Presentation on the paper Dendritic spine changes associated with hippocampal long-term synaptic plasticity by Florian Engert & Tobias Bonhoeffer.

Slides:



Advertisements
Similar presentations
Journal Club April 25 th, Paper Layout Overview Quantal transmission of CA1 synapses Properties of basal transmission: – The GluR1 sub-unit in distance-dependent.
Advertisements

Announcements Mid term room assignments posted to webpage A – HoS361 (Pavilion) Hoang – LischkaS309 Lishingham - NguiS143 Nguyen – SeguinS128 Sek – Zia.
-Neuron in Memory Formation including axons, dentrites, synapse and neurotransmitters -Role of the Temporal Lobe (including hippocampus and the amygdala)
Optical controlling reveals time- dependent roles for adult-born dentate granule cells Yan Gu, Maithe Arruda-Carvalho, Jia Wang, Stephen R Janoschka, Sheena.
Figure 8.1 Forms of short-term synaptic plasticity.
The role of spike blocking as spike-timing-dependent plasticity mechanism Eleftheria Kyriaki Pissadaki Computational Biology Laboratory Institute of Molecular.
Background Long Term Potentiation. EGTA. NMDA Receptors.
Neural Mechanisms of Memory Storage Molecular, synaptic, and cellular events store information in the nervous system. New learning and memory formation.
The Role of Calcium Entry Via Synaptically Activated NMDA Receptors in the Induction of Long-Term Potentiation
By Eamon Quick. The Rundown Long-Term Potentiation (LTP): activity-dependent increase in synaptic activity –Dependent upon NMDA receptor activation Favors.
Adult Cortical Plasticity 1.Maps in somatic sensory and motor cortex 2.Reorganization of cortical maps following sensory deprivation 3.Synaptic basis of.
Before we start: What is the question? Why is it interesting?
Synapses are everywhere neurons synapses Synapse change continuously –From msec –To hours (memory) Lack HH type model for the synapse.
Long term potentiation (LTP) of an excitatory synaptic inputs is input specific.
J. Kauer, R. Malenka, and R. Nicoll
The three main phases of neural development 1. Genesis of neurons (and migration). 2. Outgrowth of axons and dendrites, and synaptogenesis. 3. Refinement.
The authors of this paper propose two main points. These are: 1)The existence of silent synapses in hippocampal area CA1 2)The effective desilencing of.
Presynaptic Mechanisms
Bi/CNS 150 Lecture 20 Friday November 15, 2014 Learning & Memory 1. Synaptic plasticity Bruce Cohen Kandel,Chap. 12: pp , Chap
Neuron schematic  G t = RT ln (c 2 /c 1 ) + zF  E axon myelin sheath dendrites nerve endings nt release nt receptors Cell body synapse.
Critical periods A time period when environmental factors have especially strong influence in a particular behavior. –Language fluency –Birds- Are you.
Synaptic plasticity Basic Neuroscience NBL 120. classical conditioning CS (neutral) - no response US - UR After pairing: CS - CR.
Learning and Memory: Basic Mechanisms
Neural Plasticity Lecture 7. Neural Plasticity n Nervous System is malleable l learning occurs n Structural changes l increased dendritic branching l.
Vertebrate Models of Learning
Learning and Stability. Learning and Memory Ramón y Cajal, 19 th century.
 spatial learning  cells that code for space  synaptic plasticity in the hippocampus  experiments that are knockouts  summary PART 4: BEHAVIORAL PLASTICITY.
Chapter 47 Learning and Memory: Basic Mechanisms Copyright © 2014 Elsevier Inc. All rights reserved.
Chapter 18. Synaptic Plasticity Copyright © 2014 Elsevier Inc. All rights reserved.
Molecular mechanisms of memory. How does the brain achieve Hebbian plasticity? How is the co-activity of presynaptic and postsynaptic cells registered.
Neural Plasticity: Long-term Potentiation Lesson 15.
synaptic plasticity is the ability of the connection, or synapse, between two neurons to change in strength in response to either use or disuse of transmission.
Synaptic Plasticity The term synaptic plasticity refers to the variability of the strength of a signal transmitted through a synapse. Facilitation:
WHS AP Psychology Unit 2: Memory (Cognition) Essential Task 2-3: Describe the physiological systems of memory with specific attention to long-term potentiation.
Mechanisms for memory: Introduction to LTP Bailey Lorv Psych 3FA3 November 15, 2010.
Lecture 24 Learning and Memory II. Memories Long term memory stored in cortex Information is processed for memory storage in other brain regions (i.e.
The effects of metabotropic glutamate receptors in NMDA receptor dependent long-term potentiation in hippocampus Zhou Su-ya.
1960s, 1970s, converging evidence from cognitive neuropsychology, psychology, neurobiology support the view of Multiple memory systems, efforts to experimentally.
Synaptic plasticity DENT/OBHS 131 Neuroscience 2009.
LONG-TERM POTENTIATION (LTP) Introduction LTP as a candidate mechanism for the activity-dependent change in the strength of synaptic connections LTP is.
(In)stability of spines. Outline Introduction Spine size and synaptic efficacy synaptic plasticity is associated with changes in number and size of spines.
ACTION POTENTIALS Chapter 11 Part 2 HONORS ANATOMY & PHYSIOLOGY.
Trends in Biomedical Science Making Memory. The following slides are mostly derived from The Brain from Top to Bottom, an Interactive Website about the.
Copyright © 2004 Allyn and Bacon 1 Chapter 13 Learning and Memory: Basic Mechanisms This multimedia product and its contents are protected under copyright.
Synaptic plasticity. Definition Alteration of synapse response to input.
Brittany Coughlin UT Graduate School of Biomedical Sciences October 8, 2015.
Neural Mechanisms of Learning & Memory Lesson 24.
Fear conditioning… e.g., Electric shock associated with specific stimuli.
APPROACHES TO THE BIOLOGY OF MEMORY Scale of analysis: –Micro: intra, intercellular –Medio: cell assemblies and neural networks –Macro: Coordinated brain.
Synaptic Plasticity Synaptic efficacy (strength) is changing with time. Many of these changes are activity-dependent, i.e. the magnitude and direction.
Neurons: Functional Units of the Nervous System
Neural Mechanisms of Memory Storage
Ch 8. Synaptic Plasticity 8.9 ~ 8.10 Adaptive Cooperative Systems, Martin Beckerman, Summarized by Kim, S. –J. Biointelligence Laboratory, Seoul.
Long Term Potentiation
Types of Learning Associative Learning: Classical Conditioning
Section 2 Interaction between neurons
Synaptic Coupling.
Types of Learning Associative Learning: Classical Conditioning
Polarity of Long-Term Synaptic Gain Change Is Related to Postsynaptic Spike Firing at a Cerebellar Inhibitory Synapse  Carlos D Aizenman, Paul B Manis,
Nicolai T. Urban, Katrin I. Willig, Stefan W. Hell, U. Valentin Nägerl 
Christian Lüscher, Robert C Malenka, Roger A Nicoll  Neuron 
Types of Learning Associative Learning: Classical Conditioning
Types of Memory (iconic memory) (7 bits for 30seconds)
Contactin Supports Synaptic Plasticity Associated with Hippocampal Long-Term Depression but Not Potentiation  Keith K. Murai, Dinah Misner, Barbara Ranscht 
Adenosine A2A Receptors Are Essential for Long-Term Potentiation of NMDA-EPSCs at Hippocampal Mossy Fiber Synapses  Nelson Rebola, Rafael Lujan, Rodrigo.
Long-Term Depression Properties in a Simple System
Zhenglin Gu, Jerrel L. Yakel  Neuron 
The Two Sides of Hippocampal Mossy Fiber Plasticity
Volume 52, Issue 4, Pages (November 2006)
Types of Learning Associative Learning: Classical Conditioning
Presentation transcript:

Presentation on the paper Dendritic spine changes associated with hippocampal long-term synaptic plasticity by Florian Engert & Tobias Bonhoeffer

What processes can be modelled by long-term enhancement of synaptic efficacy in the hippocampus? Neuronal plasticity Circuit reorganization Maybe learning and memory

Do the changes in synaptic magnitude have any morphological reason on the subcellular level? (I.e. is there any connection between function and structure?) Let's have a closer look at some particular regions of the postsynaptic dendrite!

Techniques used Local superfusion technique to concentrate on only one active synapse Two-photon imaging to "photograph" the changing dendrite with reduced phototoxic damage

Results Long-term functional enhancement of synapses in area CA1 causes spine growth on the postsynaptic dendrite, which does not occur in other regions or after solely short-term magnitude changes

Experimental setup Pyramidal neuron in CA1 (Vrest EPSPs

Blocking solution of 10µM Cd^2+ & 0.8µM Ca^2+ stops transmitter release Only a small area of about 30µm diameter is spared --> superfusion spot

Relevant synapses are found Baseline synaptic transmission is recorded LTP (depolarization + new stimuli) 6 high-resolution 3-D image stacks of the postsynaptic neuron per hour

ExampleExample

Controls "Off-spot" regions: one case of new spines NMDA-receptor antagonist AP5 (50µM) -- > no LTP: no new spines Unsuccessful induction of LTP (e.g. only a short potentiation, <30 min): no new spines In all three conditions: randomly disappearing spines

´Blind´observer Correlation between the emergence of new spines and an increase in synaptic efficacy Slight anticorrelation between the disappearence of spines and an increase in synaptic efficacy (t-test)

Studies only of long-lasting changes What about short-term LTP & LTD? Technical difficulties Uncertainty about the spatial location of the interesting synapses --> too large region to investigate Small and contradictive structural changes --> too large sample number > Big advantages of applied techniques!

Alternative (not contoversial) view Changes in spine shape influence synaptic strength (shortening and/or widening of the neck --> reduced resistance -->increased efficacy) Answer Maybe they occur in addition to the numerical changes & below the given spatial resolution

???________Do the emerging spines contain any active synapses? AAA_______Schould be expected so in congruity with the others

???________How are the first effects of LTP to explain if the initial morphological changes detected arise no earlier than 30min after LTP induction? AAA________At first: transient changes, then: structural and permanent ones

???_____Does the disapperance of spines depend on synaptic activity or general synaptic decay (a kind of regulation of synaptic density over the lifetime)? AAA______Data support the latter alternative, but probably some functional changes depend on synaptic activity

Summary LTP in hippocampus --> new dendritic spines ???____ Also new synapses (formation within an hour after the stimulus)_____??? More experiments required Functional --> physiological & structural changes

Note added in proof Supporting evidence from another experimental set up: Strong synaptic acticity --> new dendritic processes (M. Maletic-Savatic, R.Malinow & K.Svoboda, Science 283, ; 1999)