Studying synaptic physiology remains an important endeavor for understanding the mechanisms that underlie neurotransmitter release as well as synaptic development and refinement. It is also critical to understanding brain function. The basic conceptual framework for synaptic physiology was worked out by Katz and colleagues and has coalesced around three factors: the number of releasable vesicles (N), the probability of release (P), and quantal size (Q). Here, I discuss a few key experiments related to these quantities and how they are assessed.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1101/pdb.top089680 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
β-adrenergic receptor-induced E-S potentiation in the dorsal and ventral hippocampus.
Front Synaptic Neurosci
December 2024
Laboratory of Physiology, Department of Medicine, University of Patras, Patras, Greece.
β-adrenergic receptors (β-ARs) play a critical role in modulating learning, memory, emotionality, and long-term synaptic plasticity. Recent studies indicate that β-ARs are necessary for long-term potentiation (LTP) induction in the ventral hippocampus under moderate synaptic activation conditions that do not typically induce LTP. To explore potential dorsoventral differences in β-AR-mediated effects, we applied the β-AR agonist isoproterenol (10 μM, 30 min) to dorsal and ventral hippocampal slices, recording field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs) from the CA1 region.
View Article and Find Full Text PDFSingle-nucleotide polymorphism analysis accurately predicts multiple impairments in hippocampal activity and memory performance in a murine model of idiopathic autism.
Sci Rep
January 2025
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
Autism spectrum disorder (ASD) comprises alterations in brain anatomy and physiology that ultimately affect information processing and behavior. In most cases, autism is considered idiopathic, involving alterations in numerous genes whose functions are not extensively documented. We evaluated the C58/J mouse strain as an idiopathic model of ASD, emphasizing synaptic transmission as the basis of information processing.
View Article and Find Full Text PDFPreclinical and clinical study on type 3 metabotropic glutamate receptors in Parkinson's disease.
NPJ Parkinsons Dis
January 2025
Department of Molecular Pathology, IRCCS Neuromed, Pozzilli, Italy.
Metabotropic glutamate (mGlu) receptors are candidate drug targets for therapeutic intervention in Parkinson's disease (PD). Here we focused on mGlu3, a receptor subtype involved in synaptic regulation and neuroinflammation. mGlu3 mice showed an enhanced nigro-striatal damage and microglial activation in response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
View Article and Find Full Text PDFFXR1 Deletion from Cortical Parvalbumin Interneurons Modifies their Excitatory Synaptic Responses.
eNeuro
January 2025
Department of Neuroscience, University of Wisconsin-Madison, Madison, WI, 53705
Fragile X autosomal homolog 1 (FXR1), a member of the fragile X messenger riboprotein 1 family, has been linked to psychiatric disorders including autism and schizophrenia. Parvalbumin (PV) interneurons play critical roles in cortical processing, and have been implicated in FXR1-linked mental illnesses. Targeted deletion of FXR1 from PV interneurons in mice has been shown to alter cortical excitability and elicit schizophrenia-like behavior.
View Article and Find Full Text PDFEEFSEC deficiency: A selenopathy with early-onset neurodegeneration.
Am J Hum Genet
January 2025
Institute of Medical Genetics and Applied Genomics, University of Tübingen, 72076 Tübingen, Germany; Center for Rare Disease, University of Tübingen, 72076 Tübingen, Germany; Genomics for Health in Africa (GHA), Africa-Europe Cluster of Research Excellence (CoRE).
Inborn errors of selenoprotein expression arise from deleterious variants in genes encoding selenoproteins or selenoprotein biosynthetic factors, some of which are associated with neurodegenerative disorders. This study shows that bi-allelic selenocysteine tRNA-specific eukaryotic elongation factor (EEFSEC) variants cause selenoprotein deficiency, leading to progressive neurodegeneration. EEFSEC deficiency, an autosomal recessive disorder, manifests with global developmental delay, progressive spasticity, ataxia, and seizures.
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!