Publicaciones por año
Publicaciones del Departamento de Histología y Embriología
CD200R1 modulates myelin phagocytosis and spleen response following spinal cord injury
Sci Re 2026 15(1):41013
Bruno Pannunzio 1 2 , Fabio Andrés Cawen 1 3 4 , Frances Evans 1 2 , Rubèn López-Vales 5 6 , Hugo Peluffo 1 3 4 , Natalia Lago 7 8 9
1 Institut Pasteur de Montevideo, Montevideo, Uruguay. 2 Histology and Embryology Department, Faculty of Medicine, Universidad de la República, Montevideo, Uruguay. 3 Unitat de Bioquímica i Biologia Molecular, Departament de Biomedicina, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona (UB), Barcelona, 08036, Spain. 4 Institut de Neurociències, Universitat de Barcelona (UB), Barcelona, 08036, Spain. 5 Departament de Biologia Cel·lular, Fisiologia i Immunologia, Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain. 6 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. 7 Institut Pasteur de Montevideo, Montevideo, Uruguay. Natalia.Lago@uab.cat. 8 Departament de Biologia Cel·lular, Fisiologia i Immunologia, Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain. Natalia.Lago@uab.cat. 9 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. Natalia.Lago@uab.cat.
DOI: 10.1038/s41598-025-24827-6
PMID: 41266433
Pubmed: https://pubmed.ncbi.nlm.nih.gov/41266433
Texto completo: https://doi.org/10.1038/s41598-025-24827-6
Abstract:
The interaction between CD200 and its receptor CD200R1 plays a key role in modulating immune responses in nervous system disorders. This study explored the function of CD200R1 in local and systemic inflammation following spinal cord injury (SCI) using CD200R1-knockout (CD200R1-/-) mice. Following a low thoracic contusion injury, CD200R1-/- mice exhibited increased macrophage infiltration at the injury site, with a greater proportion of pro-inflammatory Ly6C + macrophages. Myelin phagocytosis was impaired in CD200R1-/- macrophages both ex vivo and in vitro, indicating a reduced capacity to clear myelin debris. Despite these immune alterations, CD200R1 deficiency did not affect spontaneous locomotor recovery post-SCI, as measured by the Basso Mouse Scale. However, CD200R1-/- mice tended to lose more weight after injury, suggesting systemic effects. In uninjured (naïve) conditions, CD200R1-/- mice showed reduced spleen weight and lymphocyte counts, along with lower mRNA expression of inflammatory cytokines TNFα, IL6, and CCL2, though no significant differences were seen in splenic immune cell populations. Altogether, these results suggest that CD200R1 is an important factor regulating myelin phagocytosis by macrophages and maintaining normal immune and splenic homeostasis under both injured and naïve conditions.
Cannabigerol improves MK-801-induced long-term recognition memory deficit in male rats through cortical TrkB-R signaling independently of changes in BDNF
Pharmacol Biochem Behav. 2026 174260
Ximena López-Hill 1 , Soledad Marton 2 , Analía Richeri 3 , Sara Fabius 4 , Jessika Urbanavicius 5 , Lucía Lima de Almeida 6 , Carolina Echeverry 7 , Verónica Sánchez de Medina Baena 8 , Carlos Ferreiro 9 , Anna Castané 10 , Cecilia Scorza 11
1 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: ximenalopezhill@gmail.com. 2 Departamento de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. Electronic address: soledadmarton@gmail.com. 3 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: aricheri@gmail.com. 4 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: sfabiusc@gmail.com. 5 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: jessikau@gmail.com. 6 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: llima@fcien.edu.uy. 7 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: caroliecheverry@gmail.com. 8 Phytoplant Research S.L., Cordoba, Spain. Electronic address: v.sanchez@phytoplant.es. 9 Phytoplant Research S.L., Cordoba, Spain. Electronic address: c.ferreiro@phytoplant.es. 10 School of Medicine, Universitat de Vic-Universitat Central de Catalunya (UVic-UCC), Institut de Recerca i Innovació en Ciències de la Vida i de la Salut a la Catalunya Central (IRIS-CC), Spain; Department of Biomedicine, School of Medicine and Health Sciences, Institute of Neurosciences University of Barcelona, Spain; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), ISCIII, Spain. Electronic address: anna.castane@iibb.csic.es. 11 Departmento de Neurofarmacología Experimental, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay. Electronic address: cscorza@iibce.edu.uy.
DOI: 10.1016/j.pbb.2026.174260
PMID: 42648374
Pubmed: https://pubmed.ncbi.nlm.nih.gov/42648374
Texto completo: https://doi.org/10.1016/j.pbb.2026.174260
Abstract:
Interest in the therapeutic potential of cannabigerol (CBG), a non-psychotomimetic cannabinoid derived from Cannabis sativa, has increased recently. However, preclinical studies examining its effects on cognitive impairment, a core symptom domain of schizophrenia, remain limited. Based on the N-methyl-d-aspartate receptor (NMDA-R) hypofunction hypothesis of schizophrenia, MK-801, a potent NMDA-R antagonist, is widely used as a pharmacological model of schizophrenia that replicates the cognitive impairments observed in patients. This study investigated whether repeated systemic administration of CBG (10 mg/kg/i.p.) could reverse long-term recognition memory (LTM) impairment induced by a single dose of MK-801 (0.1 mg/kg/i.p.) in male rats, using the novel object recognition paradigm. Additionally, we evaluated whether these effects were associated with changes in BDNF/TrkB receptor (TrkB-R) signaling. ELISA and quantitative real-time PCR analyses were performed to evaluate BDNF protein levels and BDNF and TrkB-R mRNA expression in the hippocampus and medial prefrontal cortex (mPFC). MK-801 significantly impaired LTM compared with control group, whereas co-administration of CBG prevented this deficit. MK-801-induced memory impairment was associated with reduced hippocampal and cortical BDNF protein levels, without changes in BDNF or TrkB-R mRNA expression. CBG and MK-801 combined treatment did not restore BDNF mRNA expression and protein levels although it significantly increased TrkB-R mRNA expression in the mPFC. These results suggest that activation of TrkB-R signaling through a BDNF-independent mechanism may contribute to the preservation of LTM by CBG. Our results provide relevant evidence supporting the therapeutic potential of CBG for cognitive impairments associated with schizophrenia.
Vincristine-induced alterations in ovarian function and oocyte quality: Modulation by dichloroacetate
Reprod Biol. 2026 26(4):101267
Agustina Toledo 1 , Paulina Simoes 2 , Clara Fernández-Tabó 2 , Karina Hernández-Mir 2 , Rebeca Chávez-Genaro 3 , Gabriel Anesetti 4
1 Unidad Académica de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. Electronic address: agustinatoledo@fmed.edu.uy. 2 Unidad Académica de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 3 Unidad Académica de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. Electronic address: rchavez@fmed.edu.uy. 4 Unidad Académica de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. Electronic address: ganesett@fmed.edu.uy.
DOI: 10.1016/j.repbio.2026.101267
PMID: 42531889
Pubmed: https://pubmed.ncbi.nlm.nih.gov/42531889
Texto completo: https://linkinghub.elsevier.com/retrieve/pii/S1642-431X(26)00089-6
Abstract:
Vincristine (VCR) is used in chemotherapy regimens and is generally considered to present low gonadotoxicity; however, its effects on ovarian function and oocyte quality are still to be wholly understood. Dichloroacetate (DCA), a metabolic modulator that promotes pyruvate dehydrogenase (PDH) activation, may influence the ovarian response to chemotherapeutic agents. Adult female C57BL/6 mice were randomly assigned to four groups: control, VCR, DCA, and VCR + DCA. During weeks 1-3, subjects received DCA via drinking water, and VCR was injected intraperitoneally during weeks 2-3. Short-term effects (at the end of week 3) were evaluated using ovarian histological and immunohistochemical analyses, including FOXO3a, anti-Müllerian hormone (AMH), cleaved caspase-3, Ki-67, and oxidative stress markers. Effects on oocyte number, diameter, and meiotic spindle morphology were evaluated in week 7 (Long-term effects). VCR was found to disrupt estrous cyclicity, reduce the number of growing follicles, and increase follicular atresia. These changes were associated with decreased AMH signaling and heightened cytoplasmic localization of FOXO3a, suggesting enhanced primordial follicle activation. VCR also increased the ovarian catalase levels. Long-term effects included reduced ovulation rate and alterations in oocyte diameter and meiotic spindle length. Combined treatment with DCA exacerbated the loss of growing follicles and reduced ovulatory rate, although some oocyte parameters, such as spindle length, were comparable to those in controls. Therefore, we propose that VCR induces significant alterations in ovarian function and oocyte quality that may persist beyond treatment. In contrast, DCA exhibits a dual effect, potentially aggravating follicular depletion while improving specific aspects of oocyte morphology.
Timescales of call variability in a South American treefrog
J Comp Physiol A Neuroethol Sens Neural Behav Physiol 2026
Mariana Rodriguez-Santiago 1 , Paula Pouso 2 , Kim Hoke 3 , Erik Zornik 4
1 Department of Biology, Colorado State University, Fort Collins, CO, USA. marirod@colostate.edu. 2 Lab. Bases Neurales de la Comunicación Acústica, Depto. Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 3 Department of Biology, Colorado State University, Fort Collins, CO, USA. 4 Biology Department, Reed College, Portland, OR, USA.
DOI: 10.1007/s00359-026-01829-x
PMID: 42530601
Pubmed: https://pubmed.ncbi.nlm.nih.gov/42530601
Texto completo: https://dx.doi.org/10.1007/s00359-026-01829-x
Abstract:
Communication systems shape behavioral interactions that are crucial for recognition, territoriality, and reproduction across animals. In many anuran species, acoustic communication drives reproductive and defensive behaviors as males produce advertisement calls to establish territories and attract females. Understanding the temporal dynamics in vocalizations and their variation between and within males can provide crucial insight into the mechanisms that generate call patterning and communication. Here, we examine such dynamics in the call patterning of male Boana pulchella, a South American treefrog species that produces temporally-variant call series over time. Using rhythm analysis, we quantify the rhythmic structure of these vocalizations and characterize the variability in their temporal patterning between males. We find that rhythmic isochrony is timescale-dependent - call series are produced isochronously while the patterning of calls and notes within these series is non-isochronous yet periodic. The isochronous rhythm is maintained through an inverse relationship between series duration and the silence interval that follows it, such that longer series are followed by shorter silence intervals. Temporal features of calls and notes as well as their variation vary depending on within-series patterning dynamics and across timescales. Taken together, these results suggest that B. pulchella vocal timing is generated by hierarchically organized oscillators that produce isochronous vocalizations over a calling bout through flexible modulation at finer timescales.
Editorial: Biomarker discovery and validation in neurological diseases
Front Cell Neurosci 2026 20:1877174
Shivani Singla 1 , Bhupesh Vaidya 1 , Laura Martínez-Palma 2 3 , Dirk M Hermann 4
1 Texas Medical Center, Houston, TX, United States. 2 Academic Unit Histology & Embryology, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 3 ALS Center of Uruguay (CELAU), Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 4 Department of Neurology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
DOI: 10.3389/fncel.2026.1877174
PMID: 42282855
Pubmed: https://pubmed.ncbi.nlm.nih.gov/42282855
Texto completo: https://doi.org/10.3389/fncel.2026.1877174
Abstract:
Editorial: Biomarker discovery and validation in neurological diseases
Front Cell Neurosci 2026 20:1877174
Shivani Singla 1 , Bhupesh Vaidya 1 , Laura Martínez-Palma 2 3 , Dirk M Hermann 4
1 Texas Medical Center, Houston, TX, United States. 2 Academic Unit Histology & Embryology, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 3 ALS Center of Uruguay (CELAU), Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 4 Department of Neurology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
DOI: 10.3389/fncel.2026.1877174
PMID: 42282855
Pubmed: https://pubmed.ncbi.nlm.nih.gov/42282855
Texto completo: https://doi.org/10.3389/fncel.2026.1877174
Abstract:
Monoclonal antibodies against nitrated nerve growth factor reveal an oxidation-dependent pathogenic hallmark in ALS
Proc Natl Acad Sci U S A 2026 28;123(17):e2536562123
Valentina Varela # 1 , Santiago Garcimartín # 2 3 , Emiliano Trias # 4 , Ari Zeida 2 3 5 , Monique Richter 1 , Andrés de León 1 , Ernesto Miquel 6 , Peter H King 7 8 , Brigitte Vulliez-Le Normand 9 , Mariano Martinez 9 , Pedro M Alzari 9 , Silvina Bartesaghi 2 3 5 , Rafael Radi 2 3 5 , Luis Barbeito 1
1 Laboratorio de Neurodegeneración, Institut Pasteur de Montevideo, Montevideo 11400, Uruguay. 2 Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Montevideo 11800, Uruguay. 3 Centro de Investigaciones Biomédicas (CEINBIO), Facultad de Medicina, Universidad de la Republica, Montevideo 11800, Uruguay. 4 Departamento de Neurobiología Celular y Molecular, Instituto de Investigaciones Biológicas Clemente Estable Montevideo, Montevideo 11600, Uruguay. 5 Programa de Alimentos y Salud Humana (PAyS), Facultad de Medicina, Universidad de la República, Montevideo 11800, Uruguay. 6 Departamento de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo 11800, Uruguay. 7 Department of Neurology and Killion Center for Neurodegeneration and Experimental Therapeutics, University of Alabama, Birmingham, AL 35294. 8 Birmingham Veterans Affairs Health Care System, Birmingham, AL 35295. 9 Unité de Microbiologie Structurale, Département de Biologie Structurale et Chimie, Institut Pasteur, CNRS, Université Paris Cité, Paris 75015, France. # Contributed equally.
DOI: 10.1073/pnas.2536562123
PMID: 42030149
Pubmed: https://pubmed.ncbi.nlm.nih.gov/42030149
Texto completo: https://doi.org/10.1073/pnas.2536562123
Abstract:
Nerve growth factor (NGF) is a member of the neurotrophin family, essential for neuronal survival and phenotypic maintenance. However, in vitro, its function can be disrupted by oxidative posttranslational modifications such as tyrosine nitration. Nitrated NGF (NO2NGF) has been shown to have a gain-of-toxic, pro-apoptotic, activity in motoneuron cultures. Herein, we report the generation and characterization of monoclonal antibodies (mAbs) that specifically recognize NO2NGF to unravel its formation in vivo. Using hybridoma technology, we produced mAbs with high affinity and selectivity for NO2NGF, as demonstrated immunochemically and by surface plasmon resonance. The antibodies elicit neutralizing capacity to NO2NGF in neuronal cells. Nitrated Tyr52 within the NGF48-58 sequence was identified as the primary antigenic determinant by crystallographic analysis of antibody:peptide complexes at atomic resolution, peptide-based epitope mapping and molecular dynamics simulations, whereas local sequence NGF motifs around the nitrated tyrosine are important for protein specificity. The antibodies revealed NO2NGF accumulation in amyotrophic lateral sclerosis (ALS) rodent models and human subjects. Indeed, immunofluorescence showed selective accumulation of NO2NGF in spinal cord regions undergoing motor neuron degeneration, as well as in sciatic nerves and neuromuscular junctions. Our findings establish NGF nitration as an oxidative hallmark in ALS and demonstrate that monoclonal antibodies targeting this chemical modification are powerful tools for both mechanistic studies and biomarkers development. This work proposes a link between neurotrophin nitration and neurodegenerative disease progression and opens avenues for therapeutic exploration along the peroxynitrite-tyrosine nitration pathway.
Modulation of cofilin 1 phosphorylation induces juvenile-like plasticity in the adult mouse visual cortex
Neuroscience 2026 595:262-269
Agustina Dapueto 1 , Emilia Hayek 2 , Alejo Acuña 3 , Bruno Pannunzio 4 , Leonel Gomez 5 , Francesco M Rossi 6
1 Laboratorio de Neurociencias "Unidad de Neuroplasticidad", Instituto de Biología, Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay; Present address: Laboratorio de Mecanismos de Neurodegeneración y Neuroprotección, Departamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, Uruguay. Electronic address: agustinadapueto@gmail.com. 2 Laboratorio de Neurociencias "Unidad de Neuroplasticidad", Instituto de Biología, Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay. Electronic address: hayekemilia03@gmail.com. 3 Laboratorio de Neurociencias "Unidad de Neuroplasticidad", Instituto de Biología, Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay. Electronic address: alejoacu@gmail.com. 4 Laboratorio de Neurociencias "Unidad de Neuroplasticidad", Instituto de Biología, Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay; Present address: Departamento de Histología y Embriología, Facultad de Medicina, UdelaR / Laboratorio de Neuroinflamación y Terapia Génica del Institut Pasteur de Montevideo, Uruguay. Electronic address: brunopannunzio@gmail.com. 5 Laboratorio de Neurociencias "Unidad de Neuroplasticidad", Instituto de Biología, Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay. Electronic address: leonel.gomez@gmail.com. 6 Laboratorio de Neurociencias "Unidad de Neuroplasticidad", Instituto de Biología, Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay. Electronic address: fmrossi@fcien.edu.uy.
DOI: 10.1016/j.neuroscience.2026.01.003
PMID: 41506312
Pubmed: https://pubmed.ncbi.nlm.nih.gov/41506312
Texto completo: https://www.sciencedirect.com/science/article/pii/S0306452226000035
Abstract:
Cofilin 1 is an actin-depolymerizing protein that plays a fundamental role in actin dynamics, particularly within dendritic spines, where it has been implicated in both structural and functional plasticity. We recently demonstrated, using a combination of differential proteomics, western blot and immunohistochemistry, that the expression of cofilin 1 and its inactive phosphorylated form is dynamically regulated in the mouse visual cortex. Expression levels change across critical periods of postnatal development and are modulated by visual experience, suggesting that cofilin 1 plays a dynamic role in synaptic remodeling during windows of heightened cortical plasticity. In this study, we sought to determine whether cofilin 1 influences experience-dependent plasticity in the adult visual cortex, a stage where plasticity is more restricted but still inducible under specific conditions. Specifically, we administered a synthetic peptide inhibitor of cofilin 1 activity in vivo (PCOF). Following monocular deprivation, adult mice received either the PCOF peptide or a control peptide. Structural plasticity was assessed by quantifying dendritic spine density using Golgi-like staining, while visual plasticity was evaluated by measuring visual acuity through the optomotor response test. Our results show that, in adult mice treated with the PCOF peptide - but not in controls - monocular deprivation led to a significant reduction in dendritic spine density in the contralateral visual cortex, as well as a decrease in visual acuity of the previously deprived eye. These findings indicate that cofilin 1 activity is crucial for the regulation of experience-dependent plasticity in the adult mouse visual cortex.
Tembleque (SDtq) rat: A new model of leukodystrophy associated with hypomyelination and impaired oligodendrocyte maturation
Lab Anim. 2026 60(1):63-74
Martín Breijo 1 , Florencia Fontes 1 , Mariela Santos 1 , Laura Martínez Palma 2 , Sergio Rocha 1 , Patricia Genovesse 3 , Bin Liu 4 , David Aghado 4 , Carlos Perez 4 , Fernando Benavides 4
1 Unidad de Reactivos y Biomodelos de Experimentación, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 2 Departamento de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 3 Departamento de Histología y Embriología, Facultad de Veterinaria, Montevideo, Uruguay. 4 Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, USA.
DOI: 10.1177/00236772251369173
PMID: 41914324
Pubmed: https://pubmed.ncbi.nlm.nih.gov/41914324
Texto completo: https://doi.org/10.1177/00236772251369173
Abstract:
This work presents the characterization of tembleque (SDtq) rats as a novel animal model for myelination abnormalities, primarily manifesting as tremors and ataxia, which notably declined by 16 weeks of age. This model originated from a spontaneous autosomal recessive mutation in an outbred Sprague Dawley colony. Histological and electron microscopy analyses revealed significant hypomyelination in the central nervous system of SDtq rats compared with wild-type controls. The thoracic spinal cords of SDtq rats exhibited reduced white matter areas, while the gray matter remained consistent. Peripheral nerves showed no change in myelin thickness, though a decrease in axonal diameter was observed. Transcript analysis indicated reduced expression of mature oligodendrocyte markers and increased activity of astrocytes and microglia in SDtq rats, suggesting compensatory mechanisms. Preliminary mapping studies showed that the causative mutation is located on proximal chromosome 19. These findings highlight the SDtq rat as a promising model for studying the underlying biology of myelin disorders and the role of glial cells in leukodystrophies.
Neuroscience in Latin America Five Decades of Flourishing Neurochemistry in the Region
J Neurochem 2026 170(2):e70349
J M Pasquini 1 , F C A Gomes 2 , R A de Melo Reis 2 , P Cassina 3 , L Barbeito 4 , S Olivera 5
1 Depto Química Biológica e IQUIFIB Facultad Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina. 2 Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. 3 Unidad Académica de Histología y Embriología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. 4 Institut Pasteur, Montevideo, Uruguay. 5 Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, Uruguay.
DOI: 10.1111/jnc.70349
PMID: 41607077
Pubmed: https://pubmed.ncbi.nlm.nih.gov/41607077
Texto completo: https://doi.org/10.1111/jnc.70349
Abstract:
We describe the development of neurochemistry in Brazil, Argentina, Uruguay, and Chile in the XX century through Latin American scientists who pioneered the discipline in their countries. In addition, we analyze the research groups that succeeded the pioneers and the fields explored in greater depth in different countries. We examine the history of glial cell research and the efforts made despite financial constraints. We also highlight the role of the International Society of Neurochemistry (ISN) in the history of neurochemistry in Latin America. A special section is dedicated to neurochemistry in Venezuela, given its significant role in the past.