Dopamine D1-like receptor modulates layer- and frequency-specific short-term synaptic plasticity in rat prefrontal cortical neurons

2005 ◽  
Vol 21 (12) ◽  
pp. 3310-3320 ◽  
Author(s):  
Clint E. Young ◽  
Charles R. Yang
Keyword(s):  
Synaptic Plasticity ◽  
Cortical Neurons ◽  
Short Term ◽  
Prefrontal Cortical

Short-term sleep deprivation increases intrinsic excitability of prefrontal cortical neurons

2011 ◽  
Vol 1401 ◽  
pp. 52-58 ◽  
Author(s):  
Jie Yan ◽  
Jing-Cheng Li ◽  
Mei-Lan Xie ◽  
Dan Zhang ◽  
Ai-Ping Qi ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Cortical Neurons ◽  
Intrinsic Excitability ◽  
Short Term ◽  
Prefrontal Cortical

scholarly journals Spectral tuning of adaptation supports coding of sensory context in auditory cortex

2019 ◽  
Author(s):  
Mateo Lopez Espejo ◽  
Zachary P. Schwartz ◽  
Stephen V. David
Keyword(s):  
Synaptic Plasticity ◽  
Auditory Cortex ◽  
Cortical Neurons ◽  
Contextual Effects ◽  
Natural Sounds ◽  
Short Term ◽  
Sound Processing ◽  
Natural Sound ◽  
Evoked Activity ◽  
Better Than

AbstractPerception of vocalizations and other behaviorally relevant sounds requires integrating acoustic information over hundreds of milliseconds, but the latency of sound-evoked activity in auditory cortex typically has much shorter latency. It has been observed that the acoustic context, i.e., sound history, can modulate sound evoked activity. Contextual effects are attributed to modulatory phenomena, such as stimulus-specific adaption and contrast gain control. However, an encoding model that links context to natural sound processing has yet to be established. We tested whether a model in which spectrally tuned inputs undergo adaptation mimicking short-term synaptic plasticity can account for contextual effects during natural sound processing. Single-unit activity was recorded from primary auditory cortex of awake ferrets during presentation of noise with natural temporal dynamics and fully natural sounds. Encoding properties were characterized by a standard linear-nonlinear spectro-temporal receptive field model (LN STRF) and STRF variants that incorporated STP-like adaptation. In two models, STP was applied either globally across all spectral channels or locally to subsets of channels. For most neurons, STRFs incorporating locally tuned STP predicted neural activity as well or better than the LN and global STP STRF. The strength of nonlinear adaptation varied across neurons. Within neurons, adaptation was generally stronger for activation with excitatory than inhibitory gain. Neurons showing improved STP model performance also tended to undergo stimulus-specific adaptation, suggesting a common mechanism for these phenomena. When STP STRFs were compared between passive and active behavior conditions, response gain often changed, but average STP parameters were stable. Thus, spectrally and temporally heterogeneous adaptation, subserved by a mechanism with STP-like dynamics, may support representation of the diverse spectro-temporal patterns that comprise natural sounds.Author summarySuccessfully discriminating between behaviorally relevant sounds such as vocalizations and environmental noise requires processing how acoustic information changes over many tens to hundreds of milliseconds. The sound-evoked activity measured for most auditory cortical neurons is relatively short (< 50 ms), so it is not clear how the auditory cortex encodes sound information over longer periods. In this study, we propose that nonlinear adaptation, mimicking the effects of short-term synaptic plasticity (STP), enables auditory neurons to encode longer and more complex spectro-temporal patterns. A model in which sound history is stored in the latent state of plastic synapses is able to describe responses of single cortical neurons to natural sounds better than a standard encoding model that does not include nonlinear adaptation. Moreover, STP-like adaptation can account for contextual effects on sound evoked activity that cannot be accounted for by standard encoding models.

scholarly journals Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Emma M. Perkins ◽  
Karen Burr ◽  
Poulomi Banerjee ◽  
Arpan R. Mehta ◽  
Owen Dando ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Vesicle ◽  
Cortical Neurons ◽  
Electrode Array ◽  
Repeat Expansion ◽  
Cortical Network ◽  
Synaptic Function ◽  
Network Activity ◽  
Cortical Function ◽  
Network Function

Abstract Background Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat expansion (C9ORF72RE) mutation – the most common genetic impairment causal to ALS and FTD. Noting that perturbations in cortical function are evidenced pre-symptomatically, and that the cortex is associated with widespread pathology, cortical dysfunction is thought to be an early driver of neurodegenerative disease progression. However, our understanding of how altered network function manifests at the cellular and molecular level is not clear. Methods To address this we have generated cortical neurons from patient-derived iPSCs harbouring C9ORF72RE mutations, as well as from their isogenic expansion-corrected controls. We have established a model of network activity in these neurons using multi-electrode array electrophysiology. We have then mechanistically examined the physiological processes underpinning network dysfunction using a combination of patch-clamp electrophysiology, immunocytochemistry, pharmacology and transcriptomic profiling. Results We find that C9ORF72RE causes elevated network burst activity, associated with enhanced synaptic input, yet lower burst duration, attributable to impaired pre-synaptic vesicle dynamics. We also show that the C9ORF72RE is associated with impaired synaptic plasticity. Moreover, RNA-seq analysis revealed dysregulated molecular pathways impacting on synaptic function. All molecular, cellular and network deficits are rescued by CRISPR/Cas9 correction of C9ORF72RE. Our study provides a mechanistic view of the early dysregulated processes that underpin cortical network dysfunction in ALS-FTD. Conclusion These findings suggest synaptic pathophysiology is widespread in ALS-FTD and has an early and fundamental role in driving altered network function that is thought to contribute to neurodegenerative processes in these patients. The overall importance is the identification of previously unidentified defects in pre and postsynaptic compartments affecting synaptic plasticity, synaptic vesicle stores, and network propagation, which directly impact upon cortical function.

LY392098, a novel AMPA receptor potentiator: electrophysiological studies in prefrontal cortical neurons

2001 ◽  
Vol 40 (8) ◽  
pp. 992-1002 ◽  
Author(s):  
Polly Baumbarger ◽  
Mark Muhlhauser ◽  
Charles R Yang ◽  
Eric S Nisenbaum
Keyword(s):  
Ampa Receptor ◽  
Cortical Neurons ◽  
Prefrontal Cortical ◽  
Electrophysiological Studies

scholarly journals Taurine regulation of short term synaptic plasticity in fragile X mice

2010 ◽  
Vol 17 (Suppl 1) ◽  
pp. S15 ◽  
Author(s):  
Abdeslem El Idrissi ◽  
Lorenz S Neuwirth ◽  
William L’Amoreaux
Keyword(s):  
Synaptic Plasticity ◽  
Fragile X ◽  
Short Term
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