To assess the relationship between brain-derived neurotrophic factor (BDNF) and synapsin I in the hippocampus during exercise, we employed a novel microsphere injection method to block the action of BDNF through its tyrosine kinase (Trk) receptor and subsequently measure the mRNA levels of synapsin I, using real-time TaqMan RT-PCR for RNA quantification. After establishing a causal link between BDNF and exercise-induced synapsin I mRNA levels, we studied the exercise-induced distribution of BDNF and synapsin I in the rodent hippocampus. Quantitative immunohistochemical analysis revealed increases of BDNF and synapsin I in CA3 stratum lucidum and dentate gyrus, and synapsin I alone in CA1 stratum radiatum and stratum laconosum moleculare. These results indicate that exercise induces plasticity of select hippocampal transsynaptic circuitry, possibly comprising a spatial restriction on synapsin I regulation by BDNF.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/jnr.20077 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
BDNF/TrkB signalling, in cooperation with muscarinic signalling, retrogradely regulates PKA pathway to phosphorylate SNAP-25 and Synapsin-1 at the neuromuscular junction.
Cell Commun Signal
July 2024
Universitat Rovira i Virgili. Unitat d'Histologia i Neurobiologia (UHNeurob), Facultat de Medicina i Ciències de la Salut. c/ Sant Llorenç 21, Reus, 43201, Spain.
Background: Protein kinase A (PKA) enhances neurotransmission at the neuromuscular junction (NMJ), which is retrogradely regulated by nerve-induced muscle contraction to promote Acetylcholine (ACh) release through the phosphorylation of molecules involved in synaptic vesicle exocytosis (SNAP-25 and Synapsin-1). However, the molecular mechanism of the retrograde regulation of PKA subunits and its targets by BDNF/TrkB pathway and muscarinic signalling has not been demonstrated until now. At the NMJ, retrograde control is mainly associated with BDNF/TrkB signalling as muscle contraction enhances BDNF levels and controls specific kinases involved in the neurotransmission.
View Article and Find Full Text PDFThe role of P2X4R in regulating CA1 hippocampal synaptic impairment in LPS-induced depression.
J Affect Disord
October 2024
Department of Rehabilitation, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China. Electronic address:
Aim: To study the role of the P2X4 receptor (P2X4R) in regulating hippocampal synaptic impairment in lipopolysaccharide (LPS)-induced depression.
Methods: A rat model of depression was established by LPS injection. P2X4R expression was inhibited by 5-(3-bromophenyl)-1, 3-dihydro-2H-benzofuro[3,2-e]-1,4-diazepin-2-one (5-BDBD).
Fetal Brain-Derived Exosomal miRNAs from Maternal Blood: Potential Diagnostic Biomarkers for Fetal Alcohol Spectrum Disorders (FASDs).
Int J Mol Sci
May 2024
Center for Neural Repair and Rehabilitation (Shriners Hospitals Pediatric Research Center), Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Fetal alcohol spectrum disorders (FASDs) are leading causes of neurodevelopmental disability but cannot be diagnosed early in utero. Because several microRNAs (miRNAs) are implicated in other neurological and neurodevelopmental disorders, the effects of EtOH exposure on the expression of these miRNAs and their target genes and pathways were assessed. In women who drank alcohol (EtOH) during pregnancy and non-drinking controls, matched individually for fetal sex and gestational age, the levels of miRNAs in fetal brain-derived exosomes (FB-Es) isolated from the mothers' serum correlated well with the contents of the corresponding fetal brain tissues obtained after voluntary pregnancy termination.
View Article and Find Full Text PDFProtective effect of melatonin against metabolic disorders and neuropsychiatric injuries in type 2 diabetes mellitus mice.
Phytomedicine
August 2024
School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, PR China; The Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Medical University, Hefei, PR China; Anhui Provincial Laboratory of Inflammatory and Immune Disease, Anhui Institute of Innovative Drugs, Hefei, PR China. Electronic address:
Background: Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by hyperglycemia and progressive cognitive dysfunction, and our clinical investigation revealed that the plasma concentration of melatonin (Mlt) decreased and was closely related to cognition in T2DM patients. However, although many studies have suggested that Mlt has a certain protective effect on glucose and lipid metabolism disorders and neuropsychiatric injury, the underlying mechanism of Mlt against T2DM-related metabolic and cognitive impairments remains unclear.
Purpose: The aim of the present study was to investigate the therapeutic effect of Mlt on metabolic disorders and Alzheimer's disease (AD)-like neuropsychiatric injuries in T2DM mice and to explore the possible underlying molecular mechanism involved.
Background And Aim: Traumatic brain injury (TBI), a leading cause of high morbidity and mortality, represents a significant global public health challenge. Currently, no effective treatment for TBI exists. Curcumin, an active compound extracted from the root of , has demonstrated neuroprotective properties both and .
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!