neuropeptide-y and Hypoxia-Ischemia--Brain

To explore the effect and safety of mild hypothermia therapy combined with monosialotetrahexosylganglioside (GM1) on neural function recovery of neonatal asphyxia complicated by hypoxic ischemic encephalopathy (HIE).. The clinical data of 90 neonates with HIE were retrospectively analyzed. According to the treatment methods, the neonates were divided into a routine group, a mild hypothermia group, and a combination group, with 30 cases in each group. The differences in neural function recovery, biochemical indexes, clinical signs recovery, efficacy, and complications were observed in the three groups after treatment.. After treatment, the score of neonatal behavioral neurological assessment (NBNA) and level of superoxide dismutase (SOD) in the combination group were higher than those of the other two groups (. Mild hypothermia therapy combined with GM1 for the treatment of neonatal asphyxia complicated by HIE can promote the recovery of neural function and reduce the incidence of complications in neonates.

Topics: Asphyxia Neonatorum; Biomarkers; Combined Modality Therapy; Computational Biology; Female; G(M1) Ganglioside; Humans; Hypothermia, Induced; Hypoxia-Ischemia, Brain; Infant, Newborn; Male; Neuropeptide Y; Phosphopyruvate Hydratase; Recovery of Function; Retrospective Studies; S100 Calcium Binding Protein beta Subunit; Safety; Superoxide Dismutase

Neuronal losses are observed in the brain after neonatal hypoxia-ischemia (HI) however few studies have examined the effects of HI on specific neuronal phenotypes and their possible contribution to behavioural outcomes. In the present study we examined whether postnatal day 3 (P3) HI alters numbers of corticotropin-releasing factor (CRF) and neuropeptide-Y (NPY) neurons in the paraventricular nucleus of the hypothalamus (PVN), the bed nucleus of the stria terminalis (BNST) and the amygdala, 1 (P10) and 6 (P45) weeks after P3 HI. A significant reduction in the number of CRF-positive neurons in the PVN, central nucleus of the amygdala (CeA) and BNST ipsilateral to the carotid ligation 1 and 6 weeks after P3 HI was observed. There was also a significant reduction in the number of NPY-positive neurons in the PVN, amygdala and BNST ipsilateral to the carotid ligation 1 week after P3 HI. However after 6 weeks, only the number of PVN NPY-positive neurons decreased significantly. At 6 weeks post-insult, the number of CeA CRF-positive neurons was inversely associated with locomotor activity and exploratory behaviour in an open field. In contrast, no significant correlations between neuronal counts and early neurodevelopment tests performed on P10 were observed. Thus after P3 HI persistent losses of CRF- and NPY-positive neurons occur and the loss of CeA CRF neurons may provide a central anatomical mechanism underlying neurobehavioural deficits observed 6 weeks after P3 HI.

Topics: Amygdala; Animals; Animals, Newborn; Behavior, Animal; Cell Count; Corticotropin-Releasing Hormone; Exploratory Behavior; Gene Expression Regulation, Developmental; Hypoxia-Ischemia, Brain; Neurons; Neuropeptide Y; Rats; Rats, Sprague-Dawley; Reflex; Statistics as Topic

Hypoxic-ischemic encephalopathy (HIE) is a common cause of neonatal encephalopathy and is one of the most important causes of neonatal death and disabilities, especially those infants with moderate to severe encephalopathy. However, the pathogenesis of HIE still remains unclear. The purpose of this study was to explore the dynamic changes in plasma neuropeptide Y (NPY) and neurotensin (NT) as well as their role in regulating cerebral hemodynamics in HIE patients. The plasma levels of NPY and NT in the umbilical artery and peripheral blood on the first, third, and seventh days after birth in 40 term infants with HIE and 40 healthy controls were measured using radioimmunoassay. On the first day of life, the blood samples were collected immediately when ultrasound examinations were finished. The ultrasound transducer was placed on the temporal fontanelle to detect the hemodynamic parameters of the middle cerebral artery, including peak systolic flow velocity, end-diastolic flow velocity, time-average mean velocity, pulsatility index, and resistance index (RI) in both groups were measured by pulse Doppler ultrasound in the first day after birth. The relationship between RI and NPY or NT was analyzed by linear regression analysis. NPY levels in umbilical blood ([mean +/- standard deviation] 615.5 +/- 130.7 ng/L) and first-day peripheral blood (355.9 +/- 57.4 ng/L) in neonates with HIE were significantly higher than those in normal newborns' blood (199.1 +/- 63.2 and 214.4 +/- 58.0 ng/L, respectively; P < 0.01). NPY levels in HIE neonates then declined to control levels on the third day after birth ( P > 0.05). However, the levels of plasma NT in umbilical blood and peripheral blood were much higher in the HIE group than those in normal newborns during the first week ( P < 0.01). The results of Doppler ultrasound examinations showed that cerebral blood flow velocity significantly decreased, whereas RI increased markedly in HIE patients compared with healthy controls ( P < 0.01). Linear regression analysis revealed that the RI was positively correlated with NPY levels ( R = 0.614; P < 0.01) and negatively correlated with NT levels ( R = -0.579; P < 0.01). The results of this study showed that there was a significant increase in plasma NPY and NT levels in HIE patients and this was strongly related to the severity of HIE, and the hemodynamic parameter RI was significantly correlated with NPY and NT. Therefore, we believe that the dynamic changes in plasma NPY or

Topics: Blood Flow Velocity; Case-Control Studies; Cerebrovascular Circulation; Fetal Blood; Humans; Hypoxia-Ischemia, Brain; Infant, Newborn; Linear Models; Middle Cerebral Artery; Neuropeptide Y; Neurotensin; Radioimmunoassay; Severity of Illness Index; Transducers; Ultrasonography, Doppler, Pulsed; Vascular Resistance

Perinatal brain injury leads to chronic neurological deficits in children. Damage to the premature brain produces white matter lesions (WMLs), but the impact on cortical development is less well defined. Gamma-aminobutyric acid(GABA)ergic neurons destined for the cerebral cortex migrate through the developing white matter and form the subplate during late gestation. The authors hypothesized that GABAergic neurons are vulnerable to perinatal systemic insults in premature infants, and that damage to these neurons contributes to impaired cortical development.. An immunohistochemical analysis involving markers for oligodendrocytes, GABAergic neurons, axons, and apoptosis was performed on a consecutive series of 15 human neonatal telencephalon samples obtained postmortem from infants born at 25 to 32 weeks of gestation. The tissue samples were divided into two groups based on the presence or absence of WMLs by performing routine histological analyses. The expression of GABAergic neurons was compared between the two groups by using age-matched samples. Two-tailed t-tests were used for statistical analyses. Ten infants had WMLs and five did not. Significant losses of oligodendrocytes and axons and markedly increased apoptosis were appreciated in tissue samples from the infants with WMLs. Samples from infants with WMLs also showed significant losses of glutamic acid decarboxylase-67-positive cells and calretinin-positive cells, shorter neuropeptide Y-positive neurite lengths, and losses of cells expressing GABA(A)alpha1, GABA(B)R1, and N-acetylaspartate diethylamide NR1 receptors when these factors were compared with those in samples from infants without WMLs (all p < 0.02).. In addition to oligodendrocyte loss, axonal disruption, and excess apoptosis, a significant loss of telencephalon GABAergic neuron expression was found in neonatal brains with WMLs, compared with neonates' brains without WMLs. The loss of GABAergic subplate neurons in infants with WMLs may contribute to the pathogenesis of neurological deficits in children.

Topics: Calbindin 2; Case-Control Studies; Caspase 3; Caspases; gamma-Aminobutyric Acid; Glutamate Decarboxylase; Humans; Hypoxia-Ischemia, Brain; Infant, Newborn; Infant, Premature; Isoenzymes; Leukomalacia, Periventricular; Neuropeptide Y; Receptors, GABA; S100 Calcium Binding Protein G