scholarly journals The coincident activation of lemniscal and paralemniscal inputs can drive synaptic plasticity in layer 2/3 pyramidal neurons of the mouse somatosensory cortex in vivo

2014 ◽  
Vol 8 ◽  
Author(s):  
Kehayas Vassilis ◽  
Gambino Frédéric ◽  
Baptista Daniela ◽  
Pagès Stéphane ◽  
Holtmaat Anthony
Keyword(s):  
Synaptic Plasticity ◽  
Somatosensory Cortex ◽  
Pyramidal Neurons ◽  
Layer 2

scholarly journals Asymmetric Temporal Integration of Layer 4 and Layer 2/3 Inputs in Visual Cortex

2011 ◽  
Vol 105 (1) ◽  
pp. 347-355 ◽  
Author(s):  
Giao B. Hang ◽  
Yang Dan
Keyword(s):  
Visual Cortex ◽  
Visual Processing ◽  
Pyramidal Neurons ◽  
Temporal Integration ◽  
Cortical Inhibition ◽  
Multiple Sources ◽  
Layer 2 ◽  
Layer 4 ◽  
The Difference

Neocortical neurons in vivo receive concurrent synaptic inputs from multiple sources, including feedforward, horizontal, and feedback pathways. Layer 2/3 of the visual cortex receives feedforward input from layer 4 and horizontal input from layer 2/3. Firing of the pyramidal neurons, which carries the output to higher cortical areas, depends critically on the interaction of these pathways. Here we examined synaptic integration of inputs from layer 4 and layer 2/3 in rat visual cortical slices. We found that the integration is sublinear and temporally asymmetric, with larger responses if layer 2/3 input preceded layer 4 input. The sublinearity depended on inhibition, and the asymmetry was largely attributable to the difference between the two inhibitory inputs. Interestingly, the asymmetric integration was specific to pyramidal neurons, and it strongly affected their spiking output. Thus via cortical inhibition, the temporal order of activation of layer 2/3 and layer 4 pathways can exert powerful control of cortical output during visual processing.

scholarly journals High-order thalamic inputs to primary somatosensory cortex are stronger and longer lasting than cortical inputs

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Wanying Zhang ◽  
Randy M Bruno
Keyword(s):  
Somatosensory Cortex ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
Sensory Stimulation ◽  
Primary Somatosensory Cortex ◽  
Specific Substrate ◽  
Medial Nucleus ◽  
Posterior Medial Nucleus ◽  
Cortical Inputs

Layer (L) 2/3 pyramidal neurons in the primary somatosensory cortex (S1) are sparsely active, spontaneously and during sensory stimulation. Long-range inputs from higher areas may gate L2/3 activity. We investigated their in vivo impact by expressing channelrhodopsin in three main sources of feedback to rat S1: primary motor cortex, secondary somatosensory cortex, and secondary somatosensory thalamic nucleus (the posterior medial nucleus, POm). Inputs from cortical areas were relatively weak. POm, however, more robustly depolarized L2/3 cells and, when paired with peripheral stimulation, evoked action potentials. POm triggered not only a stronger fast-onset depolarization but also a delayed all-or-none persistent depolarization, lasting up to 1 s and exhibiting alpha/beta-range oscillations. Inactivating POm somata abolished persistent but not initial depolarization, indicating a recurrent circuit mechanism. We conclude that secondary thalamus can enhance L2/3 responsiveness over long periods. Such timescales could provide a potential modality-specific substrate for attention, working memory, and plasticity.

scholarly journals The NMDA-to-AMPA Ratio at Synapses Onto Layer 2/3 Pyramidal Neurons Is Conserved Across Prefrontal and Visual Cortices

2003 ◽  
Vol 90 (2) ◽  
pp. 771-779 ◽  
Author(s):  
Chaelon I. O. Myme ◽  
Ken Sugino ◽  
Gina G. Turrigiano ◽  
Sacha B. Nelson
Keyword(s):  
Ampa Receptor ◽  
Pyramidal Neurons ◽  
Brain Slices ◽  
Pyramidal Cells ◽  
Cell Voltage ◽  
Decay Kinetics ◽  
Excitatory Transmission ◽  
Layer 2 ◽  
Medial Pfc

To better understand regulation of N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor complements across the cortex, and to investigate NMDA receptor (NMDAR)-based models of persistent activity, we compared NMDA/AMPA ratios in prefrontal (PFC) and visual cortex (VC) in rat. Whole cell voltage-clamp responses were recorded in brain slices from layer 2/3 pyramidal cells of the medial PFC and VC of rats aged p16–p21. Mixed miniature excitatory postsynaptic currents (mEPSCs) having AMPA receptor (AMPAR)- and NMDAR-mediated components were isolated in nominally 0 Mg2+ ACSF. Averaged mEPSCs were well-fit by double exponentials. No significant differences in the NMDA/AMPA ratio (PFC: 27 ± 1%; VC: 28 ± 3%), peak mEPSC amplitude (PFC: 19.1 ± 1 pA; VC: 17.5 ± 0.7 pA), NMDAR decay kinetics (PFC: 69 ± 8 ms; VC: 67 ± 6 ms), or degree of correlation between NMDAR- and AMPAR-mediated mEPSC components were found between the areas (PFC: n = 27; VC: n = 28). Recordings from older rats (p26–29) also showed no differences. EPSCs were evoked extracellularly in 2 mM Mg2+ at depolarized potentials; although the average NMDA/AMPA ratio was larger than that observed for mEPSCs, the ratio was similar in the two regions. In nominally 0 Mg2+ and in the presence of CNQX, spontaneous activation of NMDAR increased recording noise and produced a small tonic depolarization which was similar in both areas. We conclude that this basic property of excitatory transmission is conserved across PFC and VC synapses and is therefore unlikely to contribute to differences in firing patterns observed in vivo in the two regions.

Spread of dendritic excitation in layer 2/3 pyramidal neurons in rat barrel cortex in vivo

10.1038/4569 ◽  
1999 ◽  
Vol 2 (1) ◽  
pp. 65-73 ◽  
Author(s):  
Karel Svoboda ◽  
Fritjof Helmchen ◽  
Winfried Denk ◽  
David W. Tank
Keyword(s):  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Layer 2

scholarly journals Increased excitation-inhibition ratio stabilizes synapse and circuit excitability in four autism mouse models

2018 ◽  
Author(s):  
Michelle W. Antoine ◽  
Philipp Schnepel ◽  
Tomer Langberg ◽  
Daniel E. Feldman
Keyword(s):  
Cerebral Cortex ◽  
Somatosensory Cortex ◽  
Mouse Models ◽  
Spike Threshold ◽  
Essentially Normal ◽  
Layer 2 ◽  
Conductance Changes ◽  
Conductance Ratio ◽  
Synaptic Drive

SummaryDistinct genetic forms of autism are hypothesized to share a common increase in excitation-inhibition (E-I) ratio in cerebral cortex, causing hyperexcitability and excess spiking. We provide the first systematic test of this hypothesis across 4 mouse models (Fmr1−/y,Cntnap2−/-,16p11.2del/+,Tsc2+/-), focusing on somatosensory cortex. All autism mutants showed reduced feedforward inhibition in layer 2/3 coupled with more modest, variable reductions in feedforward excitation, driving a common increase in E-I conductance ratio. Despite this, feedforward spiking, synaptic depolarization and spontaneous spiking were essentially normal. Modeling revealed that E and I conductance changes in each mutant were quantitatively matched to yield stable, not increased, synaptic depolarization for cells near spike threshold. Correspondingly, whisker-evoked spiking was not increasedin vivo, despite detectably reduced inhibition. Thus, elevated E-I ratio is a common circuit phenotype, but appears to reflect homeostatic stabilization of synaptic drive, rather than driving network hyperexcitability in autism.

Layer-specific serotonergic facilitation of IPSC in layer 2/3 pyramidal neurons of the visual cortex

2012 ◽  
Vol 107 (1) ◽  
pp. 407-416 ◽  
Author(s):  
Hyun-Jong Jang ◽  
Kwang-Hyun Cho ◽  
Sung-Won Park ◽  
Myung-Jun Kim ◽  
Shin Hee Yoon ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Pyramidal Neurons ◽  
Inhibitory Influence ◽  
Inhibitory Transmission ◽  
Layer 2 ◽  
Specific Manner ◽  
Intracellular Ca ◽  
Stimulation Of

Serotonin (5-hydroxytryptamine, 5-HT) inhibits the induction of long-term synaptic plasticity in layer 2/3 of the visual cortex at the end of its critical period in rats. However, the cellular and molecular mechanisms remain unclear. Since inhibitory influence is crucial in the induction of synaptic plasticity, the effect of 5-HT on inhibitory transmission was investigated in layer 2/3 pyramidal neurons of the primary visual cortex. The amplitude of inhibitory postsynaptic current (IPSC), but not excitatory postsynaptic current, evoked by stimulation of the underlying layer 4, was increased by ∼20% with a bath application of 5-HT. The amplitude of miniature IPSC was also increased by the application of 5-HT, while the paired-pulse ratio was not changed. The facilitating effect of 5-HT on IPSC was mediated by the activation of 5-HT2 receptors. An increase in intracellular Ca2+ via release from inositol 1,4,5-trisphosphate (IP3)-sensitive stores, which was confirmed by confocal Ca2+ imaging, and activation of Ca2+/calmodulin-dependent kinase II (CaMKII) were involved in the facilitation of IPSC by 5-HT. However, 5-HT failed to facilitate IPSC evoked by the stimulation of layer 1. These results suggest that activation of 5-HT2 receptors releases intracellular Ca2+ via IP3-sensitive stores, which facilitates GABAAergic transmission via the activation of CaMKII in layer 2/3 pyramidal neurons of the visual cortex in a layer-specific manner. Thus facilitation of inhibitory transmission by 5-HT might be involved in regulating the information flow and the induction of long-term synaptic plasticity, in a pathway-specific manner.

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