Acid-sensing ion channels (ASICs), members of the degenerin/epithelial Na+ channel superfamily, are broadly distributed in the mammalian nervous system where they play important roles in a variety of physiological processes, including neurotransmission and memory-related behaviors. In the last few years, we and others have investigated the role of ASIC1a in different forms of synaptic plasticity especially in the CA1 area of the hippocampus. This review summarizes the latest research linking ASIC1a to synaptic function either in physiological or pathological conditions. A better understanding of how these channels are regulated in brain circuitries relevant to synaptic plasticity and memory may offer novel targets for pharmacological intervention in neuropsychiatric and neurological disorders.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/112_2020_45 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The calcitron: A simple neuron model that implements many learning rules via the calcium control hypothesis.
PLoS Comput Biol
January 2025
Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Theoretical neuroscientists and machine learning researchers have proposed a variety of learning rules to enable artificial neural networks to effectively perform both supervised and unsupervised learning tasks. It is not always clear, however, how these theoretically-derived rules relate to biological mechanisms of plasticity in the brain, or how these different rules might be mechanistically implemented in different contexts and brain regions. This study shows that the calcium control hypothesis, which relates synaptic plasticity in the brain to the calcium concentration ([Ca2+]) in dendritic spines, can produce a diverse array of learning rules.
View Article and Find Full Text PDFFrom Play Date to Stress Fate: Juvenile Social Play Rescues Stress-Induced Changes in Adult Social Behavior.
Dev Psychobiol
January 2025
Department of Psychology, The University of Tennessee Knoxville, Knoxville, Tennessee, USA.
Long-term effects of social play on neural and behavioral development remain unclear. We investigated whether just 1 h of juvenile social play could rescue the effects of play deprivation on stress-related behavior and markers of neural plasticity. Syrian hamsters were reared from postnatal days 21-43 in three conditions: peer isolation, peer isolation with daily social play sessions (dyadic play), or group-housed with littermates.
View Article and Find Full Text PDFNovel De Novo Intronic Variant of SYNGAP1 Associated With the Neurodevelopmental Disorders.
Mol Genet Genomic Med
February 2025
Department of Chemistry and Molecular Biology, Gothenburg University, Gothenburg, Sweden.
Background: SYNGAP1 encodes a Ras/Rap GTPase-activating protein that is predominantly expressed in the brain with the functional roles in regulating synaptic plasticity, spine morphogenesis, and cognition function. Pathogenic variants in SYNGAP1 have been associated with a spectrum of neurodevelopmental disorders characterized by developmental delays, intellectual disabilities, epilepsy, hypotonia, and the features of autism spectrum disorder. The aim of this study was to identify a novel SYNGAP1 gene variant linked to neurodevelopmental disorders and to evaluate the pathogenicity of the detected variant.
View Article and Find Full Text PDFEpigenetic modulation rescues neurodevelopmental deficits in Syngap1 mice.
Aging Cell
January 2025
Molecular Biology and Genetics Unit, Transcription and Disease Laboratory, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, India.
SYNGAP1 is a Ras GTPase-activating protein that plays a crucial role during brain development and in synaptic plasticity. Sporadic heterozygous mutations in SYNGAP1 affect social and emotional behaviour observed in intellectual disability (ID) and autism spectrum disorder (ASD). Although neurophysiological deficits have been extensively studied, the epigenetic landscape of SYNGAP1 mutation-mediated intellectual disability is unexplored.
View Article and Find Full Text PDFThe hippocampus forms memories of our experiences by registering processed sensory information in coactive populations of excitatory principal cells or ensembles. Fast-spiking parvalbumin-expressing inhibitory neurons (PV INs) in the dentate gyrus (DG)-CA3/CA2 circuit contribute to memory encoding by exerting precise temporal control of excitatory principal cell activity through mossy fiber-dependent feed-forward inhibition. PV INs respond to input-specific information by coordinating changes in their intrinsic excitability, input-output synaptic-connectivity, synaptic-physiology and synaptic-plasticity, referred to here as experience-dependent PV IN plasticity, to influence hippocampal functions.
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!