scholarly journals Regulation and Function of Activity-Dependent Homer in Synaptic Plasticity

2019 ◽  
Vol 5 (3) ◽  
pp. 147-161 ◽  
Author(s):  
Nicholas E. Clifton ◽  
Simon Trent ◽  
Kerrie L. Thomas ◽  
Jeremy Hall
Keyword(s):  
Synaptic Plasticity ◽  
And Function ◽  
Activity Dependent

scholarly journals Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study

2016 ◽  
Vol 2016 ◽  
pp. 1-30 ◽  
Author(s):  
Maurizio De Pittà ◽  
Nicolas Brunel
Keyword(s):  
Synaptic Plasticity ◽  
Glutamate Release ◽  
Spike Timing ◽  
Biophysical Model ◽  
Dependent Manner ◽  
Inward Currents ◽  
Functional Relevance ◽  
And Function ◽  
Activity Dependent

Glutamatergic gliotransmission, that is, the release of glutamate from perisynaptic astrocyte processes in an activity-dependent manner, has emerged as a potentially crucial signaling pathway for regulation of synaptic plasticity, yet its modes of expression and function in vivo remain unclear. Here, we focus on two experimentally well-identified gliotransmitter pathways, (i) modulations of synaptic release and (ii) postsynaptic slow inward currents mediated by glutamate released from astrocytes, and investigate their possible functional relevance on synaptic plasticity in a biophysical model of an astrocyte-regulated synapse. Our model predicts that both pathways could profoundly affect both short- and long-term plasticity. In particular, activity-dependent glutamate release from astrocytes could dramatically change spike-timing-dependent plasticity, turning potentiation into depression (and vice versa) for the same induction protocol.

scholarly journals A comparison of three different methods of eliciting rapid activity-dependent synaptic plasticity at the Drosophila NMJ

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260553
Author(s):  
Carolina Maldonado-Díaz ◽  
Mariam Vazquez ◽  
Bruno Marie
Keyword(s):  
Synaptic Plasticity ◽  
Red Light ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Electrophysiological Properties ◽  
Electrophysiological Studies ◽  
Rich Solution ◽  
And Function ◽  
Synaptic Structures ◽  
Activity Dependent

The Drosophila NMJ is a system of choice for investigating the mechanisms underlying the structural and functional modifications evoked during activity-dependent synaptic plasticity. Because fly genetics allows considerable versatility, many strategies can be employed to elicit this activity. Here, we compare three different stimulation methods for eliciting activity-dependent changes in structure and function at the Drosophila NMJ. We find that the method using patterned stimulations driven by a K+-rich solution creates robust structural modifications but reduces muscle viability, as assessed by resting potential and membrane resistance. We argue that, using this method, electrophysiological studies that consider the frequency of events, rather than their amplitude, are the only reliable studies. We contrast these results with the expression of CsChrimson channels and red-light stimulation at the NMJ, as well as with the expression of TRPA channels and temperature stimulation. With both these methods we observed reliable modifications of synaptic structures and consistent changes in electrophysiological properties. Indeed, we observed a rapid appearance of immature boutons that lack postsynaptic differentiation, and a potentiation of spontaneous neurotransmission frequency. Surprisingly, a patterned application of temperature changes alone is sufficient to provoke both structural and functional plasticity. In this context, temperature-dependent TRPA channel activation induces additional structural plasticity but no further increase in the frequency of spontaneous neurotransmission, suggesting an uncoupling of these mechanisms.

scholarly journals Neuroligin 1 regulates spines and synaptic plasticity via LIMK1/cofilin-mediated actin reorganization

2016 ◽  
Vol 212 (4) ◽  
pp. 449-463 ◽  
Author(s):  
An Liu ◽  
Zikai Zhou ◽  
Rui Dang ◽  
Yuehua Zhu ◽  
Junxia Qi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synapse Development ◽  
Lim Domain ◽  
Actin Reorganization ◽  
Synaptic Regulation ◽  
Subsequent Activation ◽  
Guanosine Triphosphatase ◽  
Underlying Mechanisms ◽  
And Function ◽  
Activity Dependent

Neuroligin (NLG) 1 is important for synapse development and function, but the underlying mechanisms remain unclear. It is known that at least some aspects of NLG1 function are independent of the presynaptic neurexin, suggesting that the C-terminal domain (CTD) of NLG1 may be sufficient for synaptic regulation. In addition, NLG1 is subjected to activity-dependent proteolytic cleavage, generating a cytosolic CTD fragment, but the significance of this process remains unknown. In this study, we show that the CTD of NLG1 is sufficient to (a) enhance spine and synapse number, (b) modulate synaptic plasticity, and (c) exert these effects via its interaction with spine-associated Rap guanosine triphosphatase–activating protein and subsequent activation of LIM-domain protein kinase 1/cofilin–mediated actin reorganization. Our results provide a novel postsynaptic mechanism by which NLG1 regulates synapse development and function.

scholarly journals Activity-dependent synaptic plasticity in the supraoptic nucleus of the rat hypothalamus

2006 ◽  
Vol 573 (3) ◽  
pp. 711-721 ◽  
Author(s):  
Aude Panatier ◽  
Stephen J. Gentles ◽  
Charles W. Bourque ◽  
Stéphane H. R. Oliet
Keyword(s):  
Synaptic Plasticity ◽  
Supraoptic Nucleus ◽  
Rat Hypothalamus ◽  
Activity Dependent

scholarly journals Hebbian activity-dependent plasticity in white matter

2022 ◽  
Author(s):  
Alberto Lazari ◽  
Piergiorgio Salvan ◽  
Michiel Cottaar ◽  
Daniel Papp ◽  
Matthew FS Rushworth ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
White Matter ◽  
Associative Learning ◽  
Fiber Bundle ◽  
Cortical Excitability ◽  
Brain Plasticity ◽  
Cortical Areas ◽  
Hebbian Plasticity ◽  
Synaptic Changes ◽  
Activity Dependent

Synaptic plasticity is required for learning and follows Hebb's Rule, the computational principle underpinning associative learning. In recent years, a complementary type of brain plasticity has been identified in myelinated axons, which make up the majority of brain's white matter. Like synaptic plasticity, myelin plasticity is required for learning, but it is unclear whether it is Hebbian or whether it follows different rules. Here, we provide evidence that white matter plasticity operates following Hebb's Rule in humans. Across two experiments, we find that co-stimulating cortical areas to induce Hebbian plasticity leads to relative increases in cortical excitability and associated increases in a myelin marker within the stimulated fiber bundle. We conclude that Hebbian plasticity extends beyond synaptic changes, and can be observed in human white matter fibers.

scholarly journals Adult medial habenula neurons require GDNF receptor GFRα1 for synaptic stability and function

PLoS Biology ◽  
2021 ◽  
Vol 19 (11) ◽  
pp. e3001350
Author(s):  
Diana Fernández-Suárez ◽  
Favio A. Krapacher ◽  
Katarzyna Pietrajtis ◽  
Annika Andersson ◽  
Lilian Kisiswa ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Proximity Ligation Assay ◽  
Glutamatergic Synapses ◽  
Proximity Ligation ◽  
Postsynaptic Currents ◽  
Adult Mice ◽  
Medial Habenula ◽  
Factor Receptor Alpha ◽  
And Function ◽  
Anxiety And Fear

The medial habenula (mHb) is an understudied small brain nucleus linking forebrain and midbrain structures controlling anxiety and fear behaviors. The mechanisms that maintain the structural and functional integrity of mHb neurons and their synapses remain unknown. Using spatiotemporally controlled Cre-mediated recombination in adult mice, we found that the glial cell–derived neurotrophic factor receptor alpha 1 (GFRα1) is required in adult mHb neurons for synaptic stability and function. mHb neurons express some of the highest levels of GFRα1 in the mouse brain, and acute ablation of GFRα1 results in loss of septohabenular and habenulointerpeduncular glutamatergic synapses, with the remaining synapses displaying reduced numbers of presynaptic vesicles. Chemo- and optogenetic studies in mice lacking GFRα1 revealed impaired circuit connectivity, reduced AMPA receptor postsynaptic currents, and abnormally low rectification index (R.I.) of AMPARs, suggesting reduced Ca2+ permeability. Further biochemical and proximity ligation assay (PLA) studies defined the presence of GluA1/GluA2 (Ca2+ impermeable) as well as GluA1/GluA4 (Ca2+ permeable) AMPAR complexes in mHb neurons, as well as clear differences in the levels and association of AMPAR subunits with mHb neurons lacking GFRα1. Finally, acute loss of GFRα1 in adult mHb neurons reduced anxiety-like behavior and potentiated context-based fear responses, phenocopying the effects of lesions to septal projections to the mHb. These results uncover an unexpected function for GFRα1 in the maintenance and function of adult glutamatergic synapses and reveal a potential new mechanism for regulating synaptic plasticity in the septohabenulointerpeduncular pathway and attuning of anxiety and fear behaviors.

scholarly journals Coupling an aVLSI Neuromorphic Vision Chip to a Neurotrophic Model of Synaptic Plasticity: The Development of Topography

2002 ◽  
Vol 14 (10) ◽  
pp. 2353-2370 ◽  
Author(s):  
Terry Elliott ◽  
Jörg Kramer
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Development ◽  
Ganglion Cells ◽  
Activity Patterns ◽  
Retinal Ganglion ◽  
Biologically Inspired ◽  
Silicon Neurons ◽  
Retina Chip ◽  
Developing System ◽  
Activity Dependent

We couple a previously studied, biologically inspired neurotrophic model of activity-dependent competitive synaptic plasticity and neuronal development to a neuromorphic retina chip. Using this system, we examine the development and refinement of a topographic mapping between an array of afferent neurons (the retinal ganglion cells) and an array of target neurons. We find that the plasticity model can indeed drive topographic refinement in the presence of afferent activity patterns generated by a real-world device. We examine the resilience of the developing system to the presence of high levels of noise by adjusting the spontaneous firing rate of the silicon neurons.

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