Evidence map›Paper›PMID 28981509›Full record

ArticlePLoS computational biology2017

Differential temperature sensitivity of synaptic and firing processes in a neural mass model of epileptic discharges explains heterogeneous response of experimental epilepsy to focal brain cooling.

Jaymar Soriano, Takatomi Kubo, Takao Inoue, Hiroyuki Kida, Toshitaka Yamakawa, Michiyasu Suzuki, Kazushi Ikeda

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 50% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jaymar SorianoMathematical Informatics Laboratory, Graduate School of Information Science, Nara Institute of Science and Technology, Ikoma, Japan.ORCID http://orcid.org/0000-0001-9647-5999
Takatomi KuboMathematical Informatics Laboratory, Graduate School of Information Science, Nara Institute of Science and Technology, Ikoma, Japan.ORCID http://orcid.org/0000-0003-0192-7177
Takao InoueDepartment of Neurosurgery, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Hiroyuki KidaDepartment of Physiology, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Toshitaka YamakawaOrganization for Innovation and Excellence, Kumamoto University, Kumamoto, Japan.
Michiyasu SuzukiDepartment of Neurosurgery, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Kazushi IkedaMathematical Informatics Laboratory, Graduate School of Information Science, Nara Institute of Science and Technology, Ikoma, Japan.ORCID http://orcid.org/0000-0003-3330-6121
Nara Institute of Science and Technology · JPYamaguchi University · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experiments with drug-induced epilepsy in rat brains and epileptic human brain region reveal that focal cooling can suppress epileptic discharges without affecting the brain's normal neurological function. Findings suggest a viable treatment for intractable epilepsy cases via an implantable cooling device. However, precise mechanisms by which cooling suppresses epileptic discharges are still not clearly understood. Cooling experiments in vitro presented evidence of reduction in neurotransmitter release from presynaptic terminals and loss of dendritic spines at post-synaptic terminals offering a possible synaptic mechanism. We show that termination of epileptic discharges is possible by introducing a homogeneous temperature factor in a neural mass model which attenuates the post-synaptic impulse responses of the neuronal populations. This result however may be expected since such attenuation leads to reduced post-synaptic potential and when the effect on inhibitory interneurons is less than on excitatory interneurons, frequency of firing of pyramidal cells is consequently reduced. While this is observed in cooling experiments in vitro, experiments in vivo exhibit persistent discharges during cooling but suppressed in magnitude. This leads us to conjecture that reduction in the frequency of discharges may be compensated through intrinsic excitability mechanisms. Such compensatory mechanism is modelled using a reciprocal temperature factor in the firing response function in the neural mass model. We demonstrate that the complete model can reproduce attenuation of both magnitude and frequency of epileptic discharges during cooling. The compensatory mechanism suggests that cooling lowers the average and the variance of the distribution of threshold potential of firing across the population. Bifurcation study with respect to the temperature parameters of the model reveals how heterogeneous response of epileptic discharges to cooling (termination or suppression only) is exhibited. Possibility of differential temperature effects on post-synaptic potential generation of different populations is also explored.

Indexed as

Hypothermia, InducedModels, NeurologicalAnimalsBody TemperatureBrainCold TemperatureComputational BiologyDisease Models, AnimalEpilepsyMaleRatsRats, Sprague-DawleySynaptic PotentialsSynaptic Transmission

Identifiers

PMID28981509
PMCPMC5628798
OpenAlexW2764152570

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LicenceCC BY
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.