    Translation:HumansAnimals
    15. Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network. Neuron. 2010 Nov 04; 68(3):428-41. Harris JA, Devidze N, Verret L, Ho K, Halabisky B, Thwin MT, Kim D, Hamto P, Lo I, Yu GQ, Palop JJ, Masliah E, Mucke L. PMID: 21040845; PMCID: PMC3050043.
      View in: PubMed   Mentions: 172     Fields:    Translation:HumansAnimalsCells
    16. Arc regulates spine morphology and maintains network stability in vivo. Proc Natl Acad Sci U S A. 2010 Oct 19; 107(42):18173-8. Peebles CL, Yoo J, Thwin MT, Palop JJ, Noebels JL, Finkbeiner S. PMID: 20921410; PMCID: PMC2964216.
      View in: PubMed   Mentions: 133     Fields:    Translation:AnimalsCells
    17. Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice. Am J Pathol. 2010 Aug; 177(2):563-9. Buttini M, Masliah E, Yu GQ, Palop JJ, Chang S, Bernardo A, Lin C, Wyss-Coray T, Huang Y, Mucke L. PMID: 20595630; PMCID: PMC2913361.
      View in: PubMed   Mentions: 39     Fields:    Translation:HumansAnimalsCells
    18. Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks. Nat Neurosci. 2010 Jul; 13(7):812-8. Palop JJ, Mucke L. PMID: 20581818; PMCID: PMC3072750.
      View in: PubMed   Mentions: 733     Fields:    Translation:HumansCells
    19. Distinct roles of GABAergic interneurons in the regulation of striatal output pathways. J Neurosci. 2010 Feb 10; 30(6):2223-34. Gittis AH, Nelson AB, Thwin MT, Palop JJ, Kreitzer AC. PMID: 20147549; PMCID: PMC2836801.
      View in: PubMed   Mentions: 205     Fields:    Translation:AnimalsCells
    20. Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease. Cell Stem Cell. 2009 Dec 04; 5(6):624-33. Sun B, Halabisky B, Zhou Y, Palop JJ, Yu G, Mucke L, Gan L. PMID: 19951690; PMCID: PMC2823799.
      View in: PubMed   Mentions: 107     Fields:    Translation:HumansAnimalsCells
    21. Synaptic depression and aberrant excitatory network activity in Alzheimer's disease: two faces of the same coin? Neuromolecular Med. 2010 Mar; 12(1):48-55. Palop JJ, Mucke L. PMID: 19838821; PMCID: PMC3319077.
      View in: PubMed   Mentions: 83     Fields:    Translation:HumansAnimalsCells
    22. Epilepsy and cognitive impairments in Alzheimer disease. Arch Neurol. 2009 Apr; 66(4):435-40. Palop JJ, Mucke L. PMID: 19204149; PMCID: PMC2812914.
      View in: PubMed   Mentions: 298     Fields:    Translation:HumansAnimalsCells
    23. Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease. Nat Neurosci. 2008 Nov; 11(11):1311-8. Sanchez-Mejia RO, Newman JW, Toh S, Yu GQ, Zhou Y, Halabisky B, Cissé M, Scearce-Levie K, Cheng IH, Gan L, Palop JJ, Bonventre JV, Mucke L. PMID: 18931664; PMCID: PMC2597064.
      View in: PubMed   Mentions: 167     Fields:    Translation:HumansAnimalsCells
    24. Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease. J Neurosci. 2008 May 07; 28(19):5007-17. Meilandt WJ, Yu GQ, Chin J, Roberson ED, Palop JJ, Wu T, Scearce-Levie K, Mucke L. PMID: 18463254; PMCID: PMC3315282.
      View in: PubMed   Mentions: 40     Fields:    Translation:HumansAnimalsCells
    25. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. Neuron. 2007 Sep 06; 55(5):697-711. Palop JJ, Chin J, Roberson ED, Wang J, Thwin MT, Bien-Ly N, Yoo J, Ho KO, Yu GQ, Kreitzer A, Finkbeiner S, Noebels JL, Mucke L. PMID: 17785178; PMCID: PMC8055171.
      View in: PubMed   Mentions: 792     Fields:    Translation:HumansAnimalsCells
    26. Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. J Biol Chem. 2007 Aug 17; 282(33):23818-28. Cheng IH, Scearce-Levie K, Legleiter J, Palop JJ, Gerstein H, Bien-Ly N, Puoliväli J, Lesné S, Ashe KH, Muchowski PJ, Mucke L. PMID: 17548355.
      View in: PubMed   Mentions: 223     Fields:    Translation:HumansAnimals
    27. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model. Science. 2007 May 04; 316(5825):750-4. Roberson ED, Scearce-Levie K, Palop JJ, Yan F, Cheng IH, Wu T, Gerstein H, Yu GQ, Mucke L. PMID: 17478722.
      View in: PubMed   Mentions: 928     Fields:    Translation:HumansAnimalsCells
    28. Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease. J Neurosci. 2007 Mar 14; 27(11):2727-33. Chin J, Massaro CM, Palop JJ, Thwin MT, Yu GQ, Bien-Ly N, Bender A, Mucke L. PMID: 17360894; PMCID: PMC6672562.
      View in: PubMed   Mentions: 88     Fields:    Translation:HumansAnimalsCells
    29. Altered navigational strategy use and visuospatial deficits in hAPP transgenic mice. Neurobiol Aging. 2008 Feb; 29(2):253-66. Deipolyi AR, Fang S, Palop JJ, Yu GQ, Wang X, Mucke L. PMID: 17126954.
      View in: PubMed   Mentions: 28     Fields:    Translation:HumansAnimals
    30. A network dysfunction perspective on neurodegenerative diseases. Nature. 2006 Oct 19; 443(7113):768-73. Palop JJ, Chin J, Mucke L. PMID: 17051202.
      View in: PubMed   Mentions: 288     Fields:    Translation:HumansAnimalsCells
    31. Vulnerability of dentate granule cells to disruption of arc expression in human amyloid precursor protein transgenic mice. J Neurosci. 2005 Oct 19; 25(42):9686-93. Palop JJ, Chin J, Bien-Ly N, Massaro C, Yeung BZ, Yu GQ, Mucke L. PMID: 16237173; PMCID: PMC6725729.
      View in: PubMed   Mentions: 79     Fields:    Translation:HumansAnimals
    32. Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease. J Neurosci. 2005 Oct 19; 25(42):9694-703. Chin J, Palop JJ, Puoliväli J, Massaro C, Bien-Ly N, Gerstein H, Scearce-Levie K, Masliah E, Mucke L. PMID: 16237174; PMCID: PMC6725734.
      View in: PubMed   Mentions: 176     Fields:    Translation:HumansAnimalsCells
    33. Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation. Nat Med. 2004 Nov; 10(11):1190-2. Cheng IH, Palop JJ, Esposito LA, Bien-Ly N, Yan F, Mucke L. PMID: 15502844.
      View in: PubMed   Mentions: 54     Fields:    Translation:HumansAnimals
    34. Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic mice. J Neurosci. 2004 May 12; 24(19):4692-7. Chin J, Palop JJ, Yu GQ, Kojima N, Masliah E, Mucke L. PMID: 15140940; PMCID: PMC6729387.
      View in: PubMed   Mentions: 92     Fields:    Translation:HumansAnimalsCells
    35. Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits. Proc Natl Acad Sci U S A. 2003 Aug 05; 100(16):9572-7. Palop JJ, Jones B, Kekonius L, Chin J, Yu GQ, Raber J, Masliah E, Mucke L. PMID: 12881482; PMCID: PMC170959.
      View in: PubMed   Mentions: 189     Fields:    Translation:HumansAnimalsCells
    36. Cytochemical techniques for zinc and heavy metals localization in nerve cells. Microsc Res Tech. 2002 Mar 01; 56(5):318-31. López-García C, Varea E, Palop JJ, Nacher J, Ramirez C, Ponsoda X, Molowny A. PMID: 11877810.
      View in: PubMed   Mentions: 7     Fields:    Translation:AnimalsCells
    37. Early histological maturation in the hippocampus of the guinea pig. Brain Behav Evol. 2000 Jun; 56(1):38-44. Nacher J, Palop JJ, Ramirez C, Molowny A, Lopez-Garcia C. PMID: 11025343.
      View in: PubMed   Mentions: 3     Fields:    Translation:AnimalsCells
    38. Radial glia and cell debris removal during lesion-regeneration of the lizard medial cortex. Histol Histopathol. 1999 01; 14(1):89-101. Nacher J, Ramírez C, Palop JJ, Molowny A, Luis de la Iglesia JA, López-García C. PMID: 9987654.
      View in: PubMed   Mentions: 3     Fields:    Translation:AnimalsCells
    39. Microglial cells during the lesion-regeneration of the lizard medial cortex. Histol Histopathol. 1999 01; 14(1):103-17. Nacher J, Ramírez C, Palop JJ, Artal P, Molowny A, López-García C. PMID: 9987655.
      View in: PubMed   Mentions:    Fields:    Translation:AnimalsCells
    40. Zinc-positive presynaptic boutons of the rabbit hippocampus during early postnatal development. Brain Res Dev Brain Res. 1997 Nov 12; 103(2):171-83. Sanchez-Andres JV, Palop JJ, Ramirez C, Nacher J, Molowny A, Lopez-Gracia C. PMID: 9427481.
      View in: PubMed   Mentions:    Fields:    Translation:AnimalsCells
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