scholarly journals Parallel pathways for rapid odor processing in lateral entorhinal cortex: Rate and temporal coding by layer 2 subcircuits

2021 ◽  
Author(s):  
Sebastian H. Bitzenhofer ◽  
Elena A. Westeinde ◽  
Han-Xiong Bear Zhang ◽  
Jeffry S. Isaacson
Keyword(s):  
Entorhinal Cortex ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Temporal Coding ◽  
Odor Intensity ◽  
Inhibitory Circuits ◽  
Odor Processing ◽  
Layer 2 ◽  
Rate Coding ◽  
Olfactory Input

SummaryOlfactory information is encoded in lateral entorhinal cortex (LEC) by two classes of layer 2 (L2) principal neurons: fan and pyramidal cells. However, the functional properties of L2 neurons are unclear. Here, we show in awake mice that L2 cells respond rapidly to odors during single sniffs and that LEC is essential for discrimination of odor identity and intensity. Population analyses of L2 ensembles reveals that while rate coding distinguishes odor identity, firing rates are weakly concentration-dependent and changes in spike timing represent odor intensity. L2 principal cells differ in afferent olfactory input and connectivity with local inhibitory circuits and the relative timing of pyramidal and fan cell spikes underlies odor intensity coding. Downstream, intensity is encoded purely by spike timing in hippocampal CA1. Together, these results reveal the unique processing of odor information by parallel LEC subcircuits and highlight the importance of temporal coding in higher olfactory areas.

scholarly journals Competitive Learning in a Spiking Neural Network: Towards an Intelligent Pattern Classifier

Sensors ◽  
2020 ◽  
Vol 20 (2) ◽  
pp. 500 ◽  
Author(s):  
Sergey A. Lobov ◽  
Andrey V. Chernyshov ◽  
Nadia P. Krilova ◽  
Maxim O. Shamshin ◽  
Victor B. Kazantsev
Keyword(s):  
Supervised Learning ◽  
Hebbian Learning ◽  
Back Propagation ◽  
Spike Timing ◽  
Temporal Coding ◽  
Competitive Learning ◽  
Neuron Activity ◽  
Synaptic Competition ◽  
Rate Coding ◽  
Emg Patterns

One of the modern trends in the design of human–machine interfaces (HMI) is to involve the so called spiking neuron networks (SNNs) in signal processing. The SNNs can be trained by simple and efficient biologically inspired algorithms. In particular, we have shown that sensory neurons in the input layer of SNNs can simultaneously encode the input signal based both on the spiking frequency rate and on varying the latency in generating spikes. In the case of such mixed temporal-rate coding, the SNN should implement learning working properly for both types of coding. Based on this, we investigate how a single neuron can be trained with pure rate and temporal patterns, and then build a universal SNN that is trained using mixed coding. In particular, we study Hebbian and competitive learning in SNN in the context of temporal and rate coding problems. We show that the use of Hebbian learning through pair-based and triplet-based spike timing-dependent plasticity (STDP) rule is accomplishable for temporal coding, but not for rate coding. Synaptic competition inducing depression of poorly used synapses is required to ensure a neural selectivity in the rate coding. This kind of competition can be implemented by the so-called forgetting function that is dependent on neuron activity. We show that coherent use of the triplet-based STDP and synaptic competition with the forgetting function is sufficient for the rate coding. Next, we propose a SNN capable of classifying electromyographical (EMG) patterns using an unsupervised learning procedure. The neuron competition achieved via lateral inhibition ensures the “winner takes all” principle among classifier neurons. The SNN also provides gradual output response dependent on muscular contraction strength. Furthermore, we modify the SNN to implement a supervised learning method based on stimulation of the target classifier neuron synchronously with the network input. In a problem of discrimination of three EMG patterns, the SNN with supervised learning shows median accuracy 99.5% that is close to the result demonstrated by multi-layer perceptron learned by back propagation of an error algorithm.

Duality of Rate Coding and Temporal Coding in Multilayered Feedforward Networks

2003 ◽  
Vol 15 (1) ◽  
pp. 103-125 ◽  
Author(s):  
Naoki Masuda ◽  
Kazuyuki Aihara
Keyword(s):  
Alternative Hypothesis ◽  
Spike Timing ◽  
Temporal Coding ◽  
Model Parameters ◽  
Synchronous Firing ◽  
Feedback Strength ◽  
Common Framework ◽  
Rate Coding ◽  
Single Neural Network ◽  
Population Rate

A functional role for precise spike timing has been proposed as an alternative hypothesis to rate coding. We show in this article that both the synchronous firing code and the population rate code can be used dually in a common framework of a single neural network model. Furthermore, these two coding mechanisms are bridged continuously by several modulatable model parameters, including shared connectivity, feedback strength, membrane leak rate, and neuron heterogeneity. The rates of change of these parameters are closely related to the response time and the timescale of learning.

scholarly journals Asymmetry of the temporal code for space by hippocampal place cells

2016 ◽  
Author(s):  
Bryan C. Souza ◽  
Adriano B. L. Tort
Keyword(s):  
Firing Rate ◽  
Spatial Information ◽  
Place Cells ◽  
Spike Timing ◽  
Temporal Coding ◽  
Place Field ◽  
Phase Precession ◽  
Wide Debate ◽  
Rate Coding ◽  
Theta Phase

Hippocampal place cells convey spatial information through spike frequency (“rate coding”) and spike timing relative to the theta phase (“temporal coding”). Whether rate and temporal coding are due to independent or related mechanisms has been the subject of wide debate. Here we show that the spike timing of place cells couples to theta phase before major increases in firing rate, anticipating the animal’s entrance into the classical, rate-based place field. In contrast, spikes rapidly decouple from theta as the animal leaves the place field and firing rate decreases. Therefore, temporal coding has strong asymmetry around the place field center. We further show that the dynamics of temporal coding along space evolves in three stages: phase coupling, phase precession and phase decoupling. These results suggest that place cells represent more future than past locations through their spike timing and that independent mechanisms govern rate and temporal coding.

Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex

2012 ◽  
Vol 107 (1) ◽  
pp. 205-215 ◽  
Author(s):  
Aleksey V. Zaitsev ◽  
Roger Anwyl
Keyword(s):  
Prefrontal Cortex ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Layer 2 ◽  
Stdp Rule ◽  
Stimulation Of

The induction of long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic currents was investigated in proximal synapses of layer 2/3 pyramidal cells of the rat medial prefrontal cortex. The spike timing-dependent plasticity (STDP) induction protocol of negative timing, with postsynaptic leading presynaptic stimulation of action potentials (APs), induced LTD as expected from the classical STDP rule. However, the positive STDP protocol of presynaptic leading postsynaptic stimulation of APs predominantly induced a presynaptically expressed LTD rather than the expected postsynaptically expressed LTP. Thus the induction of plasticity in layer 2/3 pyramidal cells does not obey the classical STDP rule for positive timing. This unusual STDP switched to a classical timing rule if the slow Ca2+-dependent, K+-mediated afterhyperpolarization (sAHP) was inhibited by the selective blocker N-trityl-3-pyridinemethanamine (UCL2077), by the β-adrenergic receptor agonist isoproterenol, or by the cholinergic agonist carbachol. Thus we demonstrate that neuromodulators can affect synaptic plasticity by inhibition of the sAHP. These findings shed light on a fundamental question in the field of memory research regarding how environmental and behavioral stimuli influence LTP, thereby contributing to the modulation of memory.

scholarly journals Structural development and dorsoventral maturation of the medial entorhinal cortex

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Saikat Ray ◽  
Michael Brecht
Keyword(s):  
Entorhinal Cortex ◽  
Spatial Scales ◽  
Pyramidal Cells ◽  
Stellate Cells ◽  
Superficial Layer ◽  
Cholinergic Innervation ◽  
Structural Development ◽  
Medial Entorhinal Cortex ◽  
Functional Maturation ◽  
Layer 2

We investigated the structural development of superficial-layers of medial entorhinal cortex and parasubiculum in rats. The grid-layout and cholinergic-innervation of calbindin-positive pyramidal-cells in layer-2 emerged around birth while reelin-positive stellate-cells were scattered throughout development. Layer-3 and parasubiculum neurons had a transient calbindin-expression, which declined with age. Early postnatally, layer-2 pyramidal but not stellate-cells co-localized with doublecortin – a marker of immature neurons – suggesting delayed functional-maturation of pyramidal-cells. Three observations indicated a dorsal-to-ventral maturation of entorhinal cortex and parasubiculum: (i) calbindin-expression in layer-3 neurons decreased progressively from dorsal-to-ventral, (ii) doublecortin in layer-2 calbindin-positive-patches disappeared dorsally before ventrally, and (iii) wolframin-expression emerged earlier in dorsal than ventral parasubiculum. The early appearance of calbindin-pyramidal-grid-organization in layer-2 suggests that this pattern is instructed by genetic information rather than experience. Superficial-layer-microcircuits mature earlier in dorsal entorhinal cortex, where small spatial-scales are represented. Maturation of ventral-entorhinal-microcircuits – representing larger spatial-scales – follows later around the onset of exploratory behavior.

scholarly journals Differential inhibition of pyramidal cells and inhibitory interneurons along the rostrocaudal axis of anterior piriform cortex

2018 ◽  
Vol 115 (34) ◽  
pp. E8067-E8076 ◽  
Author(s):  
Adam M. Large ◽  
Nathan W. Vogler ◽  
Martha Canto-Bustos ◽  
F. Kathryn Friason ◽  
Paul Schick ◽  
...  
Keyword(s):  
Sensory Processing ◽  
Spatial Representation ◽  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Inhibitory Neurons ◽  
Gabaergic Interneurons ◽  
Inhibitory Circuits ◽  
Anterior Piriform Cortex ◽  
Odor Processing ◽  
Spatial Asymmetries

The spatial representation of stimuli in sensory neocortices provides a scaffold for elucidating circuit mechanisms underlying sensory processing. However, the anterior piriform cortex (APC) lacks topology for odor identity as well as afferent and intracortical excitation. Consequently, olfactory processing is considered homogenous along the APC rostral–caudal (RC) axis. We recorded excitatory and inhibitory neurons in APC while optogenetically activating GABAergic interneurons along the RC axis. In contrast to excitation, we find opposing, spatially asymmetric inhibition onto pyramidal cells (PCs) and interneurons. PCs are strongly inhibited by caudal stimulation sites, whereas interneurons are strongly inhibited by rostral sites. At least two mechanisms underlie spatial asymmetries. Enhanced caudal inhibition of PCs is due to increased synaptic strength, whereas rostrally biased inhibition of interneurons is mediated by increased somatostatin–interneuron density. Altogether, we show differences in rostral and caudal inhibitory circuits in APC that may underlie spatial variation in odor processing along the RC axis.

scholarly journals Sim1-expressing cells illuminate the origin and course of migration of the nucleus of the lateral olfactory tract in the mouse amygdala

2021 ◽  
Vol 226 (2) ◽  
pp. 519-562 ◽  
Author(s):  
Elena Garcia-Calero ◽  
Lara López-González ◽  
Margaret Martínez-de-la-Torre ◽  
Chen-Ming Fan ◽  
Luis Puelles
Keyword(s):  
Experimental Data ◽  
Mouse Line ◽  
Lateral Olfactory Tract ◽  
Migration Stream ◽  
Olfactory Tract ◽  
Basolateral Nucleus ◽  
Gene Functions ◽  
Layer 2 ◽  
Embryonic Origin ◽  
Olfactory Input

AbstractWe focus this report on the nucleus of the lateral olfactory tract (NLOT), a superficial amygdalar nucleus receiving olfactory input. Mixed with its Tbr1-expressing layer 2 pyramidal cell population (NLOT2), there are Sim1-expressing cells whose embryonic origin and mode of arrival remain unclear. We examined this population with Sim1-ISH and a Sim1-tauLacZ mouse line. An alar hypothalamic origin is apparent at the paraventricular area, which expresses Sim1 precociously. This progenitor area shows at E10.5 a Sim1-expressing dorsal prolongation that crosses the telencephalic stalk and follows the terminal sulcus, reaching the caudomedial end of the pallial amygdala. We conceive this Sim1-expressing hypothalamo-amygdalar corridor (HyA) as an evaginated part of the hypothalamic paraventricular area, which participates in the production of Sim1-expressing cells. From E13.5 onwards, Sim1-expressing cells migrated via the HyA penetrate the posterior pallial amygdalar radial unit and associate therein to the incipient Tbr1-expressing migration stream which swings medially past the amygdalar anterior basolateral nucleus (E15.5), crosses the pallio-subpallial boundary (E16.5), and forms the NLOT2 within the anterior amygdala by E17.5. We conclude that the Tbr1-expressing NLOT2 cells arise strictly within the posterior pallial amygdalar unit, involving a variety of required gene functions we discuss. Our results are consistent with the experimental data on NLOT2 origin reported by Remedios et al. (Nat Neurosci 10:1141–1150, 2007), but we disagree on their implication in this process of the dorsal pallium, observed to be distant from the amygdala.

scholarly journals Independent rate and temporal coding in hippocampal pyramidal cells

Nature ◽  
2003 ◽  
Vol 425 (6960) ◽  
pp. 828-832 ◽  
Author(s):  
John Huxter ◽  
Neil Burgess ◽  
John O'Keefe
Keyword(s):  
Pyramidal Cells ◽  
Temporal Coding ◽  
Hippocampal Pyramidal Cells

Hyperexcitability of entorhinal cortex and hippocampus after application of aminooxyacetic acid (AOAA) to layer III of the rat medial entorhinal cortex in vitro

1996 ◽  
Vol 76 (5) ◽  
pp. 2986-3001 ◽  
Author(s):  
H. E. Scharfman
Keyword(s):  
Nmda Receptor ◽  
Evoked Potentials ◽  
Entorhinal Cortex ◽  
Pyramidal Cells ◽  
Aminooxyacetic Acid ◽  
Field Potentials ◽  
Medial Entorhinal Cortex ◽  
Extracellular Recordings ◽  
Extracellular Potentials

1. Injection of aminooxyacetic acid (AOAA) into the entorhinal cortex in vivo produces acute seizures and cell loss in medial entorhinal cortex. To understand these effects, AOAA was applied directly to the medial entorhinal cortex in slices containing both the entorhinal cortex and hippocampus. Extracellular and intracellular recordings were made in both the entorhinal cortex and hippocampus to study responses to angular bundle stimulation and spontaneous activity. 2. AOAA was applied focally by leak from a micropipette or by pressure ejection. Evoked potentials increased gradually within 5 min of application, particularly the late, negative components. Evoked potentials continued to increase for up to 1 h, and these changes persisted for the remainder of the experiment (up to 5 h after drug application). 3. Paired pulse facilitation (100-ms interval) was also enhanced after AOAA application. Increasing stimulus frequency to 1-10 Hz increased evoked potentials further, and after several seconds of such stimulation multiple field potentials occurred. When stimulation was stopped at this point, repetitive field potentials occurred spontaneously for 1-2 min. These recordings, and simultaneous extracellular recordings in different layers, indicated that spontaneous synchronous activity occurred in entorhinal neurons. Intracellularly labeled cortical pyramidal cells depolarized and discharged during spontaneous and evoked field potentials. 4. The effects of AOAA were blocked reversibly by bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-amino-5-phosphonovalerate (D-APV; 25 microM) or focal application of D-APV to the medial entorhinal cortex. 5. Simultaneous extracellular recordings from the entorhinal cortex and hippocampus demonstrated that spontaneous synchronous activity in layer III was often followed within several milliseconds by negative field potentials in the terminal zones of the perforant path (stratum moleculare of the dentate gyrus and stratum lacunosum-moleculare of area CA1). The extracellular potentials recorded in the dentate gyrus corresponded to excitatory postsynaptic potentials and action potentials in dentate granule cells. However, extracellular potentials in area CA1 were small and rarely correlated with discharge in CA1 pyramidal cells. 6. The results demonstrate that AOAA application leads to an NMDA-receptor-dependent enhancement of evoked potentials in medial entorhinal cortical neurons, which appears to be irreversible. The potentials can be facilitated by repetitive stimulation, and lead to synchronized discharges of entorhinal neurons. The discharges invade other areas such as the hippocampus, indicating how seizure activity may spread after AOAA injection in vivo. These data suggest that AOAA may be a useful tool to study longlasting changes in NMDA receptor function that lead to epileptiform activity and neurodegeneration.

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