scholarly journals Pharmacological blockade of muscle afferents and perception of effort: a systematic review with meta-analysis

2021 ◽  
Author(s):  
Maxime Bergevin ◽  
James Steele ◽  
Marie Payen de la Garanderie ◽  
Camille Feral-Basin ◽  
Samuele M Marcora ◽  
...  

The perception of effort (PE) provides information on task difficulty and influences physical exercise regulation and human behavior. This perception differs from other-exercise related perceptions such as pain. There is no consensus on the role of group III-IV muscle afferents as a signal processed by the brain to generate PE. The aim of this meta-analysis was to investigate the effect of pharmacologically blocking muscle afferents on the PE. Six databases were searched to identify studies measuring the ratings of perceived effort (RPE) during physical exercise, with and without pharmacological blockade of muscle afferents. Articles were coded based on the operational measurement used to distinguish studies in which PE was assessed specifically (effort dissociated) or as a composite experience including other exercise-related perceptions (effort not dissociated). Articles that did not provide enough information for coding were assigned to the unclear group. The effort dissociated group (n=6) demonstrated a slight RPE increase with reduced muscle afferents feedback (standard mean change raw (SMCR), 0.39; 95%CI, 0.13 to 0.64). The group effort not dissociated (n=2) did not reveal conclusive results (SMCR, -0.29; 95%CI, -2.39 to 1.8). The group unclear (n=8) revealed a slight RPE decrease with reduced muscle afferents feedback (SMCR, -0.27; 95%CI, -0.50 to -0.04). The heterogeneity in results between groups reveals that the inclusion of other perceptions than effort in its rating influences the RPE scores reported by the participants. The absence of decreased RPE in the effort dissociated group suggests that muscle afferents feedback is not a sensory signal generating PE.

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  

2006 ◽  
Vol 36 (8) ◽  
pp. 705-722 ◽  
Author(s):  
Alan St Clair Gibson ◽  
Estelle V Lambert ◽  
Laurie H G Rauch ◽  
Ross Tucker ◽  
Denise A Baden ◽  
...  

2015 ◽  
Vol 100 (3) ◽  
pp. 302-311 ◽  
Author(s):  
Thales C. Barbosa ◽  
Igor A. Fernandes ◽  
Nisval Magalhães-Jr ◽  
Ismar L. Cavalcanti ◽  
Niels H. Secher ◽  
...  

2019 ◽  
Vol 13 ◽  
Author(s):  
Viviane José de Oliveira Bristot ◽  
Ana Cristina de Bem Alves ◽  
Liziane Rosa Cardoso ◽  
Débora da Luz Scheffer ◽  
Aderbal Silva Aguiar

2001 ◽  
Vol 91 (2) ◽  
pp. 755-761 ◽  
Author(s):  
Simona Bělohlávková ◽  
Jan Šimák ◽  
Alena Kokešová ◽  
Olga Hniličková ◽  
Václav Hampl

The anorexic agent fenfluramine considerably increases the risk of primary pulmonary hypertension. The mechanism of this effect is unknown. The appetite-reducing action of fenfluramine is mediated by its interaction with the metabolism of serotonin [5-hydroxytryptamine (5-HT)] in the brain. We tested the hypothesis that the pulmonary vasoconstrictive action of fenfluramine is at least in part mediated by 5-HT receptor activation. In addition, we sought to determine whether pharmacological reduction of voltage-gated potassium (KV) channel activity would potentiate the pulmonary vascular reactivity to fenfluramine. Using isolated rat lungs perfused with Krebs-albumin solution, we compared the inhibitory effect of ritanserin, an antagonist of 5-HT2 receptors, on fenfluramine- and 5-HT-induced vasoconstriction. Both 5-HT (10−5 mol/l) and fenfluramine (5 × 10−4 mol/l) caused significant increases in perfusion pressure. Ritanserin at a dose (10−7 mol/l) sufficient to inhibit >80% of the response to 5-HT reduced the response to fenfluramine by ∼50%. A higher ritanserin dose (10−5 mol/l) completely abolished the responses to 5-HT but had no more inhibitory effect on the responses to fenfluramine. A pharmacological blockade of KV channels by 4-aminopyridine (3 × 10−3 mol/l) markedly potentiated the pulmonary vasoconstrictor response to fenfluramine but was without effect on the reactivity to 5-HT. These data indicate that the pulmonary vasoconstrictor response to fenfluramine is partly mediated by 5-HT receptors. Furthermore, the pulmonary vasoconstrictor potency of fenfluramine is elevated when the KV-channel activity is low. This finding suggests that preexisting KV-channel insufficiency may predispose some patients to the development of pulmonary hypertension during fenfluramine treatment.


2018 ◽  
Author(s):  
Karbalaei Reza ◽  
Rezaei-Tavirani Mostafa ◽  
Torkzaban Bahareh ◽  
Azimzadeh Sadegh

AbstractAlzheimer’s disease (AD) is a complex neurodegenerative disease with various deleterious perturbations in regulatory pathways of various brain regions. Thus, it would be critical to understanding the role of different regions of the brain in initiation and progression of AD, However, owing to complex and multifactorial nature of this disease, the molecular mechanism of AD has yet to be fully elucidated. To confront with this challenge, we launched a meta-analytical study of current transcriptomics data in four different regions of the brain in AD (Entorhinal, Hippocampus, Temporal and Frontal) with systems analysis of identifying involved signaling and metabolic pathways. We found different regulatory patterns in Entorhinal and Hippocampus regions to be associated with progression of AD. We also identified shared versus unique biological pathways and critical proteins among different brain regions. ACACB, GAPDH, ACLY, and EGFR were the most important proteins in Entorhinal, Frontal, Hippocampus and Temporal regions, respectively. Moreover, eight proteins including CDK5, ATP5G1, DNM1, GNG3, AP2M1, ALDOA, GPI, and TPI1 were differentially expressed in all four brain regions, among which, CDK5 and ATP5G1 were enriched in KEGG Alzheimer’s disease pathway as well.


2019 ◽  
Author(s):  
Ryoji Fukabori ◽  
Yoshio Iguchi ◽  
Shigeki Kato ◽  
Kazumi Takahashi ◽  
Satoshi Eifuku ◽  
...  

AbstractThe ability to retrieve memory store in response to the environment is essential for animal behavioral adaptation. Norepinephrine (NE)-containing neurons in the brain play a key role in the modulation of synaptic plasticity underlying various processes of memory formation. However, the role of the central NE system in memory retrieval remains unclear. In this study, we developed a neural chemogenetic activation strategy using insect olfactory Ionotropic Receptors (IRs), and used it for selective stimulation of NE neurons in the locus coeruleus (LC) in transgenic mice. Ligand-induced activation of LC NE neurons resulted in enhancement of the retrieval process of conditioned taste aversion, which was mediated through at least partly adrenergic receptors in the amygdala. Pharmacological blockade of LC activity confirmed the facilitative role of these neurons in memory retrieval. Our findings indicate that the LC-amygdalar pathway is required and sufficient for enhancing the recall of taste associative memory.


2021 ◽  
Author(s):  
Manuel Seefelder ◽  
Stefan Kochanek

AbstractDescription of robust transcriptomic alterations in Huntington s disease is essential to identify targets for biochemical studies and drug development. Here, we analysed publicly available transcriptome data from the brain and blood of 449 HD patients and 212 healthy controls. We identified 737 and 661 genes with robustly altered mRNA levels in the brain and blood of HD patients, respectively. In the brain, a subnetwork of 320 genes strongly correlated with HD and was enriched in transport-related genes. Bioinformatical analysis of this subnetwork highlighted CDC42, PAK1, NFY, DLX1, HMGN3, and PRMT3. Moreover, we found that CREB1 can regulate 78.0 % of genes whose mRNA levels correlated with HD in the blood of patients. Our meta-analysis indicates that alterations in protein transport, metabolism, transcriptional regulation, and CDC42-mediated functions are central features of HD. Further our data substantiate the role of transcriptional regulators that have not been reported in the context of HD such as DLX1, HMGN3 and PRMT3 and strongly suggest transcriptional dysregulation of NFY and its target genes across tissues.


2015 ◽  
Vol 27 (2) ◽  
pp. 507-520 ◽  
Author(s):  
Madelon M. E. Riem ◽  
Lenneke R. A. Alink ◽  
Dorothée Out ◽  
Marinus H. Van Ijzendoorn ◽  
Marian J. Bakermans-Kranenburg

AbstractWe present new empirical data and meta-analytic evidence for the association of childhood maltreatment with reduced hippocampal volume. In Study 1, we examined the effects of maltreatment experiences reported during the Adult Attachment Interview on hippocampal volume in female twin pairs. We found that reduced hippocampal volume was related to childhood maltreatment. In addition, individuals who reported having experienced maltreatment at older ages had larger reductions in hippocampal volume compared to individuals who reported maltreatment in early childhood. In Study 2, we present the results of a meta-analysis of 49 studies (including 2,720 participants) examining hippocampal volume in relation to experiences of child maltreatment, and test the moderating role of the timing of the maltreatment, the severity of maltreatment, and the time after exposure to maltreatment. The results of the meta-analysis confirmed that experiences of childhood maltreatment are associated with a reduction in hippocampal volume and that the effects of maltreatment are more pronounced when the maltreatment occurs in middle childhood compared to early childhood or adolescence.


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