scholarly journals Noradrenaline Increases mEPSC Frequency in Pyramidal Cells in Layer II of Rat Barrel Cortex via Calcium Release From Presynaptic Stores

2018 ◽  
Vol 12 ◽  
Author(s):  
Julian M. C. Choy ◽  
Fransiscus A. Agahari ◽  
Li Li ◽  
Christian Stricker
Keyword(s):  
Calcium Release ◽  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Mepsc Frequency

Serotonergic Modulation of Spontaneous and Evoked Transmitter Release in Layer II Pyramidal Cells of Rat Somatosensory Cortex

2020 ◽  
Author(s):  
Fransiscus Adrian Agahari ◽  
Christian Stricker
Keyword(s):  
Somatosensory Cortex ◽  
Transmitter Release ◽  
Barrel Cortex ◽  
Signal To Noise Ratio ◽  
Pyramidal Cells ◽  
Mepsc Frequency ◽  
Spontaneous Noise ◽  
Synaptic Dynamics ◽  
Rat Somatosensory Cortex ◽  
Almost All

Abstract As axons from the raphe nuclei densely innervate the somatosensory cortex, we investigated how serotonin (5-HT) modulates transmitter release in layer II pyramidal cells of rat barrel cortex. In the presence of tetrodotoxin and gabazine, 10 μM 5-HT caused a waxing and waning in the frequency of miniature excitatory postsynaptic currents (mEPSC) with no effect on amplitude. Specifically, within 15 min of recording the mEPSC frequency initially increased by 28 ± 7%, then dropped to below control (−15 ± 3%), before resurging back to 27 ± 7% larger than control. These changes were seen in 47% of pyramidal cells (responders) and were mediated by 5-HT2C receptors (5-HT2CR). Waxing resulted from phospholipase C activation, IP3 production, and Ca2+ release from presynaptic stores. Waning was prevented if PKC was blocked. In contrast, in paired recordings, the unitary EPSC amplitude was reduced by 50 ± 3% after 5-HT exposure in almost all cases with no significant effect on paired-pulse ratio and synaptic dynamics. This sustained EPSC reduction was also caused by 5-HT2R, but was mediated by presynaptic Gβγ subunits likely limiting influx through CaV2 channels. EPSC reduction, together with enhanced spontaneous noise in a restricted subset of inputs, could temporarily diminish the signal-to-noise ratio and affect the computation in the neocortical microcircuit.

scholarly journals Direct and Collateral Alterations of Functional Cortical Circuits in a Rat Model of Subcortical Band Heterotopia

2018 ◽  
Vol 29 (10) ◽  
pp. 4253-4262 ◽  
Author(s):  
Vanessa Plantier ◽  
Françoise Watrin ◽  
Emmanuelle Buhler ◽  
Fanny Sandrine Martineau ◽  
Surajit Sahu ◽  
...  
Keyword(s):  
Barrel Cortex ◽  
Intractable Epilepsy ◽  
Pyramidal Cells ◽  
Cortical Region ◽  
Cortical Networks ◽  
Causative Gene ◽  
Double Cortex Syndrome ◽  
Subcortical Band Heterotopia ◽  
Migration Disorder ◽  
Band Heterotopia

Abstract Subcortical band heterotopia (SBH), also known as double-cortex syndrome, is a neuronal migration disorder characterized by an accumulation of neurons in a heterotopic band below the normotopic cortex. The majority of patients with SBH have mild to moderate intellectual disability and intractable epilepsy. However, it is still not clear how cortical networks are organized in SBH patients and how this abnormal organization contributes to improper brain function. In this study, cortical networks were investigated in the barrel cortex in an animal model of SBH induced by in utero knockdown of Dcx, main causative gene of this condition in human patients. When the SBH was localized below the Barrel Field (BF), layer (L) four projection to correctly positioned L2/3 pyramidal cells was weakened due to lower connectivity. Conversely, when the SBH was below an adjacent cortical region, the excitatory L4 to L2/3 projection was stronger due to increased L4 neuron excitability, synaptic strength and excitation/inhibition ratio of L4 to L2/3 connection. We propose that these developmental alterations contribute to the spectrum of clinical dysfunctions reported in patients with SBH.

scholarly journals A gradual depth-dependent change in connectivity features of supragranular pyramidal cells in rat barrel cortex

2014 ◽  
Vol 220 (3) ◽  
pp. 1317-1337 ◽  
Author(s):  
Jochen F. Staiger ◽  
Ingo Bojak ◽  
Stéphanie Miceli ◽  
Dirk Schubert
Keyword(s):  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Dependent Change

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.

scholarly journals Morphological Characteristics of Electrophysiologically Characterized Layer Vb Pyramidal Cells in Rat Barrel Cortex

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0164004 ◽  
Author(s):  
Jochen F. Staiger ◽  
Alexandre J. C. Loucif ◽  
Dirk Schubert ◽  
Martin Möck
Keyword(s):  
Barrel Cortex ◽  
Morphological Characteristics ◽  
Pyramidal Cells

scholarly journals Layer-Specific Intracolumnar and Transcolumnar Functional Connectivity of Layer V Pyramidal Cells in Rat Barrel Cortex

2001 ◽  
Vol 21 (10) ◽  
pp. 3580-3592 ◽  
Author(s):  
Dirk Schubert ◽  
Jochen F. Staiger ◽  
Nichole Cho ◽  
Rolf Kötter ◽  
Karl Zilles ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Layer V

A distinct form of calcium release down-regulates membrane excitability in neocortical pyramidal cells

Neuroscience ◽  
2002 ◽  
Vol 109 (4) ◽  
pp. 665-676 ◽  
Author(s):  
K Yamamoto ◽  
K Hashimoto ◽  
M Nakano ◽  
S Shimohama ◽  
N Kato
Keyword(s):  
Calcium Release ◽  
Pyramidal Cells ◽  
Distinct Form ◽  
Membrane Excitability

scholarly journals Layer 6A pyramidal cells subtypes form synaptic microcircuits with distinct functional and structural properties

2021 ◽  
Author(s):  
Danqing Yang ◽  
Guanxiao Qi ◽  
Dirk Feldmeyer
Keyword(s):  
Barrel Cortex ◽  
Dynamic Properties ◽  
Pyramidal Cells ◽  
Synaptic Connections ◽  
Cell Type ◽  
Short Term ◽  
Electrophysiological Properties ◽  
Cell Type Specific ◽  
Feedback Networks ◽  
Whole Cell Recordings

Neocortical layer 6 plays a crucial role in sensorimotor coordination and integration through functionally segregated circuits linking intracortical and subcortical areas. However, because of the high neuronal heterogeneity and sparse intralaminar connectivity data on the cell-type specific synaptic microcircuits in layer 6 remain few and far between. To address this issue, whole-cell recordings combined with morphological reconstructions have been used to identify morphoelectric types of layer 6A pyramidal cells (PCs) in rat barrel cortex. Cortico-thalamic (CT), corticocortical (CC) and cortico-claustral (CCla) pyramidal cells have been distinguished based on to their distinct dendritic and axonal morphologies as well as their different electrophysiological properties. Here we demonstrate that these three types of layer 6A pyramidal cells innervate neighboring excitatory neurons with distinct synaptic properties: CT PCs establish weak facilitating synapses to other L6A PCs; CC PCs form synapses of moderate efficacy; while synapses made by putative CCla PCs display the highest release probability and a marked short-term depression. Furthermore, for excitatory-inhibitory synaptic connections in layer 6 we were able to show that both the presynaptic PC type and the postsynaptic interneuron type govern the dynamic properties of the of the respective synaptic connections. We have identified a functional division of local layer 6A excitatory microcircuits which may be responsible of the differential temporal engagement of layer 6 feed-forward and feedback networks. Our results provides a basis for further investigations on the long-range cortico-cortical, cortico-thalamic and cortico-claustral pathways.

scholarly journals Novel Ca2+-dependent mechanisms regulate spontaneous release at excitatory synapses onto CA1 pyramidal cells

2018 ◽  
Vol 119 (2) ◽  
pp. 597-607 ◽  
Author(s):  
Walter E. Babiec ◽  
Thomas J. O’Dell
Keyword(s):  
Action Potential ◽  
Pyramidal Cells ◽  
Synaptic Function ◽  
Excitatory Synapses ◽  
Spontaneous Release ◽  
Ca1 Pyramidal Cells ◽  
Spontaneous Action Potential ◽  
Mepsc Frequency ◽  
Intracellular Ca ◽  
Spontaneous Action

Although long thought to simply be a source of synaptic noise, spontaneous, action potential-independent release of neurotransmitter from presynaptic terminals has multiple roles in synaptic function. We explored whether and to what extent the two predominantly proposed mechanisms for explaining spontaneous release, stochastic activation of voltage-gated Ca2+ channels (VGCCs) or activation of Ca2+-sensing receptors (CaSRs) by extracellular Ca2+, played a role in the sensitivity of spontaneous release to the level of extracellular Ca2+ concentration at excitatory synapses at CA1 pyramidal cells of the adult male mouse hippocampus. Blocking VGCCs with Cd2+ had no effect on spontaneous release, ruling out stochastic activation of VGCCs. Although divalent cation agonists of CaSRs, Co2+ and Mg2+, dramatically enhanced miniature excitatory postsynaptic current (mEPSC) frequency, potent positive and negative allosteric modulators of CaSRs had no effect. Moreover, immunoblot analysis of hippocampal lysates failed to detect CaSR expression, ruling out the CaSR. Instead, the increase in mEPSC frequency induced by Co2+ and Mg2+ was mimicked by lowering postsynaptic Ca2+ levels with BAPTA. Together, our results suggest that a reduction in intracellular Ca2+ may trigger a homeostatic-like compensatory response that upregulates spontaneous transmission at excitatory synapses onto CA1 pyramidal cells in the adult hippocampus. NEW & NOTEWORTHY We show that the predominant theories for explaining the regulation of spontaneous, action potential-independent synaptic release do not explain the sensitivity of this type of synaptic transmission to external Ca2+ concentration at excitatory synapses onto hippocampal CA1 pyramidal cells. In addition, our data indicate that intracellular Ca2+ levels in CA1 pyramidal cells regulate spontaneous release, suggesting that excitatory synapses onto CA1 pyramidal cells may express a novel, rapid form of homeostatic plasticity.

scholarly journals Synchronized gamma-frequency inhibition in neocortex depends on excitatory-inhibitory interactions but not electrical synapses

2016 ◽  
Vol 116 (2) ◽  
pp. 351-368 ◽  
Author(s):  
Garrett T. Neske ◽  
Barry W. Connors
Keyword(s):  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Inhibitory Interneurons ◽  
Electrical Synapses ◽  
Postsynaptic Currents ◽  
Gamma Frequency ◽  
Up States ◽  
Inhibitory Interactions

Synaptic inhibition plays a crucial role in the precise timing of spiking activity in the cerebral cortex. Synchronized, rhythmic inhibitory activity in the gamma (30–80 Hz) range is thought to be especially important for the active, information-processing neocortex, but the circuit mechanisms that give rise to synchronized inhibition are uncertain. In particular, the relative contributions of reciprocal inhibitory connections, excitatory-inhibitory interactions, and electrical synapses to precise spike synchrony among inhibitory interneurons are not well understood. Here we describe experiments on mouse barrel cortex in vitro as it spontaneously generates slow (<1 Hz) oscillations (Up and Down states). During Up states, inhibitory postsynaptic currents (IPSCs) are generated at gamma frequencies and are more synchronized than excitatory postsynaptic currents (EPSCs) among neighboring pyramidal cells. Furthermore, spikes in homotypic pairs of interneurons are more synchronized than in pairs of pyramidal cells. Comparing connexin36 knockout and wild-type animals, we found that electrical synapses make a minimal contribution to synchronized inhibition during Up states. Estimations of the delays between EPSCs and IPSCs in single pyramidal cells showed that excitation often preceded inhibition by a few milliseconds. Finally, tonic optogenetic activation of different interneuron subtypes in the absence of excitation led to only weak synchrony of IPSCs in pairs of pyramidal neurons. Our results suggest that phasic excitatory inputs are indispensable for synchronized spiking in inhibitory interneurons during Up states and that electrical synapses play a minimal role.

Sign in / Sign up

Export Citation Format

Share Document