Astrocytic modulation on neuronal electric mode selection induced by magnetic field effect.

Astrocytes as well as electromagnetic induction have been primarily considered as main factors in regulating neuronal firing patterns in the recent decade. In this work, an improved neuron-astrocyte model in consideration of the modulation of astrocytes and the electromagnetic induction is employed to explore the extend to which both of the factors affect the firing modes of the neurons. The "alternation mode", defined as the alternative of neural normal spiking mode with the high-frequency bursting-like mode, clearly shows the functions of astrocytes on neurons. Moreover, the firing pattern of the neuron becomes more abnormal when astrocytes are hyper-excitable, the reason why the abnormal coupling of the astrocyte leads to the "alternation mode" of the neuron have been studied. In addition, the effect of electromagnetic induction manifests nonlinear characteristic towards neurons, complex firing modes of neurons are observed in the weaker field and a switching mode consists with quiescent and spiking mode appears when there is a higher stronger field. This approved model can reveal the normal or abnormal electric activities of neuron considered electromagnetic induction induced by the degree of excitability of the astrocyte. These results can provide potential understanding about the effects of astrocyte on neuronal activity when the coupling of electromagnetic field is considered.

Modulation of Astrocytes on Mode Selection of Neuron Firing Driven by Electromagnetic Induction.

Both of astrocytes and electromagnetic induction are magnificent to modulate neuron firing by introducing feedback currents to membrane potential. An improved astro-neuron model considering both of the two factors is employed to investigate their different roles in modulation. The mixing mode, defined by combination of period bursting and depolarization blockage, characterizes the effect of astrocytes. Mixing mode and period bursting alternatively appear in parameter space with respect to the amplitude of feedback current on neuron from astrocyte modulation. However, magnetic flux obviously plays a role of neuron firing inhibition. It not only repels the mixing mode but also suppresses period bursting. The mixing mode becomes period bursting mode and even resting state when astrocytes are hyperexcitable. Abnormal activities of astrocytes are capable to induce depolarization blockage to compose the mixing mode together with bursting mode. But electromagnetic induction shows its strong ability of inhibition of neuron firing, which is also illustrated in the bifurcation diagram. Indeed, the combination of the two factors and appropriate choice of parameters show the great potential to control disorder of neuron firing like epilepsy.

Dynamic Transitions in Neuronal Network Firing Sustained by Abnormal Astrocyte Feedback.

Astrocytes play a crucial role in neuronal firing activity. Their abnormal state may lead to the pathological transition of neuronal firing patterns and even induce seizures. However, there is still little evidence explaining how the astrocyte network modulates seizures caused by structural abnormalities, such as gliosis. To explore the role of gliosis of the astrocyte network in epileptic seizures, we first established a direct astrocyte feedback neuronal network model on the basis of the hippocampal CA3 neuron-astrocyte model to simulate the condition of gliosis when astrocyte processes swell and the feedback to neurons increases in an abnormal state. We analyzed the firing pattern transitions of the neuronal network when astrocyte feedback starts to change via increases in both astrocyte feedback intensity and the connection probability of astrocytes to neurons in the network. The results show that as the connection probability and astrocyte feedback intensity increase, neuronal firing transforms from a nonepileptic synchronous firing state to an asynchronous firing state, and when astrocyte feedback starts to become abnormal, seizure-like firing becomes more severe and synchronized; meanwhile, the synchronization area continues to expand and eventually transforms into long-term seizure-like synchronous firing. Therefore, our results prove that astrocyte feedback can regulate the firing of the neuronal network, and when the astrocyte network develops gliosis, there will be an increase in the induction rate of epileptic seizures.

[Risk factors for hypoglycemia in preterm infants with a gestational age of ≤32 weeks].

OBJECTIVE: To investigate the risk factors for hypoglycemia after birth in preterm infants with a gestational age of ≤32 weeks. METHODS: A retrospective analysis was performed for 86 neonates with hypoglycemia and a gestational age of ≤32 weeks who were admitted to the neonatal intensive care unit from January 2017 to June 2020 (hypoglycemia group). A total of 172 preterm infants with normal blood glucose who were hospitalized during the same period were randomly enrolled as the control group. Univariate analysis and multivariate logistic regression analysis were used to screen out the risk factors for hypoglycemia in preterm infants. RESULTS: There were 515 preterm infants during the study, among whom 86 (16.7%) had hypoglycemia. Compared with the control group, the hypoglycemia group had significantly higher percentages of small for gestational age (SGA), cesarean section, maternal hypertension, and antenatal steroid administration (P<0.05), but significantly lower birth weight and rate of intravenous glucose use before blood glucose test (P<0.05). SGA (OR=4.311, 95%CI: 1.285-14.462, P<0.05), maternal hypertension (OR=2.469, 95%CI: 1.310-4.652, P<0.05), and antenatal steroid administration (OR=6.337, 95%CI: 1.430-28.095, P<0.05) were risk factors for hypoglycemia in preterm infants, while intravenous glucose use (OR=0.318, 95%CI: 0.171-0.591, P<0.05) was a protective factor against hypoglycemia in preterm infants. CONCLUSIONS: SGA, maternal hypertension, and antenatal steroid administration may increase the risk of early hypoglycemia in preterm infants with a gestational age of ≤32 weeks, and intravenous glucose use is recommended as soon as possible after birth for preterm infants with a gestational age of ≤32 weeks to reduce the incidence rate of hypoglycemia.

[Association between maternal pre-pregnancy body mass index and adverse outcomes of late preterm infants].

OBJECTIVE: To study the association between maternal pre-pregnancy body mass index (BMI) and adverse outcomes of late preterm infants (LPI). METHODS: A total of 367 LPI who were born from January 2011 to December 2015 and admitted to the neonatal ward were enrolled. The BMI criteria for Chinese population were used to analyze the factors for maternal pre-pregnancy BMI and its association with adverse outcomes of LPI (1 minute Apgar score ≤7, delivery room resuscitation, hospitalization days after birth >7 days, and ventilation duration ≥6 hours). RESULTS: Of all LPIs, there were 64 LPI (17.4%) in the low maternal pre-pregnancy BMI group, 243 LPI (66.2%) in the normal maternal pre-pregnancy BMI group, and 60 LPI (16.4%) in the high maternal pre-pregnancy BMI group. Low pre-pregnancy BMI was the risk factor for 1 minute Apgar score ≤7 (OR=3.243, 95% CI: 1.102-9.546) and need for delivery room resuscitation (OR=3.492, 95%CI: 1.090-11.190), and high pre-pregnancy BMI was the risk factor for hospitalization days after birth >7 days (OR=1.992, 95%CI: 1.024-3.874). CONCLUSIONS: Abnormal maternal pre-pregnancy BMI has adverse effects on the outcomes of LPI. In order to reduce these adverse outcomes BMI should be controlled within the normal range in pregnant women.