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Roles and Functions of Neurotrophins and Their Receptors in the...
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Roles and Functions of Neurotrophins and Their Receptors in the Brain

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 6797

Special Issue Editor

Prof. Dr. Oliver Von Bohlen Und Halbach

E-Mail Website
Guest Editor
Institute of Anatomy and Cell Biology, Universitätsmedizin Greifswald, Friedrich Loeffler Str. 23c, 17487 Greifswald, Germany
Interests: neuronal plasticity; adult neurogenesis; dendritic spines; neurotrophins; growth factors in the CNS; mechanisms of learning and memory

Special Issue Information

Dear Colleagues,

The neurotrophin family consists of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and the neurotrophins 3 (NT-3) and 4 (NT-4). Neurotrophins signal through specific receptors that belong to the family of tyrosine receptor kinases (NGF mainly binds to trkA; BDNF mainly binds to trkB; and NT-3 mainly binds to trkC). In addition, they can signal through the pan-neurotrophin receptor p57 (P57NTR). Neurotrophins not only have important roles during brain development, but their signaling is also essential for the postnatal brain, especially for processes that involve synaptic and neuronal plasticity. For example, neurotrophins in the postnatal brain regulate dendritic spines and are involved in the induction and/or maintenance of long-term potentiation (LTP). Disturbances in the neurotrophin system are thought to be associated with obesity and several mental illnesses including major depression. Antidepressant treatment can increase peripheral BDNF levels, which in turn may improve one’s recovery from depression. Aside from BDNF, the roles of other neurotrophins in synaptic and neuronal plasticity, as well as their involvement in mental illnesses, is much less understood.

In this Special Issue, we will highlight recent advancements in our understanding of how neurotrophins act on the brain (and thereby modulate neuronal plasticity, learning and memory, as well as behavior), both in health and disease.

Authors may submit reviews, short communications and full-size research papers which focus on the diverse roles of neurotrophins and their signaling in the brain.

I look forward to receiving your contributions.

Prof. Dr. Oliver Von Bohlen Und Halbach
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. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • aging
  • behavior
  • learning
  • memory
  • mental disorders
  • neuroanatomy
  • neurobiology
  • neuronal plasticity
  • neurophysiology
  • synaptic plasticity

Published Papers (6 papers)

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Research

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16 pages, 5008 KiB  
Article
Short- and Long-Term Effects of Subchronic Stress Exposure in Male and Female Brain-Derived Neurotrophic Factor Knock-In Val66Met Mice
by Fernando Antonio Costa Xavier, Silvia Stella Barbieri, Maurizio Popoli and Alessandro Ieraci
Biology 2024, 13(5), 303; https://doi.org/10.3390/biology13050303 - 27 Apr 2024
Viewed by 312
Abstract
Stress is an important risk factor for the onset of anxiety and depression. The ability to cope with stressful events varies among different subjects, probably depending on different genetic variants, sex and previous life experiences. The Val66Met variant of Brain-Derived Neurotrophic Factor (BDNF), [...] Read more.
Stress is an important risk factor for the onset of anxiety and depression. The ability to cope with stressful events varies among different subjects, probably depending on different genetic variants, sex and previous life experiences. The Val66Met variant of Brain-Derived Neurotrophic Factor (BDNF), which impairs the activity-dependent secretion of BDNF, has been associated with increased susceptibility to the development of various neuropsychiatric disorders. Adult male and female wild-type Val/Val (BDNFV/V) and heterozygous Val/Met (BDNFV/M) mice were exposed to two sessions of forced swimming stress (FSS) per day for two consecutive days. The mice were behaviorally tested 1 day (short-term effect) or 11 days (long-term effect) after the last stress session. Protein and mRNA levels were measured in the hippocampus 16 days after the end of stress exposure. Stressed mice showed a higher anxiety-like phenotype compared to non-stressed mice, regardless of the sex and genotype, when analyzed following the short period of stress. In the prolonged period, anxiety-like behavior persisted only in male BDNFV/M mice (p < 0.0001). Interestingly, recovery in male BDNFV/V mice was accompanied by an increase in pCREB (p < 0.001) and Bdnf4 (p < 0.01) transcript and a decrease in HDAC1 (p < 0.05) and Dnmt3a (p = 0.01) in the hippocampus. Overall, our results show that male and female BDNF Val66Met knock-in mice can recover from subchronic stress in different ways. Full article
(This article belongs to the Special Issue Roles and Functions of Neurotrophins and Their Receptors in the Brain)
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12 pages, 1455 KiB  
Article
Reduced Levels of Brain-Derived Neurotrophic Factor Affect Body Weight, Brain Weight and Behavior
by Matthias Wilhelm Voigt, Jens Schepers, Jacqueline Haas and Oliver von Bohlen und Halbach
Biology 2024, 13(3), 159; https://doi.org/10.3390/biology13030159 - 29 Feb 2024
Viewed by 914
Abstract
Neurotrophins, which belong to the family of growth factors, not only play crucial roles during development but are also involved in many processes in the postnatal brain. One representative of neurotrophins is brain-derived neurotrophic factor (BDNF). BDNF plays a role in the regulation [...] Read more.
Neurotrophins, which belong to the family of growth factors, not only play crucial roles during development but are also involved in many processes in the postnatal brain. One representative of neurotrophins is brain-derived neurotrophic factor (BDNF). BDNF plays a role in the regulation of body weight and neuronal plasticity and is, therefore, also involved in processes associated with learning and memory formation. Many of the studies on BDNF have been carried out using BDNF-deficient mice. Unfortunately, homozygous deletion of BDNF is lethal in the early postnatal stage, so heterozygous BDNF-deficient mice are often studied. Another possibility is the use of conditional BDNF-deficient mice in which the expression of BDNF is strongly downregulated in some brain cells, for example, in the neurons of the central nervous system, but the expression of BDNF in other cells in the brain is unchanged. To further reduce BDNF expression, we crossed heterozygous BDNF-deficient mice with mice carrying a deletion of BDNF in neurofilament L-positive neurons. These offspring are viable, and the animals with a strong reduction in BDNF in the brain show a strongly increased body weight, which is accompanied by a reduction in brain weight. In addition, these animals show behavioral abnormalities, particularly with regard to locomotion. Full article
(This article belongs to the Special Issue Roles and Functions of Neurotrophins and Their Receptors in the Brain)
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13 pages, 2936 KiB  
Article
Effects of Aging and Nerve Growth Factor on Neuropeptide Expression and Cholinergic Innervation of the Rat Basolateral Amygdala
by Pedro A. Pereira, Marta Tavares, Miguel Laires, Bárbara Mota, Maria Dulce Madeira, Manuel M. Paula-Barbosa and Armando Cardoso
Biology 2024, 13(3), 155; https://doi.org/10.3390/biology13030155 - 28 Feb 2024
Viewed by 921
Abstract
The basolateral amygdala (BLA) contains interneurons that express neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), both of which are involved in the regulation of functions and behaviors that undergo deterioration with aging. There is considerable evidence that, in some brain areas, the [...] Read more.
The basolateral amygdala (BLA) contains interneurons that express neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), both of which are involved in the regulation of functions and behaviors that undergo deterioration with aging. There is considerable evidence that, in some brain areas, the expression of NPY and VIP might be modulated by acetylcholine. Importantly, the BLA is one of the brain regions that has one of the densest cholinergic innervations, which arise mainly from the basal forebrain cholinergic neurons. These cholinergic neurons depend on nerve growth factor (NGF) for their survival, connectivity, and function. Thus, in this study, we sought to determine if aging alters the densities of NPY- and VIP-positive neurons and cholinergic varicosities in the BLA and, in the affirmative, if those changes might rely on insufficient trophic support provided by NGF. The number of NPY-positive neurons was significantly reduced in aged rats, whereas the number of VIP-immunoreactive neurons was unaltered. The decreased NPY expression was fully reversed by the infusion of NGF in the lateral ventricle. The density of cholinergic varicosities was similar in adult and old rats. On the other hand, the density of cholinergic varicosities is significantly higher in old rats treated with NGF than in adult and old rats. Our results indicate a dissimilar resistance of different populations of BLA interneurons to aging. Furthermore, the present data also show that the BLA cholinergic innervation is particularly resistant to aging effects. Finally, our results also show that the reduced NPY expression in the BLA of aged rats can be related to changes in the NGF neurotrophic support. Full article
(This article belongs to the Special Issue Roles and Functions of Neurotrophins and Their Receptors in the Brain)
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25 pages, 3792 KiB  
Article
Dopaminergic Input Regulates the Sensitivity of Indirect Pathway Striatal Spiny Neurons to Brain-Derived Neurotrophic Factor
by Maurilyn Ayon-Olivas, Daniel Wolf, Thomas Andreska, Noelia Granado, Patrick Lüningschrör, Chi Wang Ip, Rosario Moratalla and Michael Sendtner
Biology 2023, 12(10), 1360; https://doi.org/10.3390/biology12101360 - 23 Oct 2023
Cited by 2 | Viewed by 1270
Abstract
Motor dysfunction in Parkinson’s disease (PD) is closely linked to the dopaminergic depletion of striatal neurons and altered synaptic plasticity at corticostriatal synapses. Dopamine receptor D1 (DRD1) stimulation is a crucial step in the formation of long-term potentiation (LTP), whereas dopamine receptor D2 [...] Read more.
Motor dysfunction in Parkinson’s disease (PD) is closely linked to the dopaminergic depletion of striatal neurons and altered synaptic plasticity at corticostriatal synapses. Dopamine receptor D1 (DRD1) stimulation is a crucial step in the formation of long-term potentiation (LTP), whereas dopamine receptor D2 (DRD2) stimulation is needed for the formation of long-term depression (LTD) in striatal spiny projection neurons (SPNs). Tropomyosin receptor kinase B (TrkB) and its ligand brain-derived neurotrophic factor (BDNF) are centrally involved in plasticity regulation at the corticostriatal synapses. DRD1 activation enhances TrkB’s sensitivity for BDNF in direct pathway spiny projection neurons (dSPNs). In this study, we showed that the activation of DRD2 in cultured striatal indirect pathway spiny projection neurons (iSPNs) and cholinergic interneurons causes the retraction of TrkB from the plasma membrane. This provides an explanation for the opposing synaptic plasticity changes observed upon DRD1 or DRD2 stimulation. In addition, TrkB was found within intracellular structures in dSPNs and iSPNs from Pitx3−/− mice, a genetic model of PD with early onset dopaminergic depletion in the dorsolateral striatum (DLS). This dysregulated BDNF/TrkB signaling might contribute to the pathophysiology of direct and indirect pathway striatal projection neurons in PD. Full article
(This article belongs to the Special Issue Roles and Functions of Neurotrophins and Their Receptors in the Brain)
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17 pages, 1631 KiB  
Article
A Rat Model of the Brain-Derived Neurotrophic Factor Val66Met Polymorphism Shows Attenuated Motivation for Alcohol Self-Administration and Diminished Propensity for Cue-Induced Relapse in Females
by Emily J. Jaehne, Elizabeth McInerney, Ronan Sharma, Shannyn G. Genders, Elvan Djouma and Maarten van den Buuse
Biology 2023, 12(6), 799; https://doi.org/10.3390/biology12060799 - 31 May 2023
Cited by 1 | Viewed by 1149
Abstract
Brain-derived neurotrophic factor (BDNF) has been implicated in alcohol use disorder. The Val66Met polymorphism is a common variant of the BDNF gene (rs6265) which reduces activity-dependent BDNF release, and has been suggested as a risk factor for psychiatric disorders and substance use. Using [...] Read more.
Brain-derived neurotrophic factor (BDNF) has been implicated in alcohol use disorder. The Val66Met polymorphism is a common variant of the BDNF gene (rs6265) which reduces activity-dependent BDNF release, and has been suggested as a risk factor for psychiatric disorders and substance use. Using an operant self-administration paradigm, this study aimed to investigate ethanol preference and ethanol seeking in a novel rat model of the BDNF Val66Met polymorphism, Val68Met rats. Male and female BDNF Val68Met rats of three genotypes (Val/Val, Val/Met and Met/Met) were trained to lever press for a 10% ethanol solution. There was no effect of Val68Met genotype on acquisition of stable response to ethanol or its extinction. Met/Met rats of both sexes had a slight, but significantly lower breakpoint during progressive ratio sessions while female rats with the Met/Met genotype demonstrated a lower propensity for reinstatement of responding to cues. There were no effects of Val68Met genotype on anxiety-like behaviour or locomotor activity. In conclusion, Met/Met rats showed lower motivation to continue to press for a reward, and also a decreased propensity to relapse, suggesting a possible protective effect of the Met/Met genotype against alcohol use disorder, at least in females. Full article
(This article belongs to the Special Issue Roles and Functions of Neurotrophins and Their Receptors in the Brain)
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Review

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20 pages, 1036 KiB  
Review
Exploring Rosiglitazone’s Potential to Treat Alzheimer’s Disease through the Modulation of Brain-Derived Neurotrophic Factor
by Mackayla L. Nelson, Julia A. Pfeifer, Jordan P. Hickey, Andrila E. Collins and Bettina E. Kalisch
Biology 2023, 12(7), 1042; https://doi.org/10.3390/biology12071042 - 24 Jul 2023
Viewed by 1516
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that debilitates over 55 million individuals worldwide. Currently, treatments manage and alleviate its symptoms; however, there is still a need to find a therapy that prevents or halts disease progression. Since AD has been labeled [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that debilitates over 55 million individuals worldwide. Currently, treatments manage and alleviate its symptoms; however, there is still a need to find a therapy that prevents or halts disease progression. Since AD has been labeled as “type 3 diabetes” due to its similarity in pathological hallmarks, molecular pathways, and comorbidity with type 2 diabetes mellitus (T2DM), there is growing interest in using anti-diabetic drugs for its treatment. Rosiglitazone (RSG) is a peroxisome proliferator-activated receptor-gamma agonist that reduces hyperglycemia and hyperinsulinemia and improves insulin signaling. In cellular and rodent models of T2DM-associated cognitive decline and AD, RSG has been reported to improve cognitive impairment and reverse AD-like pathology; however, results from human clinical trials remain consistently unsuccessful. RSG has also been reported to modulate the expression of brain-derived neurotrophic factor (BDNF), a protein that regulates neuroplasticity and energy homeostasis and is implicated in both AD and T2DM. The present review investigates RSG’s limitations and potential therapeutic benefits in pre-clinical models of AD through its modulation of BDNF expression. Full article
(This article belongs to the Special Issue Roles and Functions of Neurotrophins and Their Receptors in the Brain)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: A rat model of the brain-derived neurotrophic factor Val66Met polymorphism shows association of the Met/Met genotype with reduced motivation for alcohol self-administration and reduced propensity for cue-induced relapse
Authors: Emily J. Jaehne; Elizabeth McInerney; Ronan Sharma; Shannyn Genders; Elvan Djouma; Maarten van den Buuse
Affiliation: 1. Department of Psychology, Counselling and Therapy, School of Psychology and Public Health, La Trobe University, Melbourne, Australia 2. Department of Microbiology, Anatomy, Physiology and Pharmacology, School of Agriculture, Biomedicine and Environment, La Trobe University, Melbourne, Australia 3. Department of Pharmacology, University of Melbourne, Melbourne, Australia

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