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networks*
Kerstin Lenk, Eero Risnen, and Jari AK Hyttinen, Member, IEEE
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that function in time scales longer than tens of seconds. In
biological networks, astrocytes could have plasticity or some
other kind of memory that could have long-term effects, but
these kind of functions are outside the scope of our model
and this paper.
For computational reasons, the size of the model was
limited to 250 neurons and 107 astrocytes that physically
over the electrode area of a virtual MEA. Naturally, the
number of connections of each astrocyte to neighboring
synapses was reduced compared to in vitro networks [17],
[18].
Our assumption was that GABA released by astrocytes
may be responsible for synchronous inhibition of
postsynaptic neurons [19][22]; this can be also seen in
Figure 5. Example of neuronal activity when astrocytic GABA inhibition
Figure 4. This means that astrocytes are a tonic inhibitory
is very high (yGABA = -0.3). A) spike trains of all neurons, B) summed spikes feedback system. The tonic inhibition reduces the systems
per 5 ms over all neurons, C) spike trains of the first 30 neurons for more overall activity until it is again between the boundaries set by
details, and D) number of active astrocytes. the astrocyte dynamics of our model. While in low release
networks the restriction of activity is done by reducing the
Figure 6 Figure 6. shows the medians and lower and upper activity of everything slightly, the high release shuts down
quartiles of spike rate in spikes per minute, burst rate in some neurons which results in reduction of network activity
bursts per minute, burst duration in milliseconds, and and the temporary shutdown of single neurons (Figure 4 and
average number of spikes per bursts for yGABA = [-0.01; - 5). In Alzheimers disease, this would lead to memory
0.1; -0.3]. impairment [6], [7]. Comparing Figure 5 against Figure 3 and
4, we can also see an alteration of the astrocyte dynamics. In
Figure 5, where the GABA activity is enhanced, the number
of active astrocytes remains constant over time.
In the future, we would like to compare our findings with
in vitro MEA data from human inducted pluripotent stem
cells from Alzheimers patients. Furthermore, we would like
to investigate the role of astrocytic GABA in epilepsy and see
if the model can produce epileptic signaling with altering
GABA.
V. CONCLUSION
We showed that our neural model INEXA is able to
reproduce effects by different astrocytic GABA amounts to
the neuronal network. When the amount of GABA is high
enough, the neuronal network responds with synchronous
bursts.
Figure 6. Boxplots for the spike rate, burst rate, burst duration, and
average number of spikes per bursts for yGABA = -0.01, yGABA = -0.1, and
yGABA = -0.3 respectively.
ACKNOWLEDGMENT
IV. DISCUSSION All authors thank Emre Kapucu and Inkeri Vornanen for
We simulated neural networks with three different the development and modification of the CMA algorithm.
strength of astrocytic GABA. As expected, the overall
neuronal network activity is reduced when the astrocytic
GABA effect is increased (Figure 3 to 6). This decrease can REFERENCES
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