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Brain Neurotransmitters in Genetic Control of Behavior

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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 2021) | Viewed by 13390

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Special Issue Editor

Prof. Dr. Nina K. Popova

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Guest Editor

Department of Behavioral Neurogenomics, Institute of Cytology and Genetics, Lavrentyeva av. 10, Novosibirsk 630090, Russia
Interests: brain neurotransmitters; behavior; brain serotonin system; neurotrophic factors; aggression; depression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

A Special Issue entitled “Brain Neurotransmitters in Genetic Control of Behavior" is being prepared for the IJMS journal. Brain neurotransmitters are playing crucial roles in the mechanisms of brain and behavioral plasticity. Enzymes, transporters and receptors of brain neurotransmitters are under the control of various genetic and epigenetic factors. Moreover, the majority of proteins could undergo different posttranslational modifications that significantly affect their function.

This Special Issue focuses on the role of brain neurotransmitters in the regulation of normal and pathological behavior as well as genetic predisposition to behavioral disorders. We warmly welcome submissions, including original papers and reviews dealing with different aspects of neurotransmitters contribution in behavioral control.

Dr. Nina K. Popova
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

behavioral neurogenomics
neuroplasticity
brain neurotransmitters
normal and pathological behavior
neurodegenerative diseases
gene and protein expression
posttranslational regulation
microRNA in behavioral control

Published Papers (5 papers)

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Research

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16 pages, 2321 KiB

Open AccessArticle

Genetic Background Underlying 5-HT_1A Receptor Functioning Affects the Response to Fluoxetine

by Elena M. Kondaurova, Alexander Ya. Rodnyy, Tatiana V. Ilchibaeva, Anton S. Tsybko, Dmitry V. Eremin, Yegor V. Antonov, Nina K. Popova and Vladimir S. Naumenko

Int. J. Mol. Sci. 2020, 21(22), 8784; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228784 - 20 Nov 2020

Cited by 15 | Viewed by 2287

Abstract

The influence of genetic background on sensitivity to drugs represents a topical problem of personalized medicine. Here, we investigated the effect of chronic (20 mg/kg, 14 days, i.p.) antidepressant fluoxetine treatment on recombinant B6-M76C mice, differed from control B6-M76B mice by CBA-derived 102.73–110.56 Mbp fragment of chromosome 13 and characterized by altered sensitivity of 5-HT_1A receptors to chronic 8-OH-DPAT administration and higher 5-HT_1A receptor mRNA levels in the frontal cortex and hippocampus. Significant changes in the effects of fluoxetine treatment on behavior and brain 5-HT system in recombinant B6-M76C mice were revealed. In contrast to B6-M76B mice, in B6-M76C mice, fluoxetine produced pro-depressive effects, assessed in a forced swim test. Fluoxetine decreased 5-HT_1A receptor mRNA levels in the cortex and hippocampus, reduced 5-HT_1A receptor protein levels and increased receptor silencer Freud-1 protein levels in the hippocampus of B6-M76C mice. Fluoxetine increased mRNA levels of the gene encoding key enzyme for 5-HT synthesis in the brain, tryptophan hydroxylase-2, but decreased tryptophan hydroxylase-2 protein levels in the midbrain of B6-M76B mice. These changes were accompanied by increased expression of the 5-HT transporter gene. Fluoxetine reduced 5-HT and 5-HIAA levels in cortex, hippocampus and midbrain of B6-M76B and in cortex and midbrain of B6-M76C; mice. These data demonstrate that changes in genetic background may have a dramatic effect on sensitivity to classic antidepressants from the Selective Serotonin Reuptake Inhibitors family. Additionally, the results provide new evidence confirming our idea on the disrupted functioning of 5-HT_1A autoreceptors in the brains of B6-M76C mice, suggesting these mice as a model of antidepressant resistance. Full article

(This article belongs to the Special Issue Brain Neurotransmitters in Genetic Control of Behavior)

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11 pages, 1629 KiB

Open AccessArticle

Enhanced Dopamine Transmission and Hyperactivity in the Dopamine Transporter Heterozygous Mice Lacking the D3 Dopamine Receptor

by Tatyana D. Sotnikova, Evgeniya V. Efimova and Raul R. Gainetdinov

Int. J. Mol. Sci. 2020, 21(21), 8216; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218216 - 03 Nov 2020

Cited by 4 | Viewed by 2021

Abstract

Dopamine transporter knockout (DATk) mice are known to demonstrate profound hyperactivity concurrent with elevated (5-fold) extracellular dopamine in the basal ganglia. At the same time, heterozygous DAT mice (DATh) demonstrate a 2-fold increase in dopamine levels yet only a marginal elevation in locomotor activity level. Another model of dopaminergic hyperactivity is the D3 dopamine receptor knockout (D3k) mice, which present only a modest hyperactivity phenotype, predominately manifested as stereotypical behaviors. In the D3k mice, the hyperactivity is also correlated with elevated extracellular dopamine levels (2-fold) in the basal ganglia. Cross-breeding was used to evaluate the functional consequences of the deletion of both genes. In the heterozygous DAT mice, inactivation of the D3R gene (DATh/D3k) resulted in significant hyperactivity and further elevation of striatal extracellular dopamine above levels observed in respective single mutant mice. The decreased weight of DATk mice was evident regardless of the D3 dopamine receptor genotype. In contrast, measures of thermoregulation revealed that the marked hypothermia of DATk mice (−2 °C) was reversed in double knockout mice. Thus, the extracellular dopamine levels elevated by prolonging uptake could be elevated even further by eliminating the D3 receptor. These data also suggest that the hypothermia observed in DATk mice may be mediated through D3 receptors. Full article

(This article belongs to the Special Issue Brain Neurotransmitters in Genetic Control of Behavior)

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18 pages, 2929 KiB

Open AccessArticle

Deferred Administration of Afobazole Induces Sigma1R-Dependent Restoration of Striatal Dopamine Content in a Mouse Model of Parkinson’s Disease

by Ilya A. Kadnikov, Ekaterina R. Verbovaya, Dmitry N. Voronkov, Mikhail V. Voronin and Sergei B. Seredenin

Int. J. Mol. Sci. 2020, 21(20), 7620; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207620 - 15 Oct 2020

Cited by 7 | Viewed by 2963

Abstract

Previously, we demonstrated that the immediate administration of multitarget anxiolytic afobazole slows down the progression of neuronal damage in a 6-hydroxidodamine (6-OHDA) model of Parkinson’s disease due to the activation of chaperone Sigma1R. The aim of the present study is to evaluate the therapeutic potential of deferred afobazole administration in this model. Male ICR mice received a unilateral 6-OHDA lesion of the striatum. Fourteen days after the surgery, mice were treated with afobazole, selective Sigma1R agonist PRE-084, selective Sigma1R antagonist BD-1047, and a combination of BD-1047 with afobazole or PRE-084 for another 14 days. The deferred administration of afobazole restored the intrastriatal dopamine content in the 6-OHDA-lesioned striatum and facilitated motor behavior in rotarod tests. The action of afobazole accorded with the effect of Sigma1R selective agonist PRE-084 and was blocked by Sigma1R selective antagonist BD-1047. The present study illustrates the Sigma1R-dependent effects of afobazole in a 6-OHDA model of Parkinson’s disease and reveals the therapeutic potential of Sigma1R agonists in treatment of the condition. Full article

(This article belongs to the Special Issue Brain Neurotransmitters in Genetic Control of Behavior)

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13 pages, 3113 KiB

Open AccessArticle

Cognitive Training as a Potential Activator of Hippocampal Neurogenesis in the Rat Model of Sporadic Alzheimer’s Disease

by Alena O. Burnyasheva, Tatiana A. Kozlova, Natalia A. Stefanova, Nataliya G. Kolosova and Ekaterina A. Rudnitskaya

Int. J. Mol. Sci. 2020, 21(19), 6986; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21196986 - 23 Sep 2020

Cited by 2 | Viewed by 2066

Abstract

There is a growing body of evidence that interventions like cognitive training or exercises prior to the manifestation of Alzheimer’s disease (AD) symptoms may decelerate cognitive decline. Nonetheless, evidence of prevention or a delay of dementia is still insufficient. Using OXYS rats as a suitable model of sporadic AD and Wistar rats as a control, we examined effects of cognitive training in the Morris water maze on neurogenesis in the dentate gyrus in presymptomatic (young rats) and symptomatic (adult rats) periods of development of AD signs. Four weeks after the cognitive training, we immunohistochemically estimated densities of quiescent and amplifying neuronal progenitors, neuronal-lineage cells (neuroblasts and immature and mature neurons), and astrocytes in young and adult rats, and the amyloid precursor protein and amyloid-β in adult rats. Reference memory was defective in OXYS rats. The cognitive training did not affect neuronal-lineage cells’ density in either rat strain either at the young or adult age, but activated neuronal progenitors in young rats and increased astrocyte density and downregulated amyloid-β in adult OXYS rats. Thus, to activate adult neurogenesis, cognitive training should be started before first neurodegenerative changes, whereas cognitive training accompanying amyloid-β accumulation affects only astrocytic support. Full article

(This article belongs to the Special Issue Brain Neurotransmitters in Genetic Control of Behavior)

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Review

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33 pages, 2527 KiB

Open AccessReview

Chaperone Sigma1R and Antidepressant Effect

by Mikhail V. Voronin, Yulia V. Vakhitova and Sergei B. Seredenin

Int. J. Mol. Sci. 2020, 21(19), 7088; https://doi.org/10.3390/ijms21197088 - 25 Sep 2020

Cited by 21 | Viewed by 3594

Abstract

This review analyzes the current scientific literature on the role of the Sigma1R chaperone in the pathogenesis of depressive disorders and pharmacodynamics of antidepressants. As a result of ligand activation, Sigma1R is capable of intracellular translocation from the endoplasmic reticulum (ER) into the region of nuclear and cellular membranes, where it interacts with resident proteins. This unique property of Sigma1R provides regulation of various receptors, ion channels, enzymes, and transcriptional factors. The current review demonstrates the contribution of the Sigma1R chaperone to the regulation of molecular mechanisms involved in the antidepressant effect. Full article

(This article belongs to the Special Issue Brain Neurotransmitters in Genetic Control of Behavior)

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