scholarly journals Nonreciprocal homeostatic compensation in Drosophila potassium channel mutants

2017 ◽  
Vol 117 (6) ◽  
pp. 2125-2136 ◽  
Author(s):  
Eugene Z. Kim ◽  
Julie Vienne ◽  
Michael Rosbash ◽  
Leslie C. Griffith
Keyword(s):  
Motor Neurons ◽  
Transcriptional Response ◽  
External Input ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Channel Conductance ◽  
The Face ◽  
Activity Dependent ◽  
Homeostatic Response

Homeostatic control of intrinsic excitability is important for long-term regulation of neuronal activity. In conjunction with many other forms of plasticity, intrinsic homeostasis helps neurons maintain stable activity regimes in the face of external input variability and destabilizing genetic mutations. In this study, we report a mechanism by which Drosophila melanogaster larval motor neurons stabilize hyperactivity induced by the loss of the delayed rectifying K+ channel Shaker cognate B ( Shab), by upregulating the Ca2+-dependent K+ channel encoded by the slowpoke ( slo) gene. We also show that loss of SLO does not trigger a reciprocal compensatory upregulation of SHAB, implying that homeostatic signaling pathways utilize compensatory pathways unique to the channel that was mutated. SLO upregulation due to loss of SHAB involves nuclear Ca2+ signaling and dCREB, suggesting that the slo homeostatic response is transcriptionally mediated. Examination of the changes in gene expression induced by these mutations suggests that there is not a generic transcriptional response to increased excitability in motor neurons, but that homeostatic compensations are influenced by the identity of the lost conductance. NEW & NOTEWORTHY The idea that activity-dependent homeostatic plasticity is driven solely by firing has wide credence. In this report we show that homeostatic compensation after loss of an ion channel conductance is tailored to identity of the channel lost, not its properties.

scholarly journals Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160157 ◽  
Author(s):  
Melanie A. Gainey ◽  
Daniel E. Feldman
Keyword(s):  
Visual Cortex ◽  
Sensory Deprivation ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Synaptic Scaling ◽  
Cellular Mechanisms ◽  
Firing Rates ◽  
Parvalbumin Interneuron ◽  
Activity Dependent ◽  
V1 Cortex

We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

scholarly journals BDNF Regulates the Intrinsic Excitability of Cortical Neurons

1999 ◽  
Vol 6 (3) ◽  
pp. 284-291
Author(s):  
Niraj S. Desai ◽  
Lana C. Rutherford ◽  
Gina G. Turrigiano
Keyword(s):  
Cortical Neurons ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Intrinsic Properties ◽  
General Role ◽  
Outward Currents ◽  
Visual Cortical ◽  
Activity Dependent

Neocortical pyramidal neurons respond to prolonged activity blockade by modulating their balance of inward and outward currents to become more sensitive to synaptic input, possibly as a means of homeostatically regulating firing rates during periods of intense change in synapse number or strength. Here we show that this activity-dependent regulation of intrinsic excitability depends on the neurotrophin brain-derived neurotrophic factor (BDNF). In experiments on rat visual cortical cultures, we found that exogenous BDNF prevented, and a TrkB–IgG fusion protein reproduced, the change in pyramidal neuron excitability produced by activity blockade. Most of these effects were also observed in bipolar interneurons, indicating a very general role for BDNF in regulating neuronal excitability. Moreover, earlier work has demonstrated that BDNF mediates a different kind of homeostatic plasticity present in these same cultures: scaling of the quantal amplitude of AMPA-mediated synaptic inputs up or down as a function of activity. Taken together, these results suggest that BDNF may be the signal controlling a coordinated regulation of synaptic and intrinsic properties aimed at allowing cortical networks to adapt to long-lasting changes in activity.

scholarly journals Calcineurin Participation in Hebbian and Homeostatic Plasticity Associated With Extinction

2021 ◽  
Vol 15 ◽  
Author(s):  
Salma E. Reyes-García ◽  
Martha L. Escobar
Keyword(s):  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Underlying Mechanism ◽  
Homeostatic Plasticity ◽  
Extinction Process ◽  
Hebbian Plasticity ◽  
Term Potentiation ◽  
Dependent Modification ◽  
Activity Dependent

In nature, animals need to adapt to constant changes in their environment. Learning and memory are cognitive capabilities that allow this to happen. Extinction, the reduction of a certain behavior or learning previously established, refers to a very particular and interesting type of learning that has been the basis of a series of therapies to diminish non-adaptive behaviors. In recent years, the exploration of the cellular and molecular mechanisms underlying this type of learning has received increasing attention. Hebbian plasticity (the activity-dependent modification of the strength or efficacy of synaptic transmission), and homeostatic plasticity (the homeostatic regulation of plasticity) constitute processes intimately associated with memory formation and maintenance. Particularly, long-term depression (LTD) has been proposed as the underlying mechanism of extinction, while the protein phosphatase calcineurin (CaN) has been widely related to both the extinction process and LTD. In this review, we focus on the available evidence that sustains CaN modulation of LTD and its association with extinction. Beyond the classic view, we also examine the interconnection among extinction, Hebbian and homeostatic plasticity, as well as emergent evidence of the participation of kinases and long-term potentiation (LTP) on extinction learning, highlighting the importance of the balance between kinases and phosphatases in the expression of extinction. Finally, we also integrate data that shows the association between extinction and less-studied phenomena, such as synaptic silencing and engram formation that open new perspectives in the field.

scholarly journals Kv1.1 contributes to a rapid homeostatic plasticity of intrinsic excitability in CA1 pyramidal neurons in vivo

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Peter James Morgan ◽  
Romain Bourboulou ◽  
Caroline Filippi ◽  
Julie Koenig-Gambini ◽  
Jérôme Epsztein
Keyword(s):  
Pyramidal Neurons ◽  
Place Cells ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Memory Interference ◽  
Ca1 Pyramidal Neurons ◽  
Whole Cell Patch Clamp ◽  
Activity Dependent

In area CA1 of the hippocampus, the selection of place cells to represent a new environment is biased towards neurons with higher excitability. However, different environments are represented by orthogonal cell ensembles, suggesting that regulatory mechanisms exist. Activity-dependent plasticity of intrinsic excitability, as observed in vitro, is an attractive candidate. Here, using whole-cell patch-clamp recordings of CA1 pyramidal neurons in anesthetized rats, we have examined how inducing theta-bursts of action potentials affects their intrinsic excitability over time. We observed a long-lasting, homeostatic depression of intrinsic excitability which commenced within minutes, and, in contrast to in vitro observations, was not mediated by dendritic Ih. Instead, it was attenuated by the Kv1.1 channel blocker dendrotoxin K, suggesting an axonal origin. Analysis of place cells’ out-of-field firing in mice navigating in virtual reality further revealed an experience-dependent reduction consistent with decreased excitability. We propose that this mechanism could reduce memory interference.

scholarly journals GluA2-dependent AMPA receptor endocytosis and the decay of early and late long-term potentiation: possible mechanisms for forgetting of short- and long-term memories

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130141 ◽  
Author(s):  
Oliver Hardt ◽  
Karim Nader ◽  
Yu-Tian Wang
Keyword(s):  
Ampa Receptors ◽  
Long Term Potentiation ◽  
Homeostatic Plasticity ◽  
Molecular Processes ◽  
Short Term ◽  
Receptor Endocytosis ◽  
Term Potentiation ◽  
Short And Long Term ◽  
Activity Dependent

The molecular processes involved in establishing long-term potentiation (LTP) have been characterized well, but the decay of early and late LTP (E-LTP and L-LTP) is poorly understood. We review recent advances in describing the mechanisms involved in maintaining LTP and homeostatic plasticity. We discuss how these phenomena could relate to processes that might underpin the loss of synaptic potentiation over time, and how they might contribute to the forgetting of short-term and long-term memories. We propose that homeostatic downscaling mediates the loss of E-LTP, and that metaplastic parameters determine the decay rate of L-LTP, while both processes require the activity-dependent removal of postsynaptic GluA2-containing AMPA receptors.

Structural changes and the storage of long-term memory in Aplysia

1999 ◽  
Vol 77 (9) ◽  
pp. 738-747 ◽  
Author(s):  
Craig H Bailey
Keyword(s):  
Motor Neurons ◽  
Structural Changes ◽  
Long Term Memory ◽  
Synaptic Growth ◽  
Term Memory ◽  
Molecular Logic ◽  
Dissociated Cell Culture ◽  
Synaptic Circuitry ◽  
Activity Dependent

Long-term memory for sensitization of the gill-withdrawal reflex inAplysia is associated with the growth of new synaptic connections between sensory and motor neurons. The duration of this structural change parallels the behavioral retention of the memory. Such changes can be reconstituted in dissociated cell culture by repeated presentations of the modulatory neurotransmitter serotonin (5HT) and are associated with an activity-dependent downregulation of NCAM-related cell adhesion molecules thought to contribute to cell recognition and axonal outgrowth during development. Thus, aspects of the mechanisms utilized for learning-related synaptic growth initiated by experience in the adult may eventually be understood in the context of the molecular logic that shapes synaptic circuitry during the later stages of neuronal development.Key words: learning, synapse, invertebrate, habituation, sensitization.

Challenges, Concerns, and Perspectives for Poland's Energy Transition during Global COVID-19 Pandemic

2020 ◽  
Vol 1 (2) ◽  
pp. 169-173
Author(s):  
Andrzej Lorkowski ◽  
Robert Jeszke
Keyword(s):  
Internal Energy ◽  
Energy Transition ◽  
Energy Transformation ◽  
Modern Times ◽  
Current Discussion ◽  
The Face ◽  
National Governments ◽  
The Eu ◽  
At Home

The whole world is currently struggling with one of the most disastrous pandemics to hit in modern times – Covid-19. Individual national governments, the WHO and worldwide media organisations are appealing for humanity to universally stay at home, to limit contact and to stay safe in the ongoing fight against this unseen threat. Economists are concerned about the devastating effect this will have on the markets and possible outcomes. One of the countries suffering from potential destruction of this situation is Poland. In this article we will explain how difficult internal energy transformation is, considering the long-term crisis associated with the extraction and usage of coal, the European Green Deal and current discussion on increasing the EU 2030 climate ambitions. In the face of an ongoing pandemic, the situation becomes even more challenging with each passing day.

Sign in / Sign up

Export Citation Format

Share Document