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State-of-the-Art Molecular Neurobiology in Chile, 2nd Edition
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State-of-the-Art Molecular Neurobiology in Chile, 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 5501

Special Issue Editor

Prof. Dr. Juan Orellana

E-Mail Website
Guest Editor
Departamento de Neurología, Escuela de Medicina and Centro interdisciplinario de Neurociencias, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago 7820436, Chile
Interests: glial cells; neurons; neurodegenerative processes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue follows the publication of the first edition on “State-of-the-Art Molecular Neurobiology in Chile” (https://www.mdpi.com/journal/ijms/special_issues/Mol_Neurobiol_CL )”.

Shaped by history through evolution and natural selection, diverse organisms have created complex and coordinated neural structures to ensure proper response to the external medium. The latter has allowed the increasingly sophisticated analysis of information in different clades and the desire of neuroscientists to understand the molecular mechanisms of these processes. Chilean neuroscientists have not been oblivious to this endeavor, and likely, the legacy of Joaquín Luco was crucial in this aspect. His work in neurotrophic function, innervation, and learning caused a profound impact on the following generations of Chilean neuroscientists. Nowadays, neuroscience in Chile encompasses an active scientific community whose interests cover a broad range of topics, from ion channels to whole animal behavior to real-life applications in the clinic and beyond.

This Special Issue aims to gather a collection of original research articles, short communications, perspectives, and review articles, providing the latest progress and insights in the field of molecular neurobiology in Chile. We profoundly encourage the submissions and contributions from Chilean research institutes/laboratories to consolidate our understanding of neuroscience, particularly at the molecular level.

Within this Special Issue, potential topics include, but are not limited to, the following: protein structure, channel gating, molecular modeling, electrophysiology, pharmacology, trafficking; neurophysiology, behavior, plasticity, neurogenesis, blood flow control, neuron-glia crosstalk, neuroendocrinology, cell migration, differentiation, neuroinflammation, mutation-related diseases, myelin repair, glial dysfunction, neurological disorders, and neurodegeneration.

Prof. Dr. Juan Orellana
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • neurological disorders
  • neurodegeneration
  • pharmacology
  • protein structure
  • neuroinflammation
  • neurophysiology

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Published Papers (4 papers)

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Research

19 pages, 2121 KiB  
Article
A Pro-Inflammatory Stimulus versus Extensive Passaging of DITNC1 Astrocyte Cultures as Models to Study Astrogliosis
by Leonardo A. Pérez, Esteban Palacios, María Fernanda González, Ignacio Leyton-Rivera, Samuel Martínez-Meza, Ramón Pérez-Núñez, Emanuel Jeldes, Ana María Avalos, Jorge Díaz and Lisette Leyton
Int. J. Mol. Sci. 2024, 25(17), 9454; https://doi.org/10.3390/ijms25179454 - 30 Aug 2024
Viewed by 873
Abstract
Astrogliosis is a process by which astrocytes, when exposed to inflammation, exhibit hypertrophy, motility, and elevated expression of reactivity markers such as Glial Fibrillar Acidic Protein, Vimentin, and Connexin43. Since 1999, our laboratory in Chile has been studying molecular signaling pathways associated with [...] Read more.
Astrogliosis is a process by which astrocytes, when exposed to inflammation, exhibit hypertrophy, motility, and elevated expression of reactivity markers such as Glial Fibrillar Acidic Protein, Vimentin, and Connexin43. Since 1999, our laboratory in Chile has been studying molecular signaling pathways associated with “gliosis” and has reported that reactive astrocytes upregulate Syndecan 4 and αVβ3 Integrin, which are receptors for the neuronal glycoprotein Thy-1. Thy-1 engagement stimulates adhesion and migration of reactive astrocytes and induces neurons to retract neurites, thus hindering neuronal network repair. Reportedly, we have used DITNC1 astrocytes and neuron-like CAD cells to study signaling mechanisms activated by the Syndecan 4–αVβ3 Integrin/Thy-1 interaction. Importantly, the sole overexpression of β3 Integrin in non-reactive astrocytes turns them into reactive cells. In vitro, extensive passaging is a simile for “aging”, and aged fibroblasts have shown β3 Integrin upregulation. However, it is not known if astrocytes upregulate β3 Integrin after successive cell passages. Here, we hypothesized that astrocytes undergoing long-term passaging increase β3 Integrin expression levels and behave as reactive astrocytes without needing pro-inflammatory stimuli. We used DITNC1 cells with different passage numbers to study reactivity markers using immunoblots, immunofluorescence, and astrocyte adhesion/migration assays. We also evaluated β3 Integrin levels by immunoblot and flow cytometry, as well as the neurotoxic effects of reactive astrocytes. Serial cell passaging mimicked the effects of inflammatory stimuli, inducing astrocyte reactivity. Indeed, in response to Thy-1, β3 Integrin levels, as well as cell adhesion and migration, gradually increased with multiple passages. Importantly, these long-lived astrocytes expressed and secreted factors that inhibited neurite outgrowth and caused neuronal death, just like reactive astrocytes in culture. Therefore, we describe two DITNC1 cell types: a non-reactive type that can be activated with Tumor Necrosis Factor (TNF) and another one that exhibits reactive astrocyte features even in the absence of TNF treatment. Our results emphasize the importance of passage numbers in cell behavior. Likewise, we compare the pro-inflammatory stimulus versus long-term in-plate passaging of cell cultures and introduce them as astrocyte models to study the reactivity process. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile, 2nd Edition)
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15 pages, 2310 KiB  
Article
Molecular Pharmacology of Gelsemium Alkaloids on Inhibitory Receptors
by Ana M. Marileo, César O. Lara, Anggelo Sazo, Omayra V. Contreras, Gabriel González, Patricio A. Castro, Luis G. Aguayo, Gustavo Moraga-Cid, Jorge Fuentealba, Carlos F. Burgos and Gonzalo E. Yévenes
Int. J. Mol. Sci. 2024, 25(6), 3390; https://doi.org/10.3390/ijms25063390 - 16 Mar 2024
Cited by 1 | Viewed by 1228
Abstract
Indole alkaloids are the main bioactive molecules of the Gelsemium genus plants. Diverse reports have shown the beneficial actions of Gelsemium alkaloids on the pathological states of the central nervous system (CNS). Nevertheless, Gelsemium alkaloids are toxic for mammals. To date, the molecular [...] Read more.
Indole alkaloids are the main bioactive molecules of the Gelsemium genus plants. Diverse reports have shown the beneficial actions of Gelsemium alkaloids on the pathological states of the central nervous system (CNS). Nevertheless, Gelsemium alkaloids are toxic for mammals. To date, the molecular targets underlying the biological actions of Gelsemium alkaloids at the CNS remain poorly defined. Functional studies have determined that gelsemine is a modulator of glycine receptors (GlyRs) and GABAA receptors (GABAARs), which are ligand-gated ion channels of the CNS. The molecular and physicochemical determinants involved in the interactions between Gelsemium alkaloids and these channels are still undefined. We used electrophysiological recordings and bioinformatic approaches to determine the pharmacological profile and the molecular interactions between koumine, gelsemine, gelsevirine, and humantenmine and these ion channels. GlyRs composed of α1 subunits were inhibited by koumine and gelsevirine (IC50 of 31.5 ± 1.7 and 40.6 ± 8.2 μM, respectively), while humantenmine did not display any detectable activity. The examination of GlyRs composed of α2 and α3 subunits showed similar results. Likewise, GABAARs were inhibited by koumine and were insensitive to humantenmine. Further assays with chimeric and mutated GlyRs showed that the extracellular domain and residues within the orthosteric site were critical for the alkaloid effects, while the pharmacophore modeling revealed the physicochemical features of the alkaloids for the functional modulation. Our study provides novel information about the molecular determinants and functional actions of four major Gelsemium indole alkaloids on inhibitory receptors, expanding our knowledge regarding the interaction of these types of compounds with protein targets of the CNS. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile, 2nd Edition)
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26 pages, 8953 KiB  
Article
Transcriptional and Histone Acetylation Changes Associated with CRE Elements Expose Key Factors Governing the Regulatory Circuit in the Early Stage of Huntington’s Disease Models
by Sandra Arancibia-Opazo, J. Sebastián Contreras-Riquelme, Mario Sánchez, Marisol Cisternas-Olmedo, René L. Vidal, Alberto J. M. Martin and Mauricio A. Sáez
Int. J. Mol. Sci. 2023, 24(13), 10848; https://doi.org/10.3390/ijms241310848 - 29 Jun 2023
Cited by 4 | Viewed by 1587
Abstract
Huntington’s disease (HD) is a disorder caused by an abnormal expansion of trinucleotide CAG repeats within the huntingtin (Htt) gene. Under normal conditions, the CREB Binding Protein interacts with CREB elements and acetylates Lysine 27 of Histone 3 to direct the expression of [...] Read more.
Huntington’s disease (HD) is a disorder caused by an abnormal expansion of trinucleotide CAG repeats within the huntingtin (Htt) gene. Under normal conditions, the CREB Binding Protein interacts with CREB elements and acetylates Lysine 27 of Histone 3 to direct the expression of several genes. However, mutant Htt causes depletion of CBP, which in turn induces altered histone acetylation patterns and transcriptional deregulation. Here, we have studied a differential expression analysis and H3K27ac variation in 4- and 6-week-old R6/2 mice as a model of juvenile HD. The analysis of differential gene expression and acetylation levels were integrated into Gene Regulatory Networks revealing key regulators involved in the altered transcription cascade. Our results show changes in acetylation and gene expression levels that are related to impaired neuronal development, and key regulators clearly defined in 6-week-old mice are proposed to drive the downstream regulatory cascade in HD. Here, we describe the first approach to determine the relationship among epigenetic changes in the early stages of HD. We determined the existence of changes in pre-symptomatic stages of HD as a starting point for early onset indicators of the progression of this disease. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile, 2nd Edition)
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9 pages, 1730 KiB  
Communication
BDNF and Cognitive Function in Chilean Schizophrenic Patients
by Rodrigo R. Nieto, Hernán Silva, Alejandra Armijo, Rubén Nachar, Alfonso González, Carmen Paz Castañeda, Cristián Montes and Manuel Kukuljan
Int. J. Mol. Sci. 2023, 24(13), 10569; https://doi.org/10.3390/ijms241310569 - 24 Jun 2023
Cited by 4 | Viewed by 1041
Abstract
Despite cognitive symptoms being very important in schizophrenia, not every schizophrenic patient has a significant cognitive deficit. The molecular mechanisms underlying the different degrees of cognitive functioning in schizophrenic patients are not sufficiently understood. We studied the relation between brain-derived neurotrophic factor (BDNF) [...] Read more.
Despite cognitive symptoms being very important in schizophrenia, not every schizophrenic patient has a significant cognitive deficit. The molecular mechanisms underlying the different degrees of cognitive functioning in schizophrenic patients are not sufficiently understood. We studied the relation between brain-derived neurotrophic factor (BDNF) and cognitive functioning in two groups of schizophrenic patients with different cognitive statuses. According to the Montreal Cognitive Assessment (MoCA) results, the schizophrenic patients were classified into two subgroups: normal cognition (26 or more) and cognitive deficit (25 or less). We measured their plasma BDNF levels using ELISAs. The statistical analyses were performed using Spearman’s Rho and Kruskal–Wallis tests. We found a statistically significant positive correlation between the plasma BDNF levels and MoCA score (p = 0.04) in the subgroup of schizophrenic patients with a cognitive deficit (n = 29). However, this correlation was not observed in the patients with normal cognition (n = 11) and was not observed in the total patient group (n = 40). These results support a significant role for BDNF in the cognitive functioning of schizophrenics with some degree of cognitive deficit, but suggest that BDNF may not be crucial in patients with a normal cognitive status. These findings provide information about the molecular basis underlying cognitive deficits in this illness. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile, 2nd Edition)
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