scholarly journals Reconciling Homeostatic and Use-Dependent Plasticity in the Context of Somatosensory Deprivation

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
John J. Orczyk ◽  
Preston E. Garraghty
Keyword(s):  
Temporal Correlation ◽  
Homeostatic Plasticity ◽  
Gabaergic Inhibition ◽  
Dependent Plasticity ◽  
Synaptic Inputs ◽  
Excitatory Transmission ◽  
Somatosensory Neurons ◽  
Homeostatic Mechanisms

The concept of homeostatic plasticity postulates that neurons maintain relatively stable rates of firing despite changing inputs. Homeostatic and use-dependent plasticity mechanisms operate concurrently, although they have different requirements for induction. Depriving central somatosensory neurons of their primary activating inputs reduces activity and results in compensatory changes that favor excitation. Both a reduction of GABAergic inhibition and increase in glutamatergic excitatory transmission are observed in input-deprived cortex. Topographic reorganization of the adult somatosensory cortex is likely driven by both homeostatic and use-dependent mechanisms. Plasticity is induced by changes in the strengths of synaptic inputs, as well as changes in temporal correlation of neuronal activity. However, there is less certainty regarding thein vivocontribution of homeostatic mechanisms asin vitroexperiments rely on manipulations that create states that do not normally occur in the living nervous system. Homeostatic plasticity seems to occur, but morein vivoresearch is needed to determine mechanisms.In vitroresearch is also needed but should better conform to conditions that might occur naturallyin vivo.

scholarly journals Homeostatic plasticity and external input shape neural network dynamics

2018 ◽  
Author(s):  
Johannes Zierenberg ◽  
Jens Wilting ◽  
Viola Priesemann
Keyword(s):  
Neural Network ◽  
Brain Area ◽  
External Input ◽  
Homeostatic Plasticity ◽  
Dynamic State ◽  
Network Topologies ◽  
Neural Network Dynamics ◽  
Spiking Activity

In vitro and in vivo spiking activity clearly differ. Whereas networks in vitro develop strong bursts separated by periods of very little spiking activity, in vivo cortical networks show continuous activity. This is puzzling considering that both networks presumably share similar single-neuron dynamics and plasticity rules. We propose that the defining difference between in vitro and in vivo dynamics is the strength of external input. In vitro, networks are virtually isolated, whereas in vivo every brain area receives continuous input. We analyze a model of spiking neurons in which the input strength, mediated by spike rate homeostasis, determines the characteristics of the dynamical state. In more detail, our analytical and numerical results on various network topologies show consistently that under increasing input, homeostatic plasticity generates distinct dynamic states, from bursting, to close-to-critical, reverberating and irregular states. This implies that the dynamic state of a neural network is not fixed but can readily adapt to the input strengths. Indeed, our results match experimental spike recordings in vitro and in vivo: the in vitro bursting behavior is consistent with a state generated by very low network input (< 0.1%), whereas in vivo activity suggests that on the order of 1% recorded spikes are input-driven, resulting in reverberating dynamics. Importantly, this predicts that one can abolish the ubiquitous bursts of in vitro preparations, and instead impose dynamics comparable to in vivo activity by exposing the system to weak long-term stimulation, thereby opening new paths to establish an in vivo-like assay in vitro for basic as well as neurological studies.

scholarly journals Localized adherence by enteropathogenic Escherichia coli is an inducible phenotype associated with the expression of new outer membrane proteins.

1991 ◽  
Vol 174 (5) ◽  
pp. 1167-1177 ◽  
Author(s):  
J Vuopio-Varkila ◽  
G K Schoolnik
Keyword(s):  
Escherichia Coli ◽  
Membrane Proteins ◽  
Outer Membrane ◽  
De Novo ◽  
Outer Membrane Proteins ◽  
Temporal Correlation ◽  
Enteropathogenic Escherichia Coli ◽  
E Coli

Enteropathogenic Escherichia coli grow as discrete colonies on the mucous membranes of the small intestine. A similar pattern can be demonstrated in vitro; termed localized adherence (LA), it is characterized by the presence of circumscribed clusters of bacteria attached to the surfaces of cultured epithelial cells. The LA phenotype was studied using B171, an O111:NM enteropathogenic E. coli (EPEC) strain, and HEp-2 cell monolayers. LA could be detected 30-60 min after exposure of HEp-2 cells to B171. However, bacteria transferred from infected HEp-2 cells to fresh monolayers exhibited LA within 15 min, indicating that LA is an inducible phenotype. Induction of the LA phenotype was found to be associated with de novo protein synthesis and changes in the outer membrane proteins, including the production of a new 18.5-kD polypeptide. A partial NH2-terminal amino acid sequence of this polypeptide was obtained and showed it to be identical through residue 12 to the recently described bundle-forming pilus subunit of EPEC. Expression of the 18.5-kD polypeptide required the 57-megadalton enteropathogenic E. coli adherence plasmid previously shown to be required for the LA phenotype in vitro and full virulence in vivo. This observation, the correspondence of the 18.5-kD polypeptide to an EPEC-specific pilus protein, and the temporal correlation of its expression with the development of the LA phenotype suggest that it may contribute to the EPEC colonial mode of growth.

Homeostatic Plasticity in the CNS

2019 ◽  
Author(s):  
Peter Wenner ◽  
Pernille Bülow
Keyword(s):  
Homeostatic Plasticity ◽  
Network Activity ◽  
Signaling Cascades ◽  
Neural Function ◽  
Activity Levels ◽  
Membrane Excitability ◽  
Activity Burst ◽  
Intrinsic Plasticity

Homeostatic plasticity refers to a collection of mechanisms that function to homeostatically maintain some feature of neural function. The field began with the view that homeostatic plasticity exists predominantly for the maintenance of spike rate. However, it has become clear that multiple features undergo some form of homeostatic control, including network activity, burst rate, or synaptic strength. There are several different forms of homeostatic plasticity, which are typically triggered following perturbations in activity levels. Homeostatic intrinsic plasticity (HIP) appears to compensate for the perturbation with changes in membrane excitability (voltage-gated conductances); synaptic scaling is thought to be a multiplicative increase or decrease of synaptic strengths throughout the cell following an activity perturbation; presynaptic homeostatic plasticity is a change in probability of release following a perturbation to postsynaptic receptor activity. Each form of homeostatic plasticity can be different in terms of the mechanisms that are engaged, the feature that is homeostatically regulated, the trigger that initiates the compensation, and the signaling cascades that mediate these processes. Homeostatic plasticity is often described in development, but can extend into maturity and has been described in vitro and in vivo.

scholarly journals Disrupted in schizophrenia 1 (DISC1) L100P mutants have impaired activity-dependent plasticity in vivo and in vitro

2016 ◽  
Vol 6 (1) ◽  
pp. e712-e712 ◽  
Author(s):  
D Tropea ◽  
I Molinos ◽  
E Petit ◽  
S Bellini ◽  
I Nagakura ◽  
...  
Keyword(s):  
Dependent Plasticity ◽  
Activity Dependent

scholarly journals How to build a grid cell

2014 ◽  
Vol 369 (1635) ◽  
pp. 20120520 ◽  
Author(s):  
Christoph Schmidt-Hieber ◽  
Michael Häusser
Keyword(s):  
Entorhinal Cortex ◽  
Action Potentials ◽  
Path Integration ◽  
Grid Cell ◽  
Medial Entorhinal Cortex ◽  
Synaptic Inputs ◽  
New Findings ◽  
Cell Firing

Neurons in the medial entorhinal cortex fire action potentials at regular spatial intervals, creating a striking grid-like pattern of spike rates spanning the whole environment of a navigating animal. This remarkable spatial code may represent a neural map for path integration. Recent advances using patch-clamp recordings from entorhinal cortex neurons in vitro and in vivo have revealed how the microcircuitry in the medial entorhinal cortex may contribute to grid cell firing patterns, and how grid cells may transform synaptic inputs into spike output during firing field crossings. These new findings provide key insights into the ingredients necessary to build a grid cell.

Spike Timing-Dependent Plasticity: From Synapse to Perception

2006 ◽  
Vol 86 (3) ◽  
pp. 1033-1048 ◽  
Author(s):  
Yang Dan ◽  
Mu-Ming Poo
Keyword(s):  
Neuronal Excitability ◽  
Human Perception ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Functional Changes

Information in the nervous system may be carried by both the rate and timing of neuronal spikes. Recent findings of spike timing-dependent plasticity (STDP) have fueled the interest in the potential roles of spike timing in processing and storage of information in neural circuits. Induction of long-term potentiation (LTP) and long-term depression (LTD) in a variety of in vitro and in vivo systems has been shown to depend on the temporal order of pre- and postsynaptic spiking. Spike timing-dependent modification of neuronal excitability and dendritic integration was also observed. Such STDP at the synaptic and cellular level is likely to play important roles in activity-induced functional changes in neuronal receptive fields and human perception.

scholarly journals Increased O-GlcNAcylation rapidly decreases GABAAR currents in hippocampus yet depresses neuronal output

2019 ◽  
Author(s):  
Luke T. Stewart ◽  
Kavitha Abiraman ◽  
John C. Chatham ◽  
Lori L. McMahon
Keyword(s):  
Post Translational Modification ◽  
Variable Effect ◽  
Excitatory Transmission ◽  
Hippocampal Ca3 ◽  
Health And Disease ◽  
Acute Increase ◽  
Neuronal Output

AbstractO-GlcNAcylation, a post-translational modification involving O-linkage of β-N-acetylglucosamine to Ser/Thr residues on target proteins, is increasingly recognized as a critical regulator of brain function in health and disease. Enzymes that catalyze O-GlcNAcylation are found at both presynaptic and postsynaptic sites, and O-GlcNAcylated proteins localize to synaptosomes. An acute increase in O-GlcNAcylation induces long-term depression (LTD) of excitatory transmission at hippocampal CA3-CA1 synapses, and depresses hyperexcitable circuits in vitro and in vivo. Yet, no study has investigated how O-GlcNAcylation modulates the efficacy of inhibitory neurotransmission. Here we show an acute increase in O-GlcNAc dampens GABAergic currents onto principal cells in rodent hippocampus likely through a postsynaptic mechanism, and has a variable effect on the excitation/inhibition balance. The overall effect of increased O-GlcNAc is reduced synaptically-driven spike probability via synaptic depression and decreased intrinsic excitability. Our results position O-GlcNAcylation as a novel regulator of the overall excitation/inhibition balance and neuronal output.

scholarly journals Kv4.3 channel downregulation mediates chronic post-lesional pacemaker acceleration in surviving dopamine substantia nigra neurons

2021 ◽  
Author(s):  
Lora Kovacheva ◽  
Josef Shin ◽  
Navid Farassat ◽  
Jochen Roeper
Keyword(s):  
Substantia Nigra ◽  
Mouse Model ◽  
Homeostatic Plasticity ◽  
Cellular Mechanisms ◽  
Differential Vulnerability ◽  
Autonomous Adaptation ◽  
Partial Lesion ◽  
Firing Properties

Substantia nigra dopamine (SN DA) neurons are progressively lost in Parkinson disease (PD). While the molecular and cellular mechanisms of their differential vulnerability and degeneration have been extensively studied, we still know very little about potential functional adaptations of those SN DA neurons that at least for some time manage to survive during earlier stages of PD. We utilized a partial lesion 6-OHDA mouse model to characterize initial electrophysiological impairments and chronic adaptations of surviving identified SN DA neurons, both in vivo and in vitro. Early after lesion (3 weeks), we detected a selective loss of in vivo burst firing in surviving SN DA neurons, which was accompanied by in vitro pacemaker instability. In contrast, late after lesion (>2 months), in vivo firing properties of surviving SN DA neurons had recovered in the presence of 2-fold accelerated pacemaking in vitro. Finally, we show that this chronic cell-autonomous adaptation in surviving SN DA neurons was mediated by Kv4.3 channel downregulation. Our study demonstrates substantial homeostatic plasticity of surviving SN DA neurons after a single-hit non-progressive lesion, which might contribute to the phenotype of initially surviving SN DA neurons in PD.

scholarly journals Active dendrites enable strong but sparse inputs to determine orientation selectivity

2021 ◽  
Vol 118 (30) ◽  
pp. e2017339118
Author(s):  
Lea Goetz ◽  
Arnd Roth ◽  
Michael Häusser
Keyword(s):  
Action Potential ◽  
Pyramidal Neurons ◽  
Potential Output ◽  
Synaptic Inputs ◽  
Active Dendrites ◽  
Strongly Connected ◽  
Dendritic Spikes ◽  
Sensory Responses

The dendrites of neocortical pyramidal neurons are excitable. However, it is unknown how synaptic inputs engage nonlinear dendritic mechanisms during sensory processing in vivo, and how they in turn influence action potential output. Here, we provide a quantitative account of the relationship between synaptic inputs, nonlinear dendritic events, and action potential output. We developed a detailed pyramidal neuron model constrained by in vivo dendritic recordings. We drive this model with realistic input patterns constrained by sensory responses measured in vivo and connectivity measured in vitro. We show mechanistically that under realistic conditions, dendritic Na+ and NMDA spikes are the major determinants of neuronal output in vivo. We demonstrate that these dendritic spikes can be triggered by a surprisingly small number of strong synaptic inputs, in some cases even by single synapses. We predict that dendritic excitability allows the 1% strongest synaptic inputs of a neuron to control the tuning of its output. Active dendrites therefore allow smaller subcircuits consisting of only a few strongly connected neurons to achieve selectivity for specific sensory features.

Regionally Selective Blockade of GABAergic Inhibition by Zinc in the Thalamocortical System: Functional Significance

2000 ◽  
Vol 83 (3) ◽  
pp. 1510-1521 ◽  
Author(s):  
John W. Gibbs III ◽  
Yun-Fu Zhang ◽  
Melissa D. Shumate ◽  
Douglas A. Coulter
Keyword(s):  
Cortical Neurons ◽  
Cell Voltage ◽  
Clonic Seizure ◽  
Gabaergic Inhibition ◽  
Extracellular Medium ◽  
Selective Blockade ◽  
Zinc Release ◽  
Tightly Coupled

The thalamocortical (TC) system is a tightly coupled synaptic circuit in which GABAergic inhibition originating from the nucleus reticularis thalami (NRT) serves to synchronize oscillatory TC rhythmic behavior. Zinc is colocalized within nerve terminals throughout the TC system with dense staining for zinc observed in NRT, neocortex, and thalamus. Whole cell voltage-clamp recordings of GABA-evoked responses were conducted in neurons isolated from ventrobasal thalamus, NRT, and somatosensory cortex to investigate modulation of the GABA-mediated chloride conductance by zinc. Zinc blocked GABA responses in a regionally specific, noncompetitive manner within the TC system. The regional levels of GABA blockade efficacy by zinc were: thalamus > NRT > cortex. The relationship between clonazepam and zinc sensitivity of GABAA-mediated responses was examined to investigate possible presence or absence of specific GABAAreceptor (GABAR) subunits. These properties of GABARs have been hypothesized previously to be dependent on presence or absence of the γ2 subunit and seem to display an inverse relationship. In cross-correlation plots, thalamic and NRT neurons did not show a statistically significant relationship between clonazepam and zinc sensitivity; however, a statistically significant correlation was observed in cortical neurons. Spontaneous epileptic TC oscillations can be induced in vitro by perfusion of TC slices with an extracellular medium containing no added Mg2+. Multiple varieties of oscillations are generated, including simple TC burst complexes (sTBCs), which resemble spike-wave discharge activity. A second variant was termed a complex TC burst complex (cTBC), which resembled generalized tonic clonic seizure activity. sTBCs were exacerbated by zinc, whereas cTBCs were blocked completely by zinc. This supported the concept that zinc release may modulate TC rhythms in vivo. Zinc interacts with a variety of ionic conductances, including GABAR currents, N-methyl-d-aspartate (NMDA) receptor currents, and transient potassium (A) currents.d−2-amino-5-phosphonovaleric acid and 4-aminopyridine blocked both s- and cTBCs in TC slices. Therefore NMDA and A current-blocking effects of zinc are insufficient to explain differential zinc sensitivity of these rhythms. This supports a significant role of zinc-induced GABAR modulation in differential TC rhythm effects. Zinc is localized in high levels within the TC system and appears to be released during TC activity. Furthermore application of exogenous zinc modulates TC rhythms and differentially blocks GABARs within the TC system. These data are consistent with the hypothesis that endogenously released zinc may have important neuromodulatory actions impacting generation of TC rhythms, mediated at least in part by effects on GABARs.

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