diff --git a/README.md b/README.md new file mode 100644 index 0000000..e0e76a7 --- /dev/null +++ b/README.md @@ -0,0 +1,38 @@ +# This is the readme for the model associated with the paper: + +G. G. Somjen, H. Kager, W. J. Wadman. (2008) Computer simulations of neuron-glia interactions mediated by ion flux. *J Comput Neurosci* DOI 10.1007/s10827-008-0083-9 + +## Abstract: +Extracellular potassium concentration, [K+]o, and intracellular calcium, [Ca2+]i, rise during neuron excitation, seizures and spreading depression. Astrocytes probably restrain the rise of K+ in a way that is only partly understood. To examine the effect of glial K+ uptake, we used a model neuron equipped with Na+, K+, Ca2+ and Cl− conductances, ion pumps and ion exchangers, surrounded by interstitial space and glia. The glial membrane was either "passive", incorporating only leak channels and an ion exchange pump, or it had rectifying K+ channels. We computed ion fluxes, concentration changes and osmotic volume changes. Increase of [K+]o stimulated the glial uptake by the glial 3Na/2K ion pump. The [K+]o flux through glial leak and rectifier channels was outward as long as the driving potential was outwardly directed, but it turned inward when rising [K+]o/[K+]i ratio reversed the driving potential. Adjustments of glial membrane parameters influenced the neuronal firing patterns, the length of paroxysmal afterdischarge and the ignition point of spreading depression. We conclude that voltage gated K+ currents can boost the effectiveness of the glial "potassium buffer" and that this buffer function is important even at moderate or low levels of excitation, but especially so in pathological states. + +--- + +The model files were supplied by the authors. + +## Usage: + +Autolaunch from ModelDB or download and expand the zip file. Then under Windows, run `mknrndll` and cd to the new folder and make the `nrnmech.dll`. Under MAC OS X, drag and drop the new folder onto the `mknrndll` icon, then drag the `mosinit.hoc` file onto `nrngui`. Under Linux, run `nrnivmodl` after cd'ing to the new folder, then type `nrngui mosinit.hoc`. + +Once the simulation is running in the PointProcessManager window select +**Show -> Parameters** +and change the amp (nA) to 0.1675. + +In the RunControl window select **Init & Run**. If you would like the simulation to finish faster click on Hide on the 6 Graph windows and then unhide them when the simulation time reaches 6000 (and stops). You can unhide them by selecting + +**Window -> Graph[X]** + +where X = 0 to 5 in the NEURON Main Menu window. + +This will produce graphs similar to fig 3 in the paper, for example: + +![graph similar to Fig 3a](./screenshot1.jpg) + +and + +![graph similar to Fig 3b](./screenshot2.jpg) + +Changelog +--------- +2023-04-20: fixed array variable dimension. + +2025-06-02: Standardized to Markdown. diff --git a/readme.html b/readme.html deleted file mode 100644 index 8a53974..0000000 --- a/readme.html +++ /dev/null @@ -1,66 +0,0 @@ -
-This is the readme for the model associated with the paper:
-
-G. G. Somjen, H. Kager, W. J. Wadman.  (2008) Computer simulations of
-neuron-glia interactions mediated by ion flux. J Comput Neurosci
-DOI 10.1007/s10827-008-0083-9
-
-Abstract:
-Extracellular potassium concentration, [K+]o, and intracellular
-calcium, [Ca2+]i, rise during neuron excitation, seizures and
-spreading depression.  Astrocytes probably restrain the rise of K+ in
-a way that is only partly understood.  To examine the effect of glial
-K+ uptake, we used a model neuron equipped with Na+, K+, Ca2+ and Cl−
-conductances, ion pumps and ion exchangers, surrounded by interstitial
-space and glia.  The glial membrane was either "passive",
-incorporating only leak channels and an ion exchange pump, or it had
-rectifying K+ channels. We computed ion fluxes, concentration changes
-and osmotic volume changes.  Increase of [K+]o stimulated the glial
-uptake by the glial 3Na/2K ion pump. The [K+]o flux through glial leak
-and rectifier channels was outward as long as the driving potential
-was outwardly directed, but it turned inward when rising [K+]o/[K+]i
-ratio reversed the driving potential.  Adjustments of glial membrane
-parameters influenced the neuronal firing patterns, the length of
-paroxysmal afterdischarge and the ignition point of spreading
-depression.  We conclude that voltage gated K+ currents can boost the
-effectiveness of the glial "potassium buffer" and that this buffer
-function is important even at moderate or low levels of excitation,
-but especially so in pathological states.
-
------------------------
-The model files were supplied by the authors.
-
-Usage:
-
-Autolaunch from ModelDB or download the and expand the zip zip
-file. Then under Windows, run mknrndll and cd to the new folder and
-make the nrnmech.dll under MAC OS X, drag and drop the new folder onto
-the mknrndll icon, then drag the mosinit.hoc file onto nrngui, under
-linux, run "nrnivmodl" after cd'ing to the new folder, then type
-"nrngui mosinit.hoc".
-
-Once the simulation in the PointProcessManager window select
-Show -> Parameters
-and change the amp (nA) to 0.1675
-
-In the RunControl window select "Init & Run".  If you would like the
-simulation to finish faster click on Hide on the 6 Graph windows and
-then unhide them when the simulation time reaches 6000 (and stops).
-You can unhide them by selecting
-
-Window -> Graph[X]
-
-where X =0 to 5 in the NEURON Main Menu window.
-
-This will produce graphs similar to fig 3 in the paper, for example:
-
-graph similar to Fig 3a
-
-and
-
-graph similar to Fig 3b
-
-Changelog
----------
-2023-04-20: fixed array variable dimension.
-