scholarly journals Cortical resonance selects coherent input

2020 ◽  
Author(s):  
Christopher Murphy Lewis ◽  
Jianguang Ni ◽  
Thomas Wunderle ◽  
Patrick Jendritza ◽  
Andreea Lazar ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Feedback Inhibition ◽  
Causal Analysis ◽  
Neuronal Communication ◽  
Resonance Properties ◽  
Powerful Means ◽  
Network Transmission ◽  
Noise Input ◽  
Local Circuits

SummarySynchronization has been implicated in neuronal communication, but causal evidence remains indirect. We used optogenetics to generate depolarizing currents in pyramidal neurons of cat visual cortex, emulating excitatory synaptic inputs under precise temporal control, while measuring spike output. Cortex transformed constant excitation into strong gamma-band synchronization, revealing the well-known cortical resonance. Increasing excitation with ramps increased the strength and frequency of synchronization. Slow, symmetric excitation profiles revealed hysteresis of power and frequency. Crucially, white-noise input sequences enabled causal analysis of network transmission, establishing that cortical resonance selectively transmits coherent input components. Models composed of recurrently coupled excitatory and inhibitory units uncovered a crucial role of feedback inhibition and suggest that hysteresis can arise through spike-frequency adaptation. The presented approach provides a powerful means to investigate the resonance properties of local circuits and probe how these properties transform input and shape transmission.

scholarly journals Feedback inhibition by GABAergic interneurons that are driven by dorsal raphe-projecting pyramidal neurons of the medial prefrontal cortex suppress feeding of adolescent female mice undergoing activity-based anorexia

2021 ◽  
Author(s):  
Muzi Du ◽  
Adrienne Santiago ◽  
Cenk Akiz ◽  
Chiye Aoki
Keyword(s):  
Individual Differences ◽  
Food Intake ◽  
Pyramidal Neurons ◽  
Feedback Inhibition ◽  
Dorsal Raphe ◽  
Gabaergic Interneurons ◽  
Electron Microscopic ◽  
Significant Group ◽  
Dorsal Raphé

Abstract Anorexia Nervosa (AN) is characterized by voluntary food restriction, excessive exercise and mortality rate surpassing that of major depression. Activity-based anorexia (ABA) is an animal model that captures these characteristics of AN, thus having the potential to reveal the neurobiology underlying individual differences in AN vulnerability. Dorsal raphe (DR) is known to regulate feeding but its role in ABA remains unexplored. Through chemogenetic activation, we investigated the role of mPFC pyramidal neurons projecting to DR (mPFC→DR) in an animal’s decision to eat or exercise following ABA induction. Although the DREADD ligand C21 could activate 44% of the mPFC→DR neurons, this did not generate significant group mean difference in the amount of food intake, compared to control ABA mice without chemogenetic activation. However, further analysis of individual animals’ responses to C21 revealed a significant, positive correlation between food intake and mPFC→ DR neurons that co-express cFos, a marker for neuronal activity. cFos expression by GABAergic interneurons (GABA-IN) in mPFC was significantly greater than that for the control ABA mice, indicating recruitment of GABA-IN by mPFC→DR neurons. Electron microscopic immunohistochemistry (EM-ICC) revealed that GABAergic innervation is 60% greater for the PFC→DR neurons than the Layer 5 pyramidal neurons without projections to DR. Moreover, individual differences in this innervation correlated negatively with food intake specifically on the day of C21 administration. We propose that C21 activates two antagonistic pathways: 1) PFC→DR pyramidal neurons that promote food intake; and 2) GABA-IN in the mPFC that dampen food intake through feedback inhibition of mPFC→DR neurons.

Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis

2011 ◽  
Vol 105 (4) ◽  
pp. 1574-1580 ◽  
Author(s):  
Emilie Faivre ◽  
Victor A. Gault ◽  
Bernard Thorens ◽  
Christian Hölscher
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Recognition Task ◽  
Long Term Potentiation ◽  
Spatial Learning And Memory ◽  
Neuronal Communication ◽  
Neuronal Progenitor ◽  
Term Potentiation ◽  
Spatial Water Maze

Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone, released from intestine after a meal, producing a glucose-dependent insulin secretion. The GIP receptor (GIPR) is expressed on pyramidal neurons in the cortex and hippocampus, and GIP is synthesized in a subset of neurons in the brain. However, the role of the GIPR in neuronal signaling is not clear. In this study, we used a mouse strain with GIPR gene deletion (GIPR KO) to elucidate the role of the GIPR in neuronal communication and brain function. Compared with C57BL/6 control mice, GIPR KO mice displayed higher locomotor activity in an open-field task. Impairment of recognition and spatial learning and memory of GIPR KO mice were found in the object recognition task and a spatial water maze task, respectively. In an object location task, no impairment was found. GIPR KO mice also showed impaired synaptic plasticity in paired-pulse facilitation and a block of long-term potentiation in area CA1 of the hippocampus. Moreover, a large decrease in the number of neuronal progenitor cells was found in the dentate gyrus of transgenic mice, although the numbers of young neurons was not changed. Together the results suggest that GIP receptors play an important role in cognition, neurotransmission, and cell proliferation.

scholarly journals Dysregulation of Astrocyte–Neuronal Communication in Alzheimer’s Disease

2021 ◽  
Vol 22 (15) ◽  
pp. 7887
Author(s):  
Carmen Nanclares ◽  
Andres Mateo Baraibar ◽  
Alfonso Araque ◽  
Paulo Kofuji
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Neuronal Excitability ◽  
Active Role ◽  
Ionic Homeostasis ◽  
Neuronal Communication ◽  
Structural Support

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.

scholarly journals Loss of Calretinin in L5a impairs the formation of the barrel cortex leading to abnormal whisker-mediated behaviors

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Mingzhao Su ◽  
Junhua Liu ◽  
Baocong Yu ◽  
Kaixing Zhou ◽  
Congli Sun ◽  
...  
Keyword(s):  
Information Integration ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Sensory Information ◽  
Membrane Excitability ◽  
Novelty Preference ◽  
Layer 4 ◽  
Dendritic Complexity ◽  
Cortex System

AbstractThe rodent whisker-barrel cortex system has been established as an ideal model for studying sensory information integration. The barrel cortex consists of barrel and septa columns that receive information input from the lemniscal and paralemniscal pathways, respectively. Layer 5a is involved in both barrel and septa circuits and play a key role in information integration. However, the role of layer 5a in the development of the barrel cortex remains unclear. Previously, we found that calretinin is dynamically expressed in layer 5a. In this study, we analyzed calretinin KO mice and found that the dendritic complexity and length of layer 5a pyramidal neurons were significantly decreased after calretinin ablation. The membrane excitability and excitatory synaptic transmission of layer 5a neurons were increased. Consequently, the organization of the barrels was impaired. Moreover, layer 4 spiny stellate cells were not able to properly gather, leading to abnormal formation of barrel walls as the ratio of barrel/septum size obviously decreased. Calretinin KO mice exhibited deficits in exploratory and whisker-associated tactile behaviors as well as social novelty preference. Our study expands our knowledge of layer 5a pyramidal neurons in the formation of barrel walls and deepens the understanding of the development of the whisker-barrel cortex system.

Dopamine Increases the Gain of the Input-Output Response of Rat Prefrontal Pyramidal Neurons

2008 ◽  
Vol 99 (6) ◽  
pp. 2985-2997 ◽  
Author(s):  
Kay Thurley ◽  
Walter Senn ◽  
Hans-Rudolf Lüscher
Keyword(s):  
Working Memory ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
D1 Receptors ◽  
Input Output ◽  
Prefrontal Cortical ◽  
Noisy Input ◽  
Relationship Of

Dopaminergic modulation of prefrontal cortical activity is known to affect cognitive functions like working memory. Little consensus on the role of dopamine modulation has been achieved, however, in part because quantities directly relating to the neuronal substrate of working memory are difficult to measure. Here we show that dopamine increases the gain of the frequency-current relationship of layer 5 pyramidal neurons in vitro in response to noisy input currents. The gain increase could be attributed to a reduction of the slow afterhyperpolarization by dopamine. Dopamine also increases neuronal excitability by shifting the input-output functions to lower inputs. The modulation of these response properties is mainly mediated by D1 receptors. Integrate-and-fire neurons were fitted to the experimentally recorded input-output functions and recurrently connected in a model network. The gain increase induced by dopamine application facilitated and stabilized persistent activity in this network. The results support the hypothesis that catecholamines increase the neuronal gain and suggest that dopamine improves working memory via gain modulation.

scholarly journals Regulation of Jak2 Function by Phosphorylation of Tyr317 and Tyr637 during Cytokine Signaling

2009 ◽  
Vol 29 (12) ◽  
pp. 3367-3378 ◽  
Author(s):  
Scott A. Robertson ◽  
Rositsa I. Koleva ◽  
Lawrence S. Argetsinger ◽  
Christin Carter-Su ◽  
Jarrod A. Marto ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Kinase Activity ◽  
Feedback Inhibition ◽  
Dominant Role ◽  
Kinase Domain ◽  
Cytokine Signaling ◽  
Tyrosine Kinase Domain ◽  
Phosphorylation Sites ◽  
Cytokine Stimulation

ABSTRACT Jak2, the cognate tyrosine kinase for numerous cytokine receptors, undergoes multisite phosphorylation during cytokine stimulation. To understand the role of phosphorylation in Jak2 regulation, we used mass spectrometry to identify numerous Jak2 phosphorylation sites and characterize their significance for Jak2 function. Two sites outside of the tyrosine kinase domain, Tyr317 in the FERM domain and Tyr637 in the JH2 domain, exhibited strong regulation of Jak2 activity. Mutation of Tyr317 promotes increased Jak2 activity, and the phosphorylation of Tyr317 during cytokine signaling requires prior activation loop phosphorylation, which is consistent with a role for Tyr317 in the feedback inhibition of Jak2 kinase activity after receptor stimulation. Comparison to several previously identified regulatory phosphorylation sites on Jak2 revealed a dominant role for Tyr317 in the attenuation of Jak2 signaling. In contrast, mutation of Tyr637 decreased Jak2 signaling and activity and partially suppressed the activating JH2 V617F mutation, suggesting a role for Tyr637 phosphorylation in the release of JH2 domain-mediated suppression of Jak2 kinase activity during cytokine stimulation. The phosphorylation of Tyr317 and Tyr637 act in concert with other regulatory events to maintain appropriate control of Jak2 activity and cytokine signaling.

scholarly journals Contribution of extrasynaptic N -methyl- d -aspartate and adenosine A1 receptors in the generation of dendritic glutamate-mediated plateau potentials

2015 ◽  
Vol 370 (1672) ◽  
pp. 20140193 ◽  
Author(s):  
Katerina D. Oikonomou ◽  
Mandakini B. Singh ◽  
Matthew T. Rich ◽  
Shaina M. Short ◽  
Srdjan D. Antic
Keyword(s):  
Pyramidal Neurons ◽  
Calcium Influx ◽  
Glutamate Uptake ◽  
Plateau Potentials ◽  
Adenosine A1 Receptors ◽  
Basal Dendrites ◽  
Adenosine A1 ◽  
Dendritic Spikes ◽  
Neuronal Output

Thin basal dendrites can strongly influence neuronal output via generation of dendritic spikes. It was recently postulated that glial processes actively support dendritic spikes by either ceasing glutamate uptake or by actively releasing glutamate and adenosine triphosphate (ATP). We used calcium imaging to study the role of NR2C/D-containing N -methyl- d -aspartate (NMDA) receptors and adenosine A1 receptors in the generation of dendritic NMDA spikes and plateau potentials in basal dendrites of layer 5 pyramidal neurons in the mouse prefrontal cortex. We found that NR2C/D glutamate receptor subunits contribute to the amplitude of synaptically evoked NMDA spikes. Dendritic calcium signals associated with glutamate-evoked dendritic plateau potentials were significantly shortened upon application of the NR2C/D receptor antagonist PPDA, suggesting that NR2C/D receptors prolong the duration of calcium influx during dendritic spiking. In contrast to NR2C/D receptors, adenosine A1 receptors act to abbreviate dendritic and somatic signals via the activation of dendritic K + current. This current is characterized as a slow-activating outward-rectifying voltage- and adenosine-gated current, insensitive to 4-aminopyridine but sensitive to TEA. Our data support the hypothesis that the release of glutamate and ATP from neurons or glia contribute to initiation, maintenance and termination of local dendritic glutamate-mediated regenerative potentials.

scholarly journals Learning excitatory-inhibitory neuronal assemblies in recurrent networks

2020 ◽  
Author(s):  
Owen Mackwood ◽  
Laura B. Naumann ◽  
Henning Sprekeler
Keyword(s):  
Pyramidal Neurons ◽  
Feedback Inhibition ◽  
Recent Experimental Data ◽  
Similar Stimulus ◽  
Inhibitory Circuits ◽  
Circuit Structure ◽  
Specific Feedback ◽  
Stimulus Features ◽  
Synaptic Circuitry ◽  
Activity Dependent

AbstractIn sensory circuits with poor feature topography, stimulus-specific feedback inhibition necessitates carefully tuned synaptic circuitry. Recent experimental data from mouse primary visual cortex (V1) show that synapses between pyramidal neurons and parvalbumin-expressing (PV) inhibitory interneurons tend to be stronger for neurons that respond to similar stimulus features. The mechanism that underlies the formation of such excitatory-inhibitory (E/I) assemblies is unresolved. Here, we show that activity-dependent synaptic plasticity on input and output synapses of PV interneurons generates a circuit structure that is consistent with mouse V1. Using a computational model, we show that both forms of plasticity must act synergistically to form the observed E/I assemblies. Once established, these assemblies produce a stimulus-specific competition between pyramidal neurons. Our model suggests that activity-dependent plasticity can enable inhibitory circuits to actively shape cortical computations.

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