scholarly journals Synaptic connections between layer 4 spiny neurone‐ layer 2/3 pyramidal cell pairs in juvenile rat barrel cortex: physiology and anatomy of interlaminar signalling within a cortical column

2002 ◽  
Vol 538 (3) ◽  
pp. 803-822 ◽  
Author(s):  
Dirk Feldmeyer ◽  
Joachim Lübke ◽  
R. Angus Silver ◽  
Bert Sakmann
2003 ◽  
Vol 23 (25) ◽  
pp. 8759-8770 ◽  
Author(s):  
Kevin J. Bender ◽  
Juliana Rangel ◽  
Daniel E. Feldman
Keyword(s):  
Layer 2 ◽  

2007 ◽  
Vol 97 (6) ◽  
pp. 4380-4385 ◽  
Author(s):  
Soo-Hyun Lee ◽  
Peter W. Land ◽  
Daniel J. Simons

Tactile deprivation in rats produced by whisker-trimming early in life leads to abnormally robust responses of excitatory neurons in layer 4 of primary somatosensory cortex when the re-grown whiskers are stimulated. Present findings from fast-spike neurons indicate that presumed inhibitory cells fire less robustly under the same conditions. These contrasting effects may reflect altered patterns of thalamocortical input to excitatory versus inhibitory cells and/or changes in the strength of intracortical connections. Despite increased excitability of layer 4, neurons in layer 2/3 respond at control levels even after full whisker re-growth. Layer 4 synapses onto supragranular neurons may be permanently depressed as a result of neonatal sensory deprivation.


2001 ◽  
Vol 86 (1) ◽  
pp. 354-367 ◽  
Author(s):  
Ehud Ahissar ◽  
Ronen Sosnik ◽  
Knarik Bagdasarian ◽  
Sebastian Haidarliu

Part of the information obtained by rodent whiskers is carried by the frequency of their movement. In the thalamus of anesthetized rats, the whisker frequency is represented by two different coding schemes: by amplitude and spike count (i.e., response amplitudes and spike counts decrease as a function of frequency) in the lemniscal thalamus and by latency and spike count (latencies increase and spike counts decrease as a function of frequency) in the paralemniscal thalamus (see accompanying paper). Here we investigated neuronal representations of the whisker frequency in the primary somatosensory (“barrel”) cortex of the anesthetized rat, which receives its input from both the lemniscal and paralemniscal thalamic nuclei. Single and multi-units were recorded from layers 2/3, 4 (barrels only), 5a, and 5b during vibrissal stimulation. Typically, the input frequency was represented by amplitude and spike count in the barrels of layer 4 and in layer 5b (the “lemniscal layers”) and by latency and spike count in layer 5a (the “paralemniscal layer”). Neurons of layer 2/3 displayed a mixture of the two coding schemes. When the pulse width of the stimulus was reduced from 50 to 20 ms, the latency coding in layers 5a and 2/3 was dramatically reduced, while the spike-count coding was not affected; in contrast, in layers 4 and 5b, the latencies remained constant, but the spike counts were reduced with 20-ms stimuli. The same effects were found in the paralemniscal and lemniscal thalamic nuclei, respectively (see accompanying paper). These results are consistent with the idea that thalamocortical loops of different pathways, although terminating within the same cortical columns, perform different computations in parallel. Furthermore, the mixture of coding schemes in layer 2/3 might reflect an integration of lemniscal and paralemniscal outputs.


2018 ◽  
Vol 29 (7) ◽  
pp. 3034-3047
Author(s):  
Jérémy Camon ◽  
Sandrine Hugues ◽  
Melissa A Erlandson ◽  
David Robbe ◽  
Sabria Lagoun ◽  
...  

Abstract Whisker-guided decision making in mice is thought to critically depend on information processing occurring in the primary somatosensory cortex. However, it is not clear if neuronal activity in this “early” sensory region contains information about the timing and speed of motor response. To address this question we designed a new task in which freely moving mice learned to associate a whisker stimulus to reward delivery. The task was tailored in such a way that a wide range of delays between whisker stimulation and reward collection were observed due to differences of motivation and perception. After training, mice were anesthetized and neuronal responses evoked by stimulating trained and untrained whiskers were recorded across several cortical columns of barrel cortex. We found a strong correlation between the delay of the mouse behavioral response and the timing of multiunit activity evoked by the trained whisker, outside its principal cortical column, in layers 4 and 5A but not in layer 2/3. Circuit mapping ex vivo revealed this effect was associated with a weakening of layer 4 to layer 2/3 projection. We conclude that the processes controlling the propagation of key sensory inputs to naive cortical columns and the timing of sensory-guided action are linked.


2021 ◽  
Vol 15 ◽  
Author(s):  
Yonatan Katz ◽  
Ilan Lampl

Neurons in the barrel cortex respond preferentially to stimulation of one principal whisker and weakly to several adjacent whiskers. Such integration exists already in layer 4, the pivotal recipient layer of thalamic inputs. Previous studies show that cortical neurons gradually adapt to repeated whisker stimulations and that layer 4 neurons exhibit whisker specific adaptation and no apparent interactions with other whiskers. This study aimed to study the specificity of adaptation of layer 2/3 cortical cells. Towards this aim, we compared the synaptic response of neurons to either repetitive stimulation of one of two responsive whiskers or when repetitive stimulation of the two whiskers was interleaved. We found that in most layer 2/3 cells adaptation is whisker-specific. These findings indicate that despite the multi-whisker receptive fields in the cortex, the adaptation process for each whisker-pathway is mostly independent of other whiskers. A mechanism allowing high responsiveness in complex environments.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Aleksander P. F. Domanski ◽  
Sam A. Booker ◽  
David J. A. Wyllie ◽  
John T. R. Isaac ◽  
Peter C. Kind

Abstract Sensory hypersensitivity is a common and debilitating feature of neurodevelopmental disorders such as Fragile X Syndrome (FXS). How developmental changes in neuronal function culminate in network dysfunction that underlies sensory hypersensitivities is unknown. By systematically studying cellular and synaptic properties of layer 4 neurons combined with cellular and network simulations, we explored how the array of phenotypes in Fmr1-knockout (KO) mice produce circuit pathology during development. We show that many of the cellular and synaptic pathologies in Fmr1-KO mice are antagonistic, mitigating circuit dysfunction, and hence may be compensatory to the primary pathology. Overall, the layer 4 network in the Fmr1-KO exhibits significant alterations in spike output in response to thalamocortical input and distorted sensory encoding. This developmental loss of layer 4 sensory encoding precision would contribute to subsequent developmental alterations in layer 4-to-layer 2/3 connectivity and plasticity observed in Fmr1-KO mice, and circuit dysfunction underlying sensory hypersensitivity.


2017 ◽  
Author(s):  
Jochen Meyer ◽  
Peyman Golshani ◽  
Stelios M. Smirnakis

AbstractThe influence of cortical cell spiking activity on nearby cells has been studied extensively in vitro. Less is known, however, about the impact of single cell firing on local cortical networks in vivo. In a pioneering study, Kwan et al. (Kwan et al., 2012) reported that in mouse layer 2/3 (L2/3), under anesthesia, stimulating a single pyramidal cell recruits ~1.7% of neighboring pyramidal units. Here we employ two-photon calcium imaging, in conjunction with single-cell patch clamp stimulation, to probe, in both the awake and lightly anesthetized states, how i) activating single L2/3 pyramidal neurons recruits neighboring units within L2/3 and from layer 4 (L4) to L2/3, and whether ii) activating single pyramidal neurons changes population activity in local circuit. To do this, it was essential to develop an algorithm capable of quantifying how sensitive the calcium signal is at detecting effectively recruited units (“followers”). This algorithm allowed us to estimate the chance of detecting a follower as a function of the probability that an epoch of stimulation elicits one extra action potential (AP) in the follower cell. Using this approach, we found only a small fraction (<0.75%) of L2/3 cells to be significantly activated within a radius of ~200 μm from a stimulated neighboring L2/3 pyramidal cell. This fraction did not change significantly in the awake versus the lightly anesthetized state, nor when stimulating L2/3 versus underlying L4 pyramidal neurons. These numbers are in general agreement with, though lower than, the percentage of neighboring cells (2.1%) reported by Kwan et al. to be activated upon stimulating single L2/3 pyramidal neurons under anesthesia (Kwan et al., 2012). Interestingly, despite the small number of individual units found to be reliably driven, we did observe a modest but significant elevation in aggregate population responses compared to sham stimulation. This underscores the distributed impact that single cell stimulation has on neighboring microcircuit responses, revealing only a small minority of relatively strongly connected partners.One Sentence SummaryPatch-clamp stimulation in conjunction with 2-photon imaging shows that activating single layer-2/3 or layer-4 pyramidal neurons produces few (<1% of local units) reliable singlecell followers in L2/3 of mouse area V1, either under light anesthesia or in quiet wakefulness: instead, single cell stimulation was found to elevate aggregate population activity in a weak but highly distributed fashion.


2019 ◽  
Author(s):  
Danqing Yang ◽  
Robert Günter ◽  
Guanxiao Qi ◽  
Gabriele Radnikow ◽  
Dirk Feldmeyer

AbstractAcetylcholine (ACh) is known to regulate cortical activity during different behavioral states, e.g. wakefulness and attention. Here we show a differential expression of muscarinic ACh receptors (mAChRs) and nicotinic AChRs (nAChRs) in different layer 6A (L6A) pyramidal cell (PC) types of somatosensory cortex. At low concentrations, ACh induced a persistent hyperpolarization in corticocortical (CC) but a depolarization in corticothalamic (CT) L6A PCs via M4 and M1 mAChRs, respectively. At ∼1 mM ACh depolarized exclusively CT PCs via α4β2 subunit-containing nAChRs without affecting CC PCs. Miniature EPSC frequency in CC PCs was decreased by ACh but increased in CT PCs. In synaptic connections with a presynaptic CC PC, glutamate release was suppressed via M4 mAChR activation but enhanced by nAChRs via α4β2 nAChRs when the presynaptic neuron was a CT PC. Thus, in layer 6A the interaction of mAChRs and nAChRs results in an altered excitability and synaptic release, effectively strengthening corticothalamic output while weakening corticocortical synaptic signaling.


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