The prefrontal cortex (PFC) plays a critical role in cognitive functions, including working memory, attention regulation and behavioral inhibition. Microinjection of β1-adrenoceptor (β1-AR) agonist into the PFC has been shown to impair PFC cognitive function. However, the underlying cellular and molecular mechanisms have not been determined yet. In the present study, we tested the hypothesis that β1-AR mediated modulation of excitatory synaptic transmission contributes to PFC dysfunction. We found that 1) the β1-AR agonist Dobutamine (Dobu) suppressed the amplitude evoked excitatory postsynaptic currents (eEPSCs). 2) Dobu induced a significant suppression of the frequency and amplitude of miniature EPSCs (mEPSCs). 3) Dobu-suppressed glutamate release was mediated via decreasing release probability and the number of releasable vesicles. 4) Dobu suppressed inward currents evoked by puff application of glutamate or NMDA via postsynaptic PKA-dependent pathway. The present study indicates that β1-AR activation suppresses excitatory synaptic transmission in medial PFC (mPFC) via both pre- and post-synaptic PKA-dependent mechanisms. Our results may provide a cellular and molecular mechanism that helps explain β1-AR-induced PFC dysfunction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.neuropharm.2014.03.020 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Evaluation of developmental toxicity of chlorpyrifos through new approach methodologies: a systematic review.
Arch Toxicol
January 2025
Applied Biology Department, Miguel Hernández de Elche University, Elche, Spain.
Chlorpyrifos (CPF) is an organophosphorus pesticide of concern because many in vivo animal studies have demonstrated developmental toxicity exerted by this substance; however, despite its widespread use, evidence from epidemiological studies is still limited. In this study, we have collected all the information generated in the twenty-first century on the developmental toxicity of CPF using new approach methodologies. We have critically evaluated and integrated information coming from 70 papers considering human, rodent, avian and fish models.
View Article and Find Full Text PDFA first morphological and electrophysiological characterization of Fañanas cells of the mouse cerebellum.
J Physiol
January 2025
Université Paris Cité, CNRS, Saints-Pères Paris Institute for the Neurosciences, Paris, France.
Fañanas cells (FCs) are cerebellar glia of unknown function. First described more than a century ago, they have been almost absent from the scientific literature ever since. Here, we combined whole-cell, patch clamp recordings, near-UV laser photolysis, dye-loading and confocal imaging for a first characterization of FCs in terms of their morphology, electrophysiology and glutamate-evoked currents.
View Article and Find Full Text PDFGlutamatergic Input from Arcuate Nucleus Kiss1 Neurons to Preoptic Kiss1 Neurons is Required for LH Surge in Female Mice.
Endocrinology
January 2025
Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR, USA.
Hypothalamic kisspeptin (Kiss1) neurons are vital for maintaining fertility in the mammal. In the female rodent, Kiss1 neurons populate the anteroventral periventricular/periventricular nuclei (Kiss1AVPV/PeN) and the arcuate nucleus (Kiss1ARH). Kiss1ARH neurons (a.
View Article and Find Full Text PDFBoNT/Action beyond neurons.
Toxicon
January 2025
National Research Council of Italy, Institute of Biochemistry and Cell Biology, 00015, Monterotondo, RM, Italy. Electronic address:
Botulinum neurotoxin type A (BoNT/A) has expanded its therapeutic uses beyond neuromuscular disorders to include treatments for various pain syndromes and neurological conditions. Originally recognized for blocking acetylcholine release at neuromuscular junctions, BoNT/A's effects extend to both peripheral and central nervous systems. Its ability to undergo retrograde transport allows BoNT/A to modulate synaptic transmission and reduce pain centrally, influencing neurotransmitter systems beyond muscle control.
View Article and Find Full Text PDFNrf2 Regulates Basal Glutathione Production in Astrocytes.
Int J Mol Sci
January 2025
Program in Neuroscience, Department of Biology, Syracuse University, Syracuse, NY 13210, USA.
Astrocytes produce and export glutathione (GSH), an important thiol antioxidant essential for protecting neural cells from oxidative stress and maintaining optimal brain health. While it has been established that oxidative stress increases GSH production in astrocytes, with Nrf2 acting as a critical transcription factor regulating key components of the GSH synthetic pathway, the role of Nrf2 in controlling constitutive GSH synthetic and release mechanisms remains incompletely investigated. Our data show that naïve primary mouse astrocytes cultured from the cerebral cortices of Nrf2 knockout (Nrf2) pups have significantly less intracellular and extracellular GSH levels when compared to astrocytes cultured from Nrf2 wild-type (Nrf2) pups.
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!