Synaptic and intrinsic plasticity coordinate spike output in cerebellar Purkinje cells

Mapping Intimacies ◽

10.1101/742577 ◽

2019 ◽

Author(s):

Hyun Geun Shim ◽

Sang Jeong Kim

Keyword(s):

Intracellular Signaling ◽

Synaptic Weight ◽

Spike Discharge ◽

Intrinsic Plasticity ◽

Cerebellar Purkinje Cells ◽

Dendritic Branches ◽

The Impact ◽

Activity Dependent ◽

Timing Rules

SummaryLearning has been thought to be implemented by activity-dependent modifications of synaptic weight and intrinsic excitability. Here, we highlight how long-term depression at parallel fiber to Purkinje cell synapses (PF-PC LTD) and intrinsic plasticity of PCs coordinate the postsynaptic spike discharge from C57BL/6 male mice. Intrinsic plasticity of PCs in the flocculus matched the timing rules and shared intracellular signaling for PF-PC LTD. Notably, the intrinsic plasticity was confined to the dendritic branches where the synaptic plasticity is formed. Besides, when either synaptic or intrinsic plasticity was impaired, the impact of PF inputs was less reflected by the spike output of PCs. In conclusion, synergies between synaptic and intrinsic plasticity may play a role in tuning the PC output, thereby achieving optimal ranges of output.

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The Emerging Concept of Intrinsic Plasticity: Activity-dependent Modulation of Intrinsic Excitability in Cerebellar Purkinje Cells and Motor Learning

Experimental Neurobiology ◽

10.5607/en.2018.27.3.139 ◽

2018 ◽

Vol 27 (3) ◽

pp. 139-154 ◽

Cited By ~ 15

Author(s):

Hyun Geun Shim ◽

Yong-Seok Lee ◽

Sang Jeong Kim

Keyword(s):

Motor Learning ◽

Purkinje Cells ◽

Intrinsic Excitability ◽

Intrinsic Plasticity ◽

Cerebellar Purkinje Cells ◽

Activity Dependent

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Plasticity manifolds: Conjunctive changes in multiple ion channels mediate activity-dependent plasticity in hippocampal granule cells

10.1101/747550 ◽

2019 ◽

Author(s):

Poonam Mishra ◽

Rishikesh Narayanan

Keyword(s):

Granule Cells ◽

Calcium Influx ◽

Burst Firing ◽

Action Potential Firing ◽

Whole Cell Patch Clamp ◽

Potential Firing ◽

Intrinsic Plasticity ◽

The Impact ◽

Activity Dependent ◽

Theta Burst

AbstractThe dentate gyrus (DG) was the first brain region to provide insights about synaptic and intrinsic plasticity. However, the assessment of intrinsic plasticity in DG has been surprisingly limited. We employed whole-cell patch-clamp recordings to explore the impact of behaviorally relevant theta-modulated burst firing, in the absence of synaptic stimulation, on intrinsic properties of rat DG granule cells. We found that theta burst firing induced a significant reduction in sub-threshold excitability and temporal summation, accompanied by an unexpectedly contrasting enhancement of action potential firing rate. We show that conjunctive changes in HCN, inward-rectifier potassium and persistent sodium channels mediated this form of plasticity, which was dependent on calcium influx through L-type calcium channels and inositol trisphosphate receptors. Our results unveil the expression of conjunctive plasticity in multiple channels, responding to the same activity pattern, establishing a plasticity manifold that could concomitantly mediate encoding and homeostasis in DG engram cells.

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Clustered plasticity in Long-Term Potentiation: How strong synapses persist to maintain long-term memory

Neuroforum ◽

10.1515/nf-2018-a006 ◽

2018 ◽

Vol 24 (3) ◽

pp. A127-A132

Author(s):

Marina Mikhaylova ◽

Michael R. Kreutz

Keyword(s):

Molecular Mechanisms ◽

Synaptic Weight ◽

Long Term Potentiation ◽

Long Term Memory ◽

Term Memory ◽

Term Potentiation ◽

Associated Functions ◽

Time Periods ◽

Activity Dependent

Abstract The storage of memory requires at least in part maintenance of long-term potentiation (LTP) in dendritic spine synapses. Neighboring synapses are frequently arranged into functional clusters. At present, it is still unclear how these clusters evolve, why they are stable for longer time periods and how spines interact within a cluster. In this review, we will provide an overview of current concepts of clustered plasticity and we will discuss cellular as well as molecular mechanisms that might be relevant for spine stability and associated functions in the context of LTP. We will propose that dynamics of initially formed clusters depend on compartmentalization of dendrites and that activity-dependent gene expression kicks in to preserve differences in synaptic weight. We will discuss how mechanisms of synaptic tagging, the presence of secretory organelles in dendrites and the incorporation of synaptic scaling factors that are encoded by immediate early genes interact to preserve clustered plasticity.

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Plasticity in visual cortex is disrupted in a mouse model of tauopathy and neurodegeneration

10.21203/rs.3.rs-602806/v1 ◽

2021 ◽

Author(s):

Amalia Papanikolaou ◽

Fabio Rodrigues ◽

Joanna Holeniewska ◽

Keith Phillips ◽

Aman Saleem ◽

...

Keyword(s):

Visual Cortex ◽

Neural Plasticity ◽

Cortical Plasticity ◽

Brain Plasticity ◽

Early Stages ◽

Short And Long Term ◽

Intrinsic Plasticity ◽

Visual Cortical ◽

The Impact

Abstract Neurodegeneration is a hallmark of many dementias and thought to underlie a progressive impairment of neural plasticity. Previous work in mouse models of neurodegeneration shows pronounced changes in artificially-induced plasticity in hippocampus, perirhinal and prefrontal cortex. However, it is not known how neurodegeneration disrupts intrinsic forms of brain plasticity. Here we characterised the impact of tau-driven neurodegeneration on a simple form of intrinsic plasticity in the visual system, which allowed us to track plasticity at both long (days) and short (minutes) timescales. We studied rTg4510 transgenic mice at early stages of neurodegeneration (5 months) and a more advanced stage (8 months). We recorded local field potentials in the primary visual cortex while animals were repeatedly exposed to a stimulus over 9 days. We found that both short- and long-term visual plasticity were already disrupted at early stages of neurodegeneration, and further reduced in older animals, such that it was abolished in mice expressing mutant tau. Additionally, visually evoked behaviours were disrupted in both younger and older mice expressing mutant tau. Our results show that visual cortical plasticity and visually evoked behaviours are disrupted in the rTg4510 model of tauopathy.

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Intrinsic Plasticity Complements Long-Term Potentiation in Parallel Fiber Input Gain Control in Cerebellar Purkinje Cells

Journal of Neuroscience ◽

10.1523/jneurosci.3226-10.2010 ◽

2010 ◽

Vol 30 (41) ◽

pp. 13630-13643 ◽

Cited By ~ 84

Author(s):

A. Belmeguenai ◽

E. Hosy ◽

F. Bengtsson ◽

C. M. Pedroarena ◽

C. Piochon ◽

...

Keyword(s):

Purkinje Cells ◽

Gain Control ◽

Long Term Potentiation ◽

Parallel Fiber ◽

Term Potentiation ◽

Input Gain ◽

Intrinsic Plasticity ◽

Cerebellar Purkinje Cells

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Suppressed, but Not Forgotten

Swiss Journal of Psychology ◽

10.1024/1421-0185/a000033 ◽

2011 ◽

Vol 70 (1) ◽

pp. 5-11 ◽

Cited By ~ 8

Author(s):

Beat Meier ◽

Anja König ◽

Samuel Parak ◽

Katharina Henke

Keyword(s):

Memory Trace ◽

Thought Suppression ◽

Test Phase ◽

Indirect Test ◽

Final Test ◽

Test Experiment ◽

And Control ◽

Cue Words ◽

The Impact

This study investigates the impact of thought suppression over a 1-week interval. In two experiments with 80 university students each, we used the think/no-think paradigm in which participants initially learn a list of word pairs (cue-target associations). Then they were presented with some of the cue words again and should either respond with the target word or avoid thinking about it. In the final test phase, their memory for the initially learned cue-target pairs was tested. In Experiment 1, type of memory test was manipulated (i.e., direct vs. indirect). In Experiment 2, type of no-think instructions was manipulated (i.e., suppress vs. substitute). Overall, our results showed poorer memory for no-think and control items compared to think items across all experiments and conditions. Critically, however, more no-think than control items were remembered after the 1-week interval in the direct, but not in the indirect test (Experiment 1) and with thought suppression, but not thought substitution instructions (Experiment 2). We suggest that during thought suppression a brief reactivation of the learned association may lead to reconsolidation of the memory trace and hence to better retrieval of suppressed than control items in the long term.

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