Effects of Bradykinin B2 Receptor Ablation from Tyrosine Hydroxylase Cells on Behavioral and Motor Aspects in Male and Female Mice.

B2 receptor (B2R) bradykinin metabolic aspects tyrosine hydroxylase (TH) cells

Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
25 Jan 2024
Historique:
received: 18 12 2023
revised: 16 01 2024
accepted: 21 01 2024
medline: 10 2 2024
pubmed: 10 2 2024
entrez: 10 2 2024
Statut: epublish

Résumé

The kallikrein-kinin system is a versatile regulatory network implicated in various biological processes encompassing inflammation, nociception, blood pressure control, and central nervous system functions. Its physiological impact is mediated through G-protein-coupled transmembrane receptors, specifically the B1 and B2 receptors. Dopamine, a key catecholamine neurotransmitter widely distributed in the CNS, plays a crucial role in diverse physiological functions including motricity, reward, anxiety, fear, feeding, sleep, and arousal. Notably, the potential physical interaction between bradykinin and dopaminergic receptors has been previously documented. In this study, we aimed to explore whether B2R modulation in catecholaminergic neurons influences the dopaminergic pathway, impacting behavioral, metabolic, and motor aspects in both male and female mice. B2R ablation in tyrosine hydroxylase cells reduced the body weight and lean mass without affecting body adiposity, substrate oxidation, locomotor activity, glucose tolerance, or insulin sensitivity in mice. Moreover, a B2R deficiency in TH cells did not alter anxiety levels, exercise performance, or motor coordination in female and male mice. The concentrations of monoamines and their metabolites in the substantia nigra and cortex region were not affected in knockout mice. In essence, B2R deletion in TH cells selectively influenced the body weight and composition, leaving the behavioral and motor aspects largely unaffected.

Identifiants

pubmed: 38338764
pii: ijms25031490
doi: 10.3390/ijms25031490
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : São Paulo Research Foundation
ID : 2019/07005-4 2023/01250-4 2021/09559-7 2023/09878-0 2020/01318-8
Organisme : Coordenação de Aperfeicoamento de Pessoal de Nível Superior
ID : 151318/2023-9

Auteurs

Thaina Maquedo Franco (TM)

Department of Neurology and Neurosurgery, Federal University of Sao Paulo, Sao Paulo 04039-032, Brazil.

Mariana R Tavares (MR)

Department of Neurology and Neurosurgery, Federal University of Sao Paulo, Sao Paulo 04039-032, Brazil.

Leonardo S Novaes (LS)

Department of Pharmacology, Instituto de Ciencias Biomedicas, Universidade de São Paulo, Sao Paulo 05508-000, Brazil.

Carolina D Munhoz (CD)

Department of Pharmacology, Instituto de Ciencias Biomedicas, Universidade de São Paulo, Sao Paulo 05508-000, Brazil.

Jose Eduardo Peixoto-Santos (JE)

Department of Neurology and Neurosurgery, Federal University of Sao Paulo, Sao Paulo 04039-032, Brazil.

Ronaldo C Araujo (RC)

Department of Biophysics, Federal University of Sao Paulo, Sao Paulo 04039-032, Brazil.

Jose Donato (J)

Department of Physiology and Biophysics, Instituto de Ciencias Biomedicas, Universidade de São Paulo, Sao Paulo 05508-000, Brazil.

Michael Bader (M)

Max-Delbrück Center for Molecular Medicine (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
German Center for Cardiovascular Research (DZHK), Partner Site Berlin, 10117 Berlin, Germany.
Institute for Biology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.

Frederick Wasinski (F)

Department of Neurology and Neurosurgery, Federal University of Sao Paulo, Sao Paulo 04039-032, Brazil.

Classifications MeSH