ModelDB: Homeostatic synaptic plasticity (Rabinowitch and Segev 2006a,b)

Homeostatic synaptic plasticity (Rabinowitch and Segev 2006a,b)

Accession: 114355

(2006a): "We investigated analytically and numerically the interplay between two opposing forms of synaptic plasticity: positive-feedback, long-term potentiation/depression (LTP/LTD), and negative-feedback, homeostatic synaptic plasticity (HSP). A detailed model of a CA1 pyramidal neuron, with numerous HSP-modifiable dendritic synapses, demonstrates that HSP may have an important role in selecting which spatial patterns of LTP/LTD are to last. ... Despite the negative-feedback nature of HSP, under both local and global HSP, numerous synaptic potentiations/depressions can persist. These experimentally testable results imply that HSP could be significantly involved in shaping the spatial distribution of synaptic weights in the dendrites and not just normalizing it, as is currently believed." (2006b): "Homeostatic synaptic plasticity (HSP) is an important mechanism attributed with the slow regulation of the neuron's activity. Whenever activity is chronically enhanced, HSP weakens the weights of the synapses in the dendrites and vice versa. Because dendritic morphology and its electrical properties partition the dendritic tree into functional compartments, we set out to explore the interplay between HSP and dendritic compartmentalization. ... The spatial distribution of synaptic weights throughout the dendrites will markedly differ under the local versus global HSP mechanisms. We suggest an experimental paradigm to unravel which type of HSP mechanism operates in the dendritic tree. The answer to this question will have important implications to our understanding of the functional organization of the neuron."
References:
1. Rabinowitch I, Segev I (2006b) The interplay between homeostatic synaptic plasticity and functional dendritic compartments. J Neurophysiol 96:276-83 [PubMed]
2. Rabinowitch I, Segev I (2006a) The endurance and selectivity of spatial patterns of long-term potentiation-depression in dendrites under homeostatic synaptic plasticity. J Neurosci 26:13474-84 [PubMed]
3. Rabinowitch I, Segev I (2008) Two opposing plasticity mechanisms pulling a single synapse. Trends Neurosci [PubMed]

Citations Citation Browser

Model Information (Click on a link to find other models with that property)

Model Type:	Neuron or other electrically excitable cell; Synapse;
Brain Region(s)/Organism:
Cell Type(s):	CA1 pyramidal neuron;
Channel(s):	I Na,t; I A; I K;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment:	Neuron; MATLAB;
Model Concept(s):	Synaptic Plasticity;
Implementer(s):

Search NeuronDB for information about: CA1 pyramidal neuron; I Na,t; I A; I K;

Model files

Help downloading and running models Versions

This is the readme for the model associated with the paper

Rabinowitch I, Segev I (2006) The interplay between homeostatic
synaptic plasticity and functional dendritic compartments. J
Neurophysiol 96:276-83

These files were supplied by Dr Ithai Rabinowitch.

The basic idea is:

1. Each simulation is given a RIP number and each RIP has several
   RDPs. RIP is a list of run-independent parameters such as the type
   of active channels on the dendrites. RDP is a list of run-dependent
   parameters (e.g. the simulation time). This allows you to set up a
   general RIP configuration and then run several RDP variations on
   it. The RIP and RDP parameter panels are at the top left.

2. Even above the RIP category is the neuron structure and channel
   file which are selected just before entering the main gui.

3. There are several types of simulation programs such as EPSP (which
   measures individual EPSP amplitudes for each synapse). These are
   chosen in the panel in the bottom.

4. It is possible to pre-program the simulation to run several
   simulations in sequence (if you want to leave the computer to work
   overnight and run different simulations one after the other).

Usage:

Download and extract the archive.  Then under

unix/linux:
-----------

cd main
nrnivmodl ../mechanisms
nrngui main.hoc

In the first selection window choose Spruston2 (not 3) and in the
Migliore2 Channel layout and Segment length 20.



Then click 'Done'.

You will be able to get 6 simulation configurations (RIP0: RDP0-5)
that do the following (the simulations are quite long):

RDP 0: runs in 'frozen' mode, i.e. no plasticity. This is used to get
a profile of the average membrane potential at each dendritic site (at
the end of the simulation choose Vavg in one of the two plot windows).

RDP 1: runs with plasticity so that at the end you also get gmax
values that are different from gmax0

RDP 2-5 start with the gmax distribution of RDP1 (since I have already
run this, their gmax0 is supposed to be stored).

RDP 2: local HSP RDP 3: frozen with the gmax0 obtained from RDP2's
final gmax.

RDP 4: global HSP RDP 5: frozen with the gmax0 obtained from RDP4's
final gmax.

---

Select "artificial vivo", click "add" and "go". While it is running
you can select Interaction -> distance -> gmax and Interaction ->
distance -> vmax in the graph windows, then your simulation will look
like this:



I would suggest that you create a new RDP and just set a much shorter
simulation time (TSTOP under the RDP list). You can then run it to
make the result files (under for example
./records/files/ri05-Migliore2-seg-1-20/RIP-0/RDP-0/ ) accessible
without having to run the whole simulation. If you want interesting
things to happen in the short time, you can change the time constant
of the plasticity mechanism. Create a new RIP configuration (or delete
the existing one) and change the time scale parameter in the synapse
parameter dialog box (just under the RIP list).

ModelDB Home SenseLab Home Help
Questions, comments, problems? Email the ModelDB Administrator
How to cite ModelDB
This site is Copyright 2012 Shepherd Lab, Yale University