Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
State-of-the-Art Molecular Neurobiology in Chile
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

State-of-the-Art Molecular Neurobiology in Chile

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: closed (31 January 2023) | Viewed by 34887

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,

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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

Published Papers (15 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

16 pages, 3539 KiB  
Article
Chronic Exposure to High Fat Diet Affects the Synaptic Transmission That Regulates the Dopamine Release in the Nucleus Accumbens of Adolescent Male Rats
by Wladimir Plaza-Briceño, Victoria B. Velásquez, Francisco Silva-Olivares, Karina Ceballo, Ricardo Céspedes, Gonzalo Jorquera, Gonzalo Cruz, Jonathan Martínez-Pinto, Christian Bonansco and Ramón Sotomayor-Zárate
Int. J. Mol. Sci. 2023, 24(5), 4703; https://doi.org/10.3390/ijms24054703 - 28 Feb 2023
Cited by 3 | Viewed by 2035
Abstract
Obesity is a pandemic caused by many factors, including a chronic excess in hypercaloric and high-palatable food intake. In addition, the global prevalence of obesity has increased in all age categories, such as children, adolescents, and adults. However, at the neurobiological level, how [...] Read more.
Obesity is a pandemic caused by many factors, including a chronic excess in hypercaloric and high-palatable food intake. In addition, the global prevalence of obesity has increased in all age categories, such as children, adolescents, and adults. However, at the neurobiological level, how neural circuits regulate the hedonic consumption of food intake and how the reward circuit is modified under hypercaloric diet consumption are still being unraveled. We aimed to determine the molecular and functional changes of dopaminergic and glutamatergic modulation of nucleus accumbens (NAcc) in male rats exposed to chronic consumption of a high-fat diet (HFD). Male Sprague-Dawley rats were fed a chow diet or HFD from postnatal day (PND) 21 to 62, increasing obesity markers. In addition, in HFD rats, the frequency but not amplitude of the spontaneous excitatory postsynaptic current is increased in NAcc medium spiny neurons (MSNs). Moreover, only MSNs expressing dopamine (DA) receptor type 2 (D2) increase the amplitude and glutamate release in response to amphetamine, downregulating the indirect pathway. Furthermore, NAcc gene expression of inflammasome components is increased by chronic exposure to HFD. At the neurochemical level, DOPAC content and tonic dopamine (DA) release are reduced in NAcc, while phasic DA release is increased in HFD-fed rats. In conclusion, our model of childhood and adolescent obesity functionally affects the NAcc, a brain nucleus involved in the hedonic control of feeding, which might trigger addictive-like behaviors for obesogenic foods and, through positive feedback, maintain the obese phenotype. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

11 pages, 1123 KiB  
Communication
Aromatic Bromination Abolishes Deficits in Visuospatial Learning Induced by MDMA (“Ecstasy”) in Rats While Preserving the Ability to Increase LTP in the Prefrontal Cortex
by Patricio Sáez-Briones, Boris Palma, Héctor Burgos, Rafael Barra and Alejandro Hernández
Int. J. Mol. Sci. 2023, 24(4), 3724; https://doi.org/10.3390/ijms24043724 - 13 Feb 2023
Viewed by 1408
Abstract
It has recently been demonstrated that aromatic bromination at C(2) abolishes all typical psychomotor, and some key prosocial effects of the entactogen MDMA in rats. Nevertheless, the influence of aromatic bromination on MDMA-like effects on higher cognitive functions remains unexplored. In the present [...] Read more.
It has recently been demonstrated that aromatic bromination at C(2) abolishes all typical psychomotor, and some key prosocial effects of the entactogen MDMA in rats. Nevertheless, the influence of aromatic bromination on MDMA-like effects on higher cognitive functions remains unexplored. In the present work, the effects of MDMA and its brominated analog 2Br-4,5-MDMA (1 mg/kg and 10 mg/kg i.p. each) on visuospatial learning, using a radial, octagonal Olton maze (4 × 4) which may discriminate between short-term and long-term memory, were compared with their influence on in vivo long-term potentiation (LTP) in the prefrontal cortex in rats. The results obtained indicate that MDMA diminishes both short- and long-term visuospatial memory but increases LTP. In contrast, 2Br-4,5-MDMA preserves long-term visuospatial memory and slightly accelerates the occurrence of short-term memory compared to controls, but increases LTP, like MDMA. Taken together, these data are consistent with the notion that the modulatory effects induced by the aromatic bromination of the MDMA template, which abolishes typical entactogenic-like responses, might be extended to those effects affecting higher cognitive functions, such as visuospatial learning. This effect seems not to be associated with the increase of LTP in the prefrontal cortex. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

15 pages, 2435 KiB  
Article
GABAergic Regulation of Astroglial Gliotransmission through Cx43 Hemichannels
by Ivanka Jiménez-Dinamarca, Rachel Reyes-Lizana, Yordan Lemunao-Inostroza, Kevin Cárdenas, Raimundo Castro-Lazo, Francisca Peña, Claudia M. Lucero, Juan Prieto-Villalobos, Mauricio Antonio Retamal, Juan Andrés Orellana and Jimmy Stehberg
Int. J. Mol. Sci. 2022, 23(21), 13625; https://doi.org/10.3390/ijms232113625 - 7 Nov 2022
Cited by 3 | Viewed by 1774
Abstract
Gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain. It is produced by interneurons and recycled by astrocytes. In neurons, GABA activates the influx of Cl- via the GABAA receptor or efflux or K+ via the GABAB [...] Read more.
Gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain. It is produced by interneurons and recycled by astrocytes. In neurons, GABA activates the influx of Cl- via the GABAA receptor or efflux or K+ via the GABAB receptor, inducing hyperpolarization and synaptic inhibition. In astrocytes, the activation of both GABAA and GABAB receptors induces an increase in intracellular Ca2+ and the release of glutamate and ATP. Connexin 43 (Cx43) hemichannels are among the main Ca2+-dependent cellular mechanisms for the astroglial release of glutamate and ATP. However, no study has evaluated the effect of GABA on astroglial Cx43 hemichannel activity and Cx43 hemichannel-mediated gliotransmission. Here we assessed the effects of GABA on Cx43 hemichannel activity in DI NCT1 rat astrocytes and hippocampal brain slices. We found that GABA induces a Ca2+-dependent increase in Cx43 hemichannel activity in astrocytes mediated by the GABAA receptor, as it was blunted by the GABAA receptor antagonist bicuculline but unaffected by GABAB receptor antagonist CGP55845. Moreover, GABA induced the Cx43 hemichannel-dependent release of glutamate and ATP, which was also prevented by bicuculline, but unaffected by CGP. Gliotransmission in response to GABA was also unaffected by pannexin 1 channel blockade. These results are discussed in terms of the possible role of astroglial Cx43 hemichannel-mediated glutamate and ATP release in regulating the excitatory/inhibitory balance in the brain and their possible contribution to psychiatric disorders. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

19 pages, 3364 KiB  
Article
Type 1 Corticotropin-Releasing Factor Receptor Differentially Modulates Neurotransmitter Levels in the Nucleus Accumbens of Juvenile versus Adult Rats
by Juan Zegers-Delgado, Alejandro Aguilera-Soza, Florencia Calderón, Harley Davidson, Daniel Verbel-Vergara, Hector E. Yarur, Javier Novoa, Camila Blanlot, Cristian P. Bastias, María Estela Andrés and Katia Gysling
Int. J. Mol. Sci. 2022, 23(18), 10800; https://doi.org/10.3390/ijms231810800 - 16 Sep 2022
Cited by 2 | Viewed by 1723
Abstract
Adversity is particularly pernicious in early life, increasing the likelihood of developing psychiatric disorders in adulthood. Juvenile and adult rats exposed to social isolation show differences in anxiety-like behaviors and significant changes in dopamine (DA) neurotransmission in the nucleus accumbens (NAc). Brain response [...] Read more.
Adversity is particularly pernicious in early life, increasing the likelihood of developing psychiatric disorders in adulthood. Juvenile and adult rats exposed to social isolation show differences in anxiety-like behaviors and significant changes in dopamine (DA) neurotransmission in the nucleus accumbens (NAc). Brain response to stress is partly mediated by the corticotropin-releasing factor (CRF) system, composed of CRF and its two main receptors, CRF-R1 and CRF-R2. In the NAc shell of adult rats, CRF induces anxiety-like behavior and changes local DA balance. However, the role of CRF receptors in the control of neurotransmission in the NAc is not fully understood, nor is it known whether there are differences between life stages. Our previous data showed that infusion of a CRF-R1 antagonist into the NAc of juvenile rats increased DA levels in response to a depolarizing stimulus and decreased basal glutamate levels. To extend this analysis, we now evaluated the effect of a CRF-R1 antagonist infusion in the NAc of adult rats. Here, we describe that the opposite occurred in the NAc of adult compared to juvenile rats. Infusion of a CRF-R1 antagonist decreased DA and increased glutamate levels in response to a depolarizing stimulus. Furthermore, basal levels of DA, glutamate, and γ-Aminobutyric acid (GABA) were similar in juvenile animals compared to adults. CRF-R1 protein levels and localization were not different in juvenile compared to adult rats. Interestingly, we observed differences in the signaling pathways of CRF-R1 in the NAc of juveniles compared to adult rats. We propose that the function of CRF-R1 receptors is differentially modulated in the NAc according to life stage. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

13 pages, 1475 KiB  
Communication
Prefrontal Cortical Control of Activity in Nucleus Accumbens Core Is Weakened by High-Fat Diet and Prevented by Co-Treatment with N-Acetylcysteine: Implications for the Development of Obesity
by Carlos Morgan, Patricio Sáez-Briones, Rafael Barra, Andrea Reyes, Katherine Zepeda-Morales, Luis Constandil, Miguel Ríos, Paulina Ramírez, Héctor Burgos and Alejandro Hernández
Int. J. Mol. Sci. 2022, 23(17), 10089; https://doi.org/10.3390/ijms231710089 - 3 Sep 2022
Cited by 1 | Viewed by 1800
Abstract
A loss of neuroplastic control on nucleus accumbens (NAc) neuronal activity exerted by the medial prefrontal cortex (mPFC) through long-term depression (LTD) is involved in triggering drug-seeking behavior and relapse on several substances of abuse due to impaired glutamate homeostasis in tripartite synapses [...] Read more.
A loss of neuroplastic control on nucleus accumbens (NAc) neuronal activity exerted by the medial prefrontal cortex (mPFC) through long-term depression (LTD) is involved in triggering drug-seeking behavior and relapse on several substances of abuse due to impaired glutamate homeostasis in tripartite synapses of the nucleus accumbens (NAc) core. To test whether this maladaptive neuroplastic mechanism underlies the addiction-like behavior induced in young mice by a high-fat diet (HFD), we utilized 28-days-old male mice fed HFD ad-libitum over 2 weeks, followed by 5 days of HFD abstinence. Control groups were fed a regular diet. HFD fed mice showed increased ΔFosB levels in the NAc core region, whereas LTD triggered from the mPFC became suppressed. Interestingly, LTD suppression was prevented by an i.p. injection of 100 mg/kg N-acetylcysteine 2.5 h before inducing LTD from the mPFC. In addition, excessive weight gain due to HFD feeding was diminished by adding 2mg/mL N-acetylcysteine in drinking water. Those results show a loss of neuroplastic mPFC control over NAc core activity induced by HFD consumption in young subjects. In conclusion, ad libitum consumption of HFD can lead to neuroplastic changes an addiction-like behavior that can be prevented by N-acetylcysteine, helping to decrease the rate of excessive weight gain. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

18 pages, 3203 KiB  
Article
Dlg Is Required for Short-Term Memory and Interacts with NMDAR in the Drosophila Brain
by Francisca Bertin, Guillermo Moya-Alvarado, Eduardo Quiroz-Manríquez, Andrés Ibacache, Andrés Köhler-Solis, Carlos Oliva and Jimena Sierralta
Int. J. Mol. Sci. 2022, 23(16), 9187; https://doi.org/10.3390/ijms23169187 - 16 Aug 2022
Viewed by 2002
Abstract
The vertebrates’ scaffold proteins of the Dlg-MAGUK family are involved in the recruitment, clustering, and anchoring of glutamate receptors to the postsynaptic density, particularly the NMDA subtype glutamate-receptors (NRs), necessary for long-term memory and LTP. In Drosophila, the only gene of the [...] Read more.
The vertebrates’ scaffold proteins of the Dlg-MAGUK family are involved in the recruitment, clustering, and anchoring of glutamate receptors to the postsynaptic density, particularly the NMDA subtype glutamate-receptors (NRs), necessary for long-term memory and LTP. In Drosophila, the only gene of the subfamily generates two main products, dlgA, broadly expressed, and dlgS97, restricted to the nervous system. In the Drosophila brain, NRs are expressed in the adult brain and are involved in memory, however, the role of Dlg in these processes and its relationship with NRs has been scarcely explored. Here, we show that the dlg mutants display defects in short-term memory in the olfactory associative-learning paradigm. These defects are dependent on the presence of DlgS97 in the Mushroom Body (MB) synapses. Moreover, Dlg is immunoprecipitated with NRs in the adult brain. Dlg is also expressed in the larval neuromuscular junction (NMJ) pre and post-synaptically and is important for development and synaptic function, however, NR is absent in this synapse. Despite that, we found changes in the short-term plasticity paradigms in dlg mutant larval NMJ. Together our results show that larval NMJ and the adult brain relies on Dlg for short-term memory/plasticity, but the mechanisms differ in the two types of synapses. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

17 pages, 2112 KiB  
Article
NMDA and P2X7 Receptors Require Pannexin 1 Activation to Initiate and Maintain Nociceptive Signaling in the Spinal Cord of Neuropathic Rats
by David Bravo, Katherine Zepeda-Morales, Carola J. Maturana, Jeffri S. Retamal, Alejandro Hernández, Teresa Pelissier, Rafael Barra, Patricio Sáez-Briones, Héctor Burgos and Luis Constandil
Int. J. Mol. Sci. 2022, 23(12), 6705; https://doi.org/10.3390/ijms23126705 - 16 Jun 2022
Cited by 6 | Viewed by 2002
Abstract
Pannexin 1 (Panx1) is involved in the spinal central sensitization process in rats with neuropathic pain, but its interaction with well-known, pain-related, ligand-dependent receptors, such as NMDA receptors (NMDAR) and P2X7 purinoceptors (P2X7R), remains largely unexplored. Here, we studied whether NMDAR- and P2X7R-dependent [...] Read more.
Pannexin 1 (Panx1) is involved in the spinal central sensitization process in rats with neuropathic pain, but its interaction with well-known, pain-related, ligand-dependent receptors, such as NMDA receptors (NMDAR) and P2X7 purinoceptors (P2X7R), remains largely unexplored. Here, we studied whether NMDAR- and P2X7R-dependent nociceptive signaling in neuropathic rats require the activation of Panx1 channels to generate spinal central sensitization, as assessed by behavioral (mechanical hyperalgesia) and electrophysiological (C-reflex wind-up potentiation) indexes. Administration of either a selective NMDAR agonist i.t. (NMDA, 2 mM) or a P2X7R agonist (BzATP, 150 μM) significantly increased both the mechanical hyperalgesia and the C-reflex wind-up potentiation, effects that were rapidly reversed (minutes) by i.t. administration of a selective pannexin 1 antagonist (10panx peptide, 300 μM), with the scores even reaching values of rats without neuropathy. Accordingly, 300 μM 10panx completely prevented the effects of NMDA and BzATP administered 1 h later, on mechanical hyperalgesia and C-reflex wind-up potentiation. Confocal immunofluorescence imaging revealed coexpression of Panx1 with NeuN protein in intrinsic dorsal horn neurons of neuropathic rats. The results indicate that both NMDAR- and P2X7R-mediated increases in mechanical hyperalgesia and C-reflex wind-up potentiation require neuronal Panx1 channel activation to initiate and maintain nociceptive signaling in neuropathic rats. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

12 pages, 2166 KiB  
Article
Effects of Early Life Exposure to Sex Hormones on Neurochemical and Behavioral Responses to Psychostimulants in Adulthood: Implications in Drug Addiction
by Maximiliano Elgueta-Reyes, Victoria B. Velásquez, Pedro Espinosa, Raúl Riquelme, Tatiana Dib, Nicole K. Sanguinetti, Angélica P. Escobar, Jonathan Martínez-Pinto, Georgina M. Renard and Ramón Sotomayor-Zárate
Int. J. Mol. Sci. 2022, 23(12), 6575; https://doi.org/10.3390/ijms23126575 - 12 Jun 2022
Cited by 3 | Viewed by 1854
Abstract
Early life exposure to sex hormones affects several brain areas involved in regulating locomotor and motivation behaviors. Our group has shown that neonatal exposure to testosterone propionate (TP) or estradiol valerate (EV) affected the brain dopamine (DA) system in adulthood. Here, we studied [...] Read more.
Early life exposure to sex hormones affects several brain areas involved in regulating locomotor and motivation behaviors. Our group has shown that neonatal exposure to testosterone propionate (TP) or estradiol valerate (EV) affected the brain dopamine (DA) system in adulthood. Here, we studied the long-lasting effects of neonatal exposure to sex hormones on behavioral and neurochemical responses to amphetamine (AMPH) and methylphenidate (MPD). Our results show that AMPH-induced locomotor activity was higher in female than male control rats. The conditioned place preference (CPP) to AMPH was only observed in EV male rats. In EV female rats, AMPH did not increase locomotor activity, but MPD-induced CPP was observed in control, EV and TP female rats. Using in vivo brain microdialysis, we observed that AMPH-induced extracellular DA levels were lower in nucleus accumbens (NAcc) of EV and TP female rats than control rats. In addition, MPD did not increase NAcc extracellular DA levels in EV rats. Using in vivo fast-scan cyclic voltammetry in striatum, MPD-induced DA reuptake was higher in EV than control rats. In summary, our results show that early life exposure to sex hormones modulates mesolimbic and nigrostriatal DA neurons producing opposite neurochemical effects induced by psychostimulant drugs in NAcc or striatum. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 1745 KiB  
Review
Navigating Like a Fly: Drosophila melanogaster as a Model to Explore the Contribution of Serotonergic Neurotransmission to Spatial Navigation
by Ivana Gajardo, Simón Guerra and Jorge M. Campusano
Int. J. Mol. Sci. 2023, 24(5), 4407; https://doi.org/10.3390/ijms24054407 - 23 Feb 2023
Cited by 1 | Viewed by 2299
Abstract
Serotonin is a monoamine that acts in vertebrates and invertebrates as a modulator promoting changes in the structure and activity of brain areas relevant to animal behavior, ranging from sensory perception to learning and memory. Whether serotonin contributes in Drosophila to human-like cognitive [...] Read more.
Serotonin is a monoamine that acts in vertebrates and invertebrates as a modulator promoting changes in the structure and activity of brain areas relevant to animal behavior, ranging from sensory perception to learning and memory. Whether serotonin contributes in Drosophila to human-like cognitive abilities, including spatial navigation, is an issue little studied. Like in vertebrates, the serotonergic system in Drosophila is heterogeneous, meaning that distinct serotonergic neurons/circuits innervate specific fly brain regions to modulate precise behaviors. Here we review the literature that supports that serotonergic pathways modify different aspects underlying the formation of navigational memories in Drosophila. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

25 pages, 12538 KiB  
Review
Ca2+- and Voltage-Activated K+ (BK) Channels in the Nervous System: One Gene, a Myriad of Physiological Functions
by Carlos Ancatén-González, Ignacio Segura, Rosangelina Alvarado-Sánchez, Andrés E. Chávez and Ramon Latorre
Int. J. Mol. Sci. 2023, 24(4), 3407; https://doi.org/10.3390/ijms24043407 - 8 Feb 2023
Cited by 8 | Viewed by 2903
Abstract
BK channels are large conductance potassium channels characterized by four pore-forming α subunits, often co-assembled with auxiliary β and γ subunits to regulate Ca2+ sensitivity, voltage dependence and gating properties. BK channels are abundantly expressed throughout the brain and in different compartments [...] Read more.
BK channels are large conductance potassium channels characterized by four pore-forming α subunits, often co-assembled with auxiliary β and γ subunits to regulate Ca2+ sensitivity, voltage dependence and gating properties. BK channels are abundantly expressed throughout the brain and in different compartments within a single neuron, including axons, synaptic terminals, dendritic arbors, and spines. Their activation produces a massive efflux of K+ ions that hyperpolarizes the cellular membrane. Together with their ability to detect changes in intracellular Ca2+ concentration, BK channels control neuronal excitability and synaptic communication through diverse mechanisms. Moreover, increasing evidence indicates that dysfunction of BK channel-mediated effects on neuronal excitability and synaptic function has been implicated in several neurological disorders, including epilepsy, fragile X syndrome, mental retardation, and autism, as well as in motor and cognitive behavior. Here, we discuss current evidence highlighting the physiological importance of this ubiquitous channel in regulating brain function and its role in the pathophysiology of different neurological disorders. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

13 pages, 1106 KiB  
Review
Obesogenic Diet-Induced Neuroinflammation: A Pathological Link between Hedonic and Homeostatic Control of Food Intake
by José Luis Marcos, Rossy Olivares-Barraza, Karina Ceballo, Melisa Wastavino, Víctor Ortiz, Julio Riquelme, Jonathan Martínez-Pinto, Pablo Muñoz, Gonzalo Cruz and Ramón Sotomayor-Zárate
Int. J. Mol. Sci. 2023, 24(2), 1468; https://doi.org/10.3390/ijms24021468 - 11 Jan 2023
Cited by 7 | Viewed by 2411
Abstract
Obesity-induced neuroinflammation is a chronic aseptic central nervous system inflammation that presents systemic characteristics associated with increased pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and interleukin 18 (IL-18) and the presence of microglia and reactive astrogliosis as well as the activation of [...] Read more.
Obesity-induced neuroinflammation is a chronic aseptic central nervous system inflammation that presents systemic characteristics associated with increased pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and interleukin 18 (IL-18) and the presence of microglia and reactive astrogliosis as well as the activation of the NLRP3 inflammasome. The obesity pandemic is associated with lifestyle changes, including an excessive intake of obesogenic foods and decreased physical activity. Brain areas such as the lateral hypothalamus (LH), lateral septum (LS), ventral tegmental area (VTA), and nucleus accumbens (NAcc) have been implicated in the homeostatic and hedonic control of feeding in experimental models of diet-induced obesity. In this context, a chronic lipid intake triggers neuroinflammation in several brain regions such as the hypothalamus, hippocampus, and amygdala. This review aims to present the background defining the significant impact of neuroinflammation and how this, when induced by an obesogenic diet, can affect feeding control, triggering metabolic and neurological alterations. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

22 pages, 1628 KiB  
Review
How Are Synapses Born? A Functional and Molecular View of the Role of the Wnt Signaling Pathway
by Christian Bonansco, Waldo Cerpa and Nibaldo C. Inestrosa
Int. J. Mol. Sci. 2023, 24(1), 708; https://doi.org/10.3390/ijms24010708 - 31 Dec 2022
Cited by 2 | Viewed by 1702
Abstract
Synaptic transmission is a dynamic process that requires precise regulation. Early in life, we must be able to forge appropriate connections (add and remove) to control our behavior. Neurons must recognize appropriate targets, and external soluble factors that activate specific signaling cascades provide [...] Read more.
Synaptic transmission is a dynamic process that requires precise regulation. Early in life, we must be able to forge appropriate connections (add and remove) to control our behavior. Neurons must recognize appropriate targets, and external soluble factors that activate specific signaling cascades provide the regulation needed to achieve this goal. Wnt signaling has been implicated in several forms of synaptic plasticity, including functional and structural changes associated with brain development. The analysis of synapses from an electrophysiological perspective allows us to characterize the functional role of cellular signaling pathways involved in brain development. The application of quantal theory to principles of developmental plasticity offers the possibility of dissecting the function of structural changes associated with the birth of new synapses as well as the maturation of immature silent synapses. Here, we focus on electrophysiological and molecular evidence that the Wnt signaling pathway regulates glutamatergic synaptic transmission, specifically N-methyl-d-aspartate receptors (NMDARs), to control the birth of new synapses. We also focus on the role of Wnts in the conversion of silent synapses into functional synapses. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

19 pages, 1179 KiB  
Review
The Role of the Paraventricular-Coerulear Network on the Programming of Hypertension by Prenatal Undernutrition
by Bernardita Cayupe, Blanca Troncoso, Carlos Morgan, Patricio Sáez-Briones, Ramón Sotomayor-Zárate, Luis Constandil, Alejandro Hernández, Eugenia Morselli and Rafael Barra
Int. J. Mol. Sci. 2022, 23(19), 11965; https://doi.org/10.3390/ijms231911965 - 8 Oct 2022
Cited by 1 | Viewed by 1841
Abstract
A crucial etiological component in fetal programming is early nutrition. Indeed, early undernutrition may cause a chronic increase in blood pressure and cardiovascular diseases, including stroke and heart failure. In this regard, current evidence has sustained several pathological mechanisms involving changes in central [...] Read more.
A crucial etiological component in fetal programming is early nutrition. Indeed, early undernutrition may cause a chronic increase in blood pressure and cardiovascular diseases, including stroke and heart failure. In this regard, current evidence has sustained several pathological mechanisms involving changes in central and peripheral targets. In the present review, we summarize the neuroendocrine and neuroplastic modifications that underlie maladaptive mechanisms related to chronic hypertension programming after early undernutrition. First, we analyzed the role of glucocorticoids on the mechanism of long-term programming of hypertension. Secondly, we discussed the pathological plastic changes at the paraventricular nucleus of the hypothalamus that contribute to the development of chronic hypertension in animal models of prenatal undernutrition, dissecting the neural network that reciprocally communicates this nucleus with the locus coeruleus. Finally, we propose an integrated and updated view of the main neuroendocrine and central circuital alterations that support the occurrence of chronic increases of blood pressure in prenatally undernourished animals. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

32 pages, 6634 KiB  
Review
Behavioral, Neural, and Molecular Mechanisms of Conditioned Mate Preference: The Role of Opioids and First Experiences of Sexual Reward
by Gonzalo R. Quintana, Conall E. Mac Cionnaith and James G. Pfaus
Int. J. Mol. Sci. 2022, 23(16), 8928; https://doi.org/10.3390/ijms23168928 - 10 Aug 2022
Cited by 6 | Viewed by 3346
Abstract
Although mechanisms of mate preference are thought to be relatively hard-wired, experience with appetitive and consummatory sexual reward has been shown to condition preferences for partner related cues and even objects that predict sexual reward. Here, we reviewed evidence from laboratory species and [...] Read more.
Although mechanisms of mate preference are thought to be relatively hard-wired, experience with appetitive and consummatory sexual reward has been shown to condition preferences for partner related cues and even objects that predict sexual reward. Here, we reviewed evidence from laboratory species and humans on sexually conditioned place, partner, and ejaculatory preferences in males and females, as well as the neurochemical, molecular, and epigenetic mechanisms putatively responsible. From a comprehensive review of the available data, we concluded that opioid transmission at μ opioid receptors forms the basis of sexual pleasure and reward, which then sensitizes dopamine, oxytocin, and vasopressin systems responsible for attention, arousal, and bonding, leading to cortical activation that creates awareness of attraction and desire. First experiences with sexual reward states follow a pattern of sexual imprinting, during which partner- and/or object-related cues become crystallized by conditioning into idiosyncratic “types” that are found sexually attractive and arousing. These mechanisms tie reward and reproduction together, blending proximate and ultimate causality in the maintenance of variability within a species. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

20 pages, 916 KiB  
Review
Roles of the Unsaturated Fatty Acid Docosahexaenoic Acid in the Central Nervous System: Molecular and Cellular Insights
by Ana B. Petermann, Mauricio Reyna-Jeldes, Lorena Ortega, Claudio Coddou and Gonzalo E. Yévenes
Int. J. Mol. Sci. 2022, 23(10), 5390; https://doi.org/10.3390/ijms23105390 - 12 May 2022
Cited by 18 | Viewed by 4383
Abstract
Fatty acids (FAs) are essential components of the central nervous system (CNS), where they exert multiple roles in health and disease. Among the FAs, docosahexaenoic acid (DHA) has been widely recognized as a key molecule for neuronal function and cell signaling. Despite its [...] Read more.
Fatty acids (FAs) are essential components of the central nervous system (CNS), where they exert multiple roles in health and disease. Among the FAs, docosahexaenoic acid (DHA) has been widely recognized as a key molecule for neuronal function and cell signaling. Despite its relevance, the molecular pathways underlying the beneficial effects of DHA on the cells of the CNS are still unclear. Here, we summarize and discuss the molecular mechanisms underlying the actions of DHA in neural cells with a special focus on processes of survival, morphological development, and synaptic maturation. In addition, we examine the evidence supporting a potential therapeutic role of DHA against CNS tumor diseases and tumorigenesis. The current results suggest that DHA exerts its actions on neural cells mainly through the modulation of signaling cascades involving the activation of diverse types of receptors. In addition, we found evidence connecting brain DHA and ω-3 PUFA levels with CNS diseases, such as depression, autism spectrum disorders, obesity, and neurodegenerative diseases. In the context of cancer, the existing data have shown that DHA exerts positive actions as a coadjuvant in antitumoral therapy. Although many questions in the field remain only partially resolved, we hope that future research may soon define specific pathways and receptor systems involved in the beneficial effects of DHA in cells of the CNS, opening new avenues for innovative therapeutic strategies for CNS diseases. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Chile)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-15
Back to TopTop