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Dataset of molecular docking data of neuropeptides to acid-sensing ion channels
<p>The *.dock4 files are result files of molecular docking with the software Autodock Vina to the human ASIC1a closed state model, of the peptides FRRFa and KNFLRFa (FRRF.dock4, KNFLRF.dock4) that can be visualized with structure viewing programs such as UCSF Chimera on the closed ASIC1a model file (closed_ASIC_pH7.4.pdb). The file “FRRF_KNFLRF_complexes.pdb” provides the structures of selected poses of FRRFa and KNFLRFa peptides docked to the closed conformation of the human ASIC1a model.</p>
DNA loss model explains the evolution of the neuropeptide LWamide, APGWamide, APGW/AKH, RPCH, AKH, ACP, CRZ, and GnRH families
<p><strong>R1: Establishment and purification of neuropeptide sequences</strong></p> <p>The LW, APGW, RPCH, AKH, CRZ, and GnRH neuropeptide families were searched in the GenBank database using 10 keywords: the neuropeptide name, the precursor abbreviation, the full name of the precursor, the full name of the precursor with the word “prepropeptide,” and the combinations of these terms. The candidate sequences were downloaded in FASTA format using the appropriate commands in the GenBank database. The AKH neuropeptide family was classified according to the groups published in the literature, as well as the amino acid number and sequence. Furthermore, the ACP hybrid family was identified in the GenBank database using BLAST alignments.</p> <p><strong>C00: Neuropeptide Precursor. </strong>Eight folders were named with the initials of each neuropeptide family. The AKH family folder was the only one containing four subfolders. All of the folders contained the same type of files: three text files named after the neuropeptide initials and the obtained result. The files identified with the words “<em>with codes</em>” contained the sequences with the codes generated for this study, whereas the documents with the word “<em>Full</em>” contained the GenBank database search results obtained with the 10 aforementioned keywords. These files were located in a folder named “<em>Fasta Keywords.</em>” Each file contained the results from each respective keyword. The files with the words “<em>selected EA</em>” contained the sequences that were selected for evolutionary analyses.</p> <p><strong>C01: BLAST ACP</strong>. The text file named “00 BLAST ACP” contains the BLAST alignment results obtained from the NCBI database generated with the Adipokinetic Hormone/Corazonin-related peptide from the transcriptome of <em>Callinectes toxotes</em>. The file named “01 ACP Selected” contains the precursors selected for this study. All sequences were in FASTA format and contained the codes summarized in Supplementary Material 3 “<em>Database Sequences.</em>”</p> <p>The file named “<em>02 ACP selected EA</em>” contains the ACP precursors of other species, which were used for the evolutionary analyses of <em>C. toxotes</em> ACP. The PDF file titled “<em>03 ACP ProP 1.0 Serv</em>” contains the results of the proteolytic cleavage sites of the precursors indicated in the file named “<em>02 ACP selected EA,</em>” which were generated using the aforementioned software.</p> <p><strong>C02: BLAST VP.</strong> The folder contains the results of the BLAST alignment against the NCBI database, which were generated with the virtual peptide sequences reported by Martinez-Perez et al. (2007). This folder contains seven text files. The name of each file corresponds to the precursor and species in which it was identified. Moreover, the PDF document named “<em>Virtual peptides ProP 1.0 Serv</em>” contains the results of the proteolytic cleavage sites generated with the aforementioned software.</p> <p><strong>C03: Debugging sequences with software.</strong> This folder contains three subfolders containing the results obtained with each software used in this study for the detection of each of the neuropeptide sequences using the appropriate keywords.</p> <p>The folder named “<em>BioDataToolKit</em>” contains six subfolders with the abbreviated name of each neuropeptide. Additionally, there is a file containing the sequences downloaded from the GenBank database, as well as a Microsoft Excel file containing the details generated by the software. The name of each file corresponds to the keywords used for each search. The software used in this study can be found in the following repository: <a href="https://github.com/rduarte24/BiodataToolkit">https://github.com/rduarte24/BiodataToolkit</a>.</p> <p>The folder named “<em>Pro1.0Server</em>” was organized in the same way as the results derived for the “<em>BioDataToolKit</em>” for each neuropeptide family. However, each of the neuropeptide folders contained a file with the pertinent sequences whereas another file contained the endoproteolytic cleavage sites of the neuropeptide precursors obtained with the software.</p> <p>The folder named “Proteios” contains seven files. The file names indicate the precursor analyzed with the software and the identified sequences in FASTA format. The Proteios software is available in the following website: <a href="https://github.com/Martin-Munive/Proteios">https://github.com/Martin-Munive/Proteios</a>.</p> <p><strong>C04: Neuropeptide precursors for evolutionary analysis.</strong> Files with the sequences of the neuropeptide precursors used for the generation of the phylogenetic trees in Supplementary Materials 4 and 7. The name of each file corresponds to the name of each of the analyzed neuropeptides.</p> <p><strong>R2: Transcriptome BLAST</strong></p> <p>Microsoft Excel file containing the BLAST alignments conducted using the sequences of the AKH/CRZ-related peptide (ACP) from <em>C. toxotes</em> and Corazonin (CRZ) from <em>C. arcuatus</em>. The following information is summarized in the spreadsheets named <em>C. toxotes</em> and <em>C. arcuatus</em>: Column A, neuropeptide name; Column B, species name; Columns C–G, BLAST alignment results; Column H, GenBank protein accession number; Column I, precursor sequence.</p> <p><strong>R3: </strong><strong>Construction of neuropeptide database</strong></p> <p>Microsoft Excel file with information pertaining to the database and a detailed description of each of the neuropeptide precursors analyzed in this study. The Excel file contains seven spreadsheet tabs. Each of the tabs contains the following columns:</p> <p><strong>Neuropeptides.</strong> Column A, sequence numbering in descending order; Column B, neuropeptide name; Column C, identification code used in this study; Column D, accession number; Columns E–G, species taxonomy; Columns H–L, GenBank sequence description; Columns M–N, literature reference and link. <strong>Taxonomy.</strong> Taxonomic description of each of the examined species derived from the NCBI database. <strong>Sequences evolutionary anal</strong>. This tab contains the code developed for this work in Column C; the GenBank accession codes of each neuropeptide are summarized in Column D and species taxonomy details are summarized in Columns E y F. <strong>Table of differences.</strong> Column B shows the codes of identical sequences and Column C shows the code of the sequence selected for this study. <strong>Codes deleted. </strong>This tab contains the accession codes of the species and the species name but contains no details on the properties of the neuropeptide precursors. <strong>Sequences Paper</strong>. Neuropeptide sequences reported in previous studies that were later reported in the GenBank database. The sequences marked with asterisks have not been previously reported in public databases. The codes used in this study to designate the sequences are also included. <strong>Keywords. </strong>Keywords used to conduct the GenBank database searches to obtain the members of each neuropeptide family.</p> <p><strong>R4: <em>In silico</em> validation, alignments, and phylogenetic relationships</strong></p> <p>Generated phylogenetic trees and results obtained from individual runs for each of the neuropeptide families with the DNA-LM and Kalign parameters using the IQ-TREE software.</p> <p>The folder named “<em>RUN</em>” contains the “<em>DNALM and kalign 2.0 default parameters</em>” subfolder. Both folders contain 11 subfolders with the names of each of the neuropeptide families, as well as the results obtained with the IQ-TREE software. The folder named “<em>Trees</em>” contains the folder “<em>DNALM and kalign 2.0 default parameters</em>” containing the phylogenetic trees for each of the neuropeptide families, which were created with the Itol software.</p> <p><strong>R5: BLAST alignment of the virtual peptide precursors</strong></p> <p>Results of the BLAST alignment of the virtual peptides described by Martinez-Perez et al. (2007) with respect to the sequences in the GenBank database. The files follow the same nomenclature as in the folder named “<em>Carpeta 02 BLAST VP</em><strong>”</strong> in Repository 1.</p> <p><strong>R6: Alignment of neuropeptide precursors</strong></p> <p>“<em>DNALM and Kalign 2.0 default parameter</em>” folders. Each of these folders contains the alignments of the examined neuropeptide precursors from each family and each folder is named after the corresponding neuropeptide. The remaining files contain the alignments in ascending order in the evolutionary scale and are appropriately named after the corresponding neuropeptide. The file named “<em>All Sequence FASTA</em>” contains the sequences used in our study in FASTA format.</p> <p><strong>R7: Phylogenetic clustering of the precursors </strong></p> <p> “<em>DNALM and Kalign 2.0 default parameter</em>” folders. Both folders contain the phylogenetic tree clustering results from Supplementary Material 6, which were obtained using the DNA-LM y Kalign parameters and the IQ-TREE software. All analyses were conducted using the GUANE-1 supercomputer (Universidad Industrial de Santander). The phylogenetic clustering results of all of the precursors are contained in the folders with the respective precursor name. The folder also contains Figure 6, which was included in our main manuscript.</p> <p>Additionally, a folder entitled "Orthofinder and Robinson-Foulds" is included, which corresponds to the analyses carried out for: the Robinson-Foulds metric and the Orthofinder software.</p>
A dataset of 3D fly (Drosophila melanogaster) flight trajectories to study the role of neuropeptide degradation in visuo-motor behaviors.
<p>As part of a wide study on the role of neuropeptides in the visuo-motor behavior of Drosophila melanogaster, we exposed three fly strains with impaired neuropeptide degradation function, and corresponding controls, to different visual stimuli.</p> <p>Find further details in the provided README.</p>
Figure 4 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 4. Body weight on the 120th offspring from mothers submitted the control diet or the high-fat diet. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiple-comparison test. *p<0,05; **p<0,005.
Figure 3 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 3. Body weight on the second day life's of offspring from mothers submitted the control diet (C) or the high-fat diet (H). Values are presented as mean + SEM using Student t-test. C: n = 23; H: n = 23.
Figure 2 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 2. Pomc (A) and npy (B) gene expression in the hypothalamus of offspring exposed or not to a control diet or high-fat diet during perinatal and/or postnatal period. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiplecomparison test. Level of significance: *p<0,05; "a": compared to CC, "b": compared to CH; "c": compared to HC; "d": compared to HH.
Figure 1. Drd1 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 1. Drd1 (A) and drd2 (B) gene expression in the nucleus accumbens of offspring exposed or not to a control diet or high-fat diet during perinatal and/or postnatal period. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiplecomparison test. Level of significance: *p<0,05; "a": compared to CC, "b": compared to CH; "c": compared to HC; "d": compared to HH.
Data from: Neuropeptide receptor distributions in male and female Eulemur vary between female-dominant and egalitarian species
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Short neuropeptide F regulates the starvation mediated enhanced locomotor activity in Drosophila
<p class="normal"><span>The circadian clock regulates various behavioral, metabolic and physiological processes to occur at the most suitable time of the day. Internal energy stores and nutrient availability modulates the most apparent circadian clock mediated locmotor activity rhythm in <i>Drosophila</i>. </span>Although previous studies unraveled the role of circadian clock in metabolism and activity rest rhythm, the precise pathway through which the circadian neuropeptidergic signaling regulates internal energy storage and the starvation-mediated increase in activity resembling foraging remains largely unclear. This study was aimed to elucidate the role of circadian neuropeptide, short neuropeptide F (sNPF) in triglyceride metabolism, starvation resistance and starvation-mediated increased locomotor activity in <i>Drosophila</i>. The results showed that <i>snpf </i>transcripts exhibits significant rhythmicity in wild type flies under 12:12 hour light-dark cycles (LD) and constant darkness (DD) whereas <i>snpf</i> transcript level in <i>period</i> null flies did not exhibit any significant rhythmicity under LD. Knockdown of sNPF in circadian clock neurons reduced the triglyceride level, starvation resistance and increased the starvation-mediated hyperactivity response after 24 hour of starvation. Further studies showed that knock down of sNPF receptors (sNPFR) expressed in insulin producing cells (IPC) increased the starvation resistance and reduced starvation-induced hyperactivity response after 24 hour of starvation. Collectively, our results suggest that transcriptional oscillation of <i>snpf </i>mRNA is endogenously controlled by the circadian clock and elucidate the role of sNPF in modulating locomotor activity in accordance with the nutrient availability in <i>Drosophila</i>. </p>
Failure to mate enhances investment in behaviors that may promote mating reward and impairs the ability to cope with stressors via a subpopulation of Neuropeptide F receptor neurons
<p><span>Living in dynamic environments such as the social domain, where interaction with others determines the reproductive success of individuals, requires the ability to recognize opportunities to obtain natural rewards and cope with challenges that are associated with achieving them. As such, actions that promote survival and reproduction are reinforced by the brain reward system, whereas coping with the challenges associated with obtaining these rewards is mediated by stress-response pathways, the activation of which can impair health and shorten lifespan. While much research has been devoted to understanding mechanisms underlying the way by which natural rewards are processed by the reward system, less attention has been given to the consequences of failure to obtain a desirable reward. As a model system to study the impact of failure to obtain a natural reward, we used the well-established courtship suppression paradigm in <em>Drosophila</em> <em>melanogaster</em> as means to induce repeated failures to obtain sexual reward in male flies. We discovered that beyond the known reduction in courtship actions caused by interaction with non-receptive females, repeated failures to mate induce a stress response characterized by persistent motivation to obtain the sexual reward, reduced male-male social interaction, and enhanced aggression. This frustrative-like state caused by the conflict between high motivation to obtain sexual reward and the inability to fulfill their mating drive impairs the capacity of rejected males to tolerate stressors such as starvation and oxidative stress. We further show that sensitivity to starvation and enhanced social arousal is mediated by the disinhibition of a small population of neurons that express receptors for the fly homologue of<em> neuropeptide Y</em>. Our findings demonstrate for the first time the existence of social stress in flies and offers a framework to study mechanisms underlying the crosstalk between reward, stress, and reproduction in a simple nervous system that is highly amenable to genetic manipulation.</span></p>
Identification and expression of short neuropeptide F and its receptors in the tick Ixodes ricinus
<p>The open datasets include raw data covering results published in paper by Medla et al., 2023 (https://doi.org/10.1016/j.jinsphys.2023.104524)</p>
Data from: Neuropeptide signalling shapes feeding and reproductive behaviours in male C. elegans
<p><span><span>Sexual dimorphism occurs where different sexes of the same species display differences in characteristics not limited to reproduction. For the nematode <em><span>Caenorhabditis elegans</span></em>, in which the complete neuroanatomy has been solved for both hermaphrodites and males, sexually dimorphic features have been observed both in terms of the number of neurons and in synaptic connectivity. In addition, male behaviours, such as food-leaving to prioritise searching for mates, have been attributed to neuropeptides released from sex-shared or sex-specific neurons.</span></span></p> <p><span> </span></p> <p>This dataset compiles the results obtained in our investigation of how LURY-1 neuropeptides regulate feeding and mating behaviours in <em>C. elegans</em>. These contain confocal micrographs and z-stacks of fluorescence reporter imaging used to demonstrate the expression pattern of<em> lury-1</em> and <em>npr-22</em>, including micrographs used for cell identification of <em>lury-1</em> expressing neurons in the male worm. Other behavioural data from mating efficiency assays, pharyngeal pumping assays and food leaving assays are also shown. These include male turning behaviour examined through video recordings of male mating; the videos are also included as part of this dataset.</p> <p>In this study ("Neuropeptide signalling shapes feeding and reproductive behaviours in male <em>C. elegans</em>"), our findings indicate sex-specific roles of this peptide in feeding and reproduction in <em>C. elegans</em>. This provides further insight into neuromodulatory control of sexually dimorphic behaviours.</p>
Table 2 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
<p><b>Table 2.</b> Relative food intake of the high-fat diet and control diet during the food preference study in offspring exposed or not a control diet or high-fat diet during perinatal and/or postnatal period.</p><table><tbody><tr><th></th><th><i>High-fat diet (g/100 g body weight)</i></th><th></th></tr></tbody><tbody><tr><th></th><td><i>102º day</i></td><td><i>110º day</i></td><td><i>116º day</i></td></tr><tr><th><i>CC</i></th><td>12.6 ± 0.6</td><td>11.3 ± 0.2</td><td>11.1 ± 0.7</td></tr><tr><th><i>CH</i></th><td>12.8 ± 0.6</td><td>12.4 ± 0.3</td><td>11.4 ± 0.4</td></tr><tr><th><i>HC</i></th><td>16.7 ± 1.1 <b>a.b*</b></td><td>13.7 ± 0.9</td><td>10.0 ± 0.5</td></tr><tr><th><i>HH</i></th><td>15.3 ± 0.7 <b>a.b*</b></td><td>11.7 ± 0.9</td><td>10.7 ± 0.5</td></tr><tr><th></th><td><i>Control diet (g/100 g body weight)</i></td><td></td></tr><tr><th></th><td><i>102º day</i></td><td><i>110º day</i></td><td><i>116º day</i></td></tr><tr><th><i>CC</i></th><td>1.4 ± 0.2</td><td>1.1 ± 0.1</td><td>1.1 ± 0.3</td></tr><tr><th><i>CH</i></th><td>2.1 ± 0.2</td><td>1.5 ± 0.3</td><td>0.9 ± 0.1</td></tr><tr><th><i>HC</i></th><td>1.8 ± 0.2</td><td>1.0 ± 0.3</td><td>1.0 ± 0.3</td></tr><tr><th><i>HH</i></th><td>1.9 ± 0.2</td><td>1.1 ± 0.2</td><td>0.7 ± 0.1</td></tr></tbody></table><p>Values are presented as mean + SEM using two-way ANOVA followed by the Bonferroni multiple-comparison test. *p<0,005; “a”: compared to CC, “b”: compared to CH; “c”: compared to HC; “d”: compared to HH.</p>
Table 1 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
<p><b>Table 1.</b> Experimental design. The rats were fed commercial standard diet for rodents control diet or high-fat diet during pregnancy, lactation and post-weaning (up to 100 days of life).During the feeding period, rats consumed both diets (control diet and high-fat diet). The numbers in parentheses indicate the animals number in each nutritional group.</p><table><tbody><tr><th><b>Experimental Design</b></th></tr></tbody><tbody><tr><th><b>Genitors (n)</b></th><td><b>Gestation and lactation</b></td><td><b>Offspring during lactation (n)</b></td><td><b>Offspring (n)</b></td><td><b>Post-weaning (21-100° life’s day)</b></td><td><b>Food preference (102-116º life’s day)</b></td></tr><tr><th></th><td></td><td></td><td>CC (12)</td><td>Control diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th>GC (5)</th><td>Control diet</td><td>C (23)</td><td>CH (11)</td><td>High-fat diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th></th><td></td><td></td><td>HC (11)</td><td>Control diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th>GH (5)</th><td>High-fat diet</td><td>H (23)</td><td>HH (12)</td><td>High-fat diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr></tbody></table>
Resource limitation, intragroup aggression, and brain neuropeptide expression in a social wasp
<p>1. Nourishment can have profound effects on social behavior, including aggressive interactions between individuals. However, how nutritional resource availability and limitation affects intraspecific aggression remains somewhat contested. The prevailing theoretical and empirical understanding is that when nutritional resources are limited, inter-individual competition and aggression will increase. However, findings from several social animals suggest that limited nutrition can lead to increased cooperation, including by a reduction in inter-individual aggression.</p> <p>2. We suggest that in social insect colonies, where nourishment is often important in determining differences between the reproductive and non-reproductive worker behavioral castes, the link between an individual's nourishment and their future reproductive potential may be a key missing element of models that predict how nutritional resource availability affects inter-individual aggression.</p> <p>3. We investigated how nourishment influenced intra-colony aggression and its molecular correlates in colonies of the social paper wasp <i>Polistes fuscatus</i>, which workers that maintain flexible reproductive potential as adults. We subjected colonies to either a high or low feeding treatment, and examined subsequent effects on behavior, physiology, and brain gene expression.</p> <p>4. We found that nutritional restriction reduced aggressive interactions, suggesting increased social cohesion when resources are limiting. Thus, individual worker paper wasps appear to have the capacity to adjust their behavior (e.g., reduced aggression) in response to nutritional stress, investing nutritional resources in the colony when resources are limiting, and in the self when resources are abundant.</p> <p>5. Differential brain gene expression results implicate two well-known neuropeptides associated with aggression and/or nutrient signaling across taxa, <i>Tachykinin </i>and <i>Neuropeptide-F</i>, as possible mediators of nutritionally-dependent intra-colony aggression. This adds to a growing understanding that deeply conserved genes associated with core, conserved behaviors such as feeding and aggression in solitary insects can play a role in the regulation of social plasticity in more highly social species.</p>
Periprandial changes in brain serotonergic system and food intake related neuropeptides
<p><span>In this work, we assessed periprandial serotonin and 5-hydroxyindolacetic acid abundance in several brain areas of rainbow trout, in parallel with the evaluation of gene expression of tryptophan hydroxilase 1 and 2, neuropeptides involved in the central control of food intake, and the quantification of plasma glucose and cortisol. The results showed severe changes in serotonergic systems around mealtime, the most prominent being the increase in their activity just after food intake, suggesting that serotonin has a relevant role in relation to the daily timing of food intake, probably triggering satiety signals. In addition, a temporal adjustment of neuropeptide expression and plasma cortisol was found in relation to food intake, supporting its role in the regulation of feeding behaviour.</span></p>
Is the neuropeptide PEN a ligand of GPR83?
<p>Numerical dataset for the manuscript by Giesecke et al., Is the neuropeptide PEN a ligand of GPR83?</p>
Neuropeptide Treatment for Hot Flushes During the Menopause
ClinicalTrials.gov study NCT02668185. IPD Sharing: NO. Countries: 1. Publications: 3.
Intranasal Administration of Neuropeptide Y in Healthy Male Volunteers
ClinicalTrials.gov study NCT00748956. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Short neuropeptide F regulates the starvation mediated enhanced locomotor activity in Drosophila
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Allen Brain Atlas
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