Scientists have revealed new mechanisms by which small glial cells play a protective role in complex thermal convulsions

On November 3rd, Professor Hu Weiwei of Zhejiang University's School of Basic Medicine/Affiliated Second College and Professor Chen Zhong of the School of Pharmacy published a research paper entitled "Microglial class of GABAergic synapses is a protective event when complex febrile resed" online at Cell Reports, which revealed for the first time the small Glial cells can synapse by replacing γ-amino butyric acid (GABA) around glutamate-energy neurons, reducing neuron excitability and playing a protective role in the occurrence of complex heat convulsions, a role that is mediated by P2Y12.
fever convulsions are a convulsive behavior caused by high fever, one-third of which is complex febrile seizures, which can cause lasting damage to the nervous system, but the pathogenesis of complex thermal convulsions is not yet clear.
small glial cells are activated during complex thermal convulsions, and their inflammatory effects are assumed to promote the occurrence of heat convulsions.
Research Group carried out a study on the synactal stripping of small glial cells in the early stages, thus proposing the idea of whether the small glial cells activated in complex heat convulsions will have a certain effect on neurons and their synapses, which in turn will affect the occurrence of complex thermal convulsions.
In the study, the authors found that after complex heat convulsions, small glial cells activated and were widely close to glutamate-energy neurons, replacing, rather than devouring, GABA synapses around neurons, while neurons with no small glial cells that were widely approached after heat convulsions increased significantly in the number of GABAs around the cells.
To further clarify the effect of small glial cells on the electrophysiological properties of neurons, the authors recorded the GABA transmission of neurons and neuron-induced motor potential through diaphragm clamps, and found that complex thermal convulsions can cause neuron GABA transmission enhancement, neuron excitability increases, and small glial cells peeling GABA can reverse this phenomenon.
also determines that GABA can act as an excitable effect after complex thermal convulsions at an early stage by recording the reversal potential of GABA's synapses.
based on this, the team inhibited the activation of small glial cells by pharmacological means, or by killing small glial cells in CD11bDTR mice, which significantly promoted the onset of complex heat convulsions.
At the same time, the study also found that small glial cells close to neurons express higher P2Y12 subjects, antagonist P2Y12 subjects or knock out P2Y12 subjects can inhibit small glial cells peeling GABA can synapse, accelerate complex heat convulsions.
the study further studied the pathogenesis of complex heat convulsions and provided an important experimental and theoretical basis for explaining the protective role of small glial cells.
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