Anatomical and sensory experiential determinants of synaptic plasticity in layer 2/3 pyramidal neurons of mouse barrel cortex

2011 ◽  
Vol 519 (11) ◽  
pp. 2090-2124 ◽  
Author(s):  
Neil R. Hardingham ◽  
Tim Gould ◽  
Kevin Fox
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Layer 2

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

Development of Intrinsic Properties and Excitability of Layer 2/3 Pyramidal Neurons During a Critical Period for Sensory Maps in Rat Barrel Cortex

2004 ◽  
Vol 92 (1) ◽  
pp. 144-156 ◽  
Author(s):  
Miguel Maravall ◽  
Edward A. Stern ◽  
Karel Svoboda
Keyword(s):  
Critical Period ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Membrane Properties ◽  
Sensory Maps ◽  
Layer 2 ◽  
Whole Cell Recordings ◽  
Passive Membrane Properties

The development of layer 2/3 sensory maps in rat barrel cortex (BC) is experience dependent with a critical period around postnatal days (PND) 10–14. The role of intrinsic response properties of neurons in this plasticity has not been investigated. Here we characterize the development of BC layer 2/3 intrinsic responses to identify possible sites of plasticity. Whole cell recordings were performed on pyramidal cells in acute BC slices from control and deprived rats, over ages spanning the critical period (PND 12, 14, and 17). Vibrissa trimming began at PND 9. Spiking behavior changed from phasic (more spike frequency adaptation) to regular (less adaptation) with age, such that the number of action potentials per stimulus increased. Changes in spiking properties were related to the strength of a slow Ca2+-dependent afterhyperpolarization. Maturation of the spiking properties of layer 2/3 pyramidal neurons coincided with the close of the critical period and was delayed by deprivation. Other measures of excitability, including I-f curves and passive membrane properties, were affected by development but unaffected by whisker deprivation.

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.

scholarly journals NMDA receptor–BK channel coupling regulates synaptic plasticity in the barrel cortex

2021 ◽  
Vol 118 (35) ◽  
pp. e2107026118 ◽  
Author(s):  
Ricardo Gómez ◽  
Laura E. Maglio ◽  
Alberto J. Gonzalez-Hernandez ◽  
Belinda Rivero-Pérez ◽  
David Bartolomé-Martín ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Feedback Inhibition ◽  
Bk Channels ◽  
Bk Channel ◽  
Spike Timing ◽  
Ability To Act ◽  
Nmdar Activation ◽  
Molecular Context

Postsynaptic N-methyl-D-aspartate receptors (NMDARs) are crucial mediators of synaptic plasticity due to their ability to act as coincidence detectors of presynaptic and postsynaptic neuronal activity. However, NMDARs exist within the molecular context of a variety of postsynaptic signaling proteins, which can fine-tune their function. Here, we describe a form of NMDAR suppression by large-conductance Ca2+- and voltage-gated K+ (BK) channels in the basal dendrites of a subset of barrel cortex layer 5 pyramidal neurons. We show that NMDAR activation increases intracellular Ca2+ in the vicinity of BK channels, thus activating K+ efflux and strong negative feedback inhibition. We further show that neurons exhibiting such NMDAR–BK coupling serve as high-pass filters for incoming synaptic inputs, precluding the induction of spike timing–dependent plasticity. Together, these data suggest that NMDAR-localized BK channels regulate synaptic integration and provide input-specific synaptic diversity to a thalamocortical circuit.

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