LTD, Spike Timing and Somatosensory Barrel Cortex Plasticity

2003 ◽  
pp. 229-240
Author(s):  
Daniel E. Feldman ◽  
Cara B. Allen ◽  
Tansu Celikel
Keyword(s):  
2014 ◽  
Vol 2 (3) ◽  
pp. e00271 ◽  
Author(s):  
Abhishek Banerjee ◽  
Ana González-Rueda ◽  
Cassandra Sampaio-Baptista ◽  
Ole Paulsen ◽  
Antonio Rodríguez-Moreno

2007 ◽  
Vol 98 (4) ◽  
pp. 1871-1882 ◽  
Author(s):  
Marcelo A. Montemurro ◽  
Stefano Panzeri ◽  
Miguel Maravall ◽  
Andrea Alenda ◽  
Michael R. Bale ◽  
...  

Rats discriminate texture by whisking their vibrissae across the surfaces of objects. This process induces corresponding vibrissa vibrations, which must be accurately represented by neurons in the somatosensory pathway. In this study, we investigated the neural code for vibrissa motion in the ventroposterior medial (VPm) nucleus of the thalamus by single-unit recording. We found that neurons conveyed a great deal of information (up to 77.9 bits/s) about vibrissa dynamics. The key was precise spike timing, which typically varied by less than a millisecond from trial to trial. The neural code was sparse, the average spike being remarkably informative (5.8 bits/spike). This implies that as few as four VPm spikes, coding independent information, might reliably differentiate between 106 textures. To probe the mechanism of information transmission, we compared the role of time-varying firing rate to that of temporally correlated spike patterns in two ways: 93.9% of the information encoded by a neuron could be accounted for by a hypothetical neuron with the same time-dependent firing rate but no correlations between spikes; moreover, ≥93.4% of the information in the spike trains could be decoded even if temporal correlations were ignored. Taken together, these results suggest that the essence of the VPm code for vibrissa motion is firing rate modulation on a submillisecond timescale. The significance of such a code may be that it enables a small number of neurons, firing only few spikes, to convey distinctions between very many different textures to the barrel cortex.


2009 ◽  
Vol 19 (12) ◽  
pp. 2959-2969 ◽  
Author(s):  
Abhishek Banerjee ◽  
Rhiannon M. Meredith ◽  
Antonio Rodríguez-Moreno ◽  
Susanna B. Mierau ◽  
Yves P. Auberson ◽  
...  

2021 ◽  
Vol 118 (35) ◽  
pp. e2107026118 ◽  
Author(s):  
Ricardo Gómez ◽  
Laura E. Maglio ◽  
Alberto J. Gonzalez-Hernandez ◽  
Belinda Rivero-Pérez ◽  
David Bartolomé-Martín ◽  
...  

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.


eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Miou Zhou ◽  
Stuart Greenhill ◽  
Shan Huang ◽  
Tawnie K Silva ◽  
Yoshitake Sano ◽  
...  

Although the role of CCR5 in immunity and in HIV infection has been studied widely, its role in neuronal plasticity, learning and memory is not understood. Here, we report that decreasing the function of CCR5 increases MAPK/CREB signaling, long-term potentiation (LTP), and hippocampus-dependent memory in mice, while neuronal CCR5 overexpression caused memory deficits. Decreasing CCR5 function in mouse barrel cortex also resulted in enhanced spike timing dependent plasticity and consequently, dramatically accelerated experience-dependent plasticity. These results suggest that CCR5 is a powerful suppressor for plasticity and memory, and CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits. Consistent with this hypothesis, the HIV V3 peptide caused LTP, signaling and memory deficits that were prevented by Ccr5 knockout or knockdown. Overall, our results demonstrate that CCR5 plays an important role in neuroplasticity, learning and memory, and indicate that CCR5 has a role in the cognitive deficits caused by HIV.


2019 ◽  
Author(s):  
Hyun Jae Jang ◽  
Hyowon Chung ◽  
James M. Rowland ◽  
Blake A. Richards ◽  
Michael M. Kohl ◽  
...  

AbstractSynchronization of precise spike-times across multiple neurons carries information about sensory stimuli. Inhibitory interneurons are suggested to promote this synchronization, but it is unclear whether distinct interneuron subtypes provide different contributions. To test this, we examined single-unit recordings from barrel cortex in vivo and used optogenetics to determine the contribution of two classes of inhibitory interneurons: parvalbumin (PV)- and somatostatin (SST)-positive interneurons to spike-timing synchronization across cortical layers. We found that PV interneurons preferentially promote the synchronization of spike-times when instantaneous firing-rates are low (<12 Hz), whereas SST interneurons preferentially promote the synchronization of spike-times when instantaneous firing-rates are high (>12 Hz). Furthermore, using a computational model, we demonstrate that these effects can be explained by PV and SST interneurons having preferential contribution to feedforward and feedback inhibition, respectively. Our findings demonstrate that distinct subtypes of inhibitory interneurons have frequency-selective roles in spatio-temporal synchronization of precise spike-times.


2001 ◽  
Vol 13 (6) ◽  
pp. 1311-1349 ◽  
Author(s):  
Stefano Panzeri ◽  
Simon R. Schultz

We demonstrate that the information contained in the spike occurrence times of a population of neurons can be broken up into a series of terms, each reflecting something about potential coding mechanisms. This is possible in the coding regime in which few spikes are emitted in the relevant time window. This approach allows us to study the additional information contributed by spike timing beyond that present in the spike counts and to examine the contributions to the whole information of different statistical properties of spike trains, such as firing rates and correlation functions. It thus forms the basis for a new quantitative procedure for analyzing simultaneous multiple neuron recordings and provides theoretical constraints on neural coding strategies. We find a transition between two coding regimes, depending on the size of the relevant observation timescale. For time windows shorter than the timescale of the stimulus-induced response fluctuations, there exists a spike count coding phase, in which the purely temporal information is of third order in time. For time windows much longer than the characteristic timescale, there can be additional timing information of first order, leading to a temporal coding phase in which timing information may affect the instantaneous information rate. In this new framework, we study the relative contributions of the dynamic firing rate and correlation variables to the full temporal information, the interaction of signal and noise correlations in temporal coding, synergy between spikes and between cells, and the effect of refractoriness. We illustrate the utility of the technique by analyzing a few cells from the rat barrel cortex.


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