Objective To explore the effects and mechanism of autonomic nervous control on the proliferation of human hepatocytes. And to examine the cellular localization of some related receptors expression in human hepatocytes. MethodsNorepinephrine (NE), and its agonist, antagonist, acetylcholine (Ach), and its antagonist have been added to human hepatocyte line L02 and hepatoma cell line Bel7402. Modified MTT assay was employed to test the effects of them on the proliferation of the two cell lines at 4 h, 24 h, 48 h and 72 h. Immuocytochemical staining was used to examine the cellular localization of alpha1Badrenoceptor (α1BAR), β2AR and epidermal growth factor receptor (EGFR) expression in human hepatocyte line L02. ResultsNE potentiated the proliferation of human hepatocyte and hepatoma cell, which was enhanced significantly with dose increased. The proliferative rate of 4 h were higher than that of the other time points (P＜0.05). There were no significant differences between the group of NE combined with propanolol and the group of NE alone. Metaproterenol had no significant effect. Ach significantly inhibited the proliferation of human hepatocyte. Its effect was enhanced with dose increased. Atropine significantly attenuated the inhibitory effect of Ach at 24 h and 48 h (P＜0.05). Scoline alone inhibited hepatocyte proliferation at 24 h, 48 h and 72 h (P＜0.05, P＜0.01). In immunocytochemical staining, there were positive responses to α1BAR, β2AR and EGFR in all cultures. It was observed that the responses to α1BAR, β2AR and EGFR were mainly both cytoplasmic and cell membrane localized. Conclusion NE, the sympathetic neurotransmitter, acts via α1BAR potentiate the proliferation of human hepatocyte and hepatoma cell in the presence of serum. Ach, the vagus neurotransmitter acting via mAchR and nAchR inhibits hepatocyte proliferation.
Purpose To identify the expression of alternatively spliced mRNA isoforms of the NMDA-R1 in the visual cortex of strabismic cats. Methods Two pai rs of normal and strabismic cats were used．The amblyopic cats had been made monocularly esotropic (by tenotomy) at the age of weeks，resulting in behavioral am blyopia．Animals were sacrificed about 6 months by intraperitoneal administration of Nembutal．Cryostat sections of fresh，frozen central visual cortex of the ats were cut to 20 micron thickness．A series of digoxygenin-labelled oligonucle otide probes basing on the human gene sequence were used for ISH．Control probes included sense oligonucleotides and short segment probes which were adjacent to ，but did not，span the splice junctions．A computer-assisted systematic morphometric ounting procedure was used to enumerate hybridising cells． Results The number of positive cells expressing NMDA-R1 mRNA in t he strabismic amblyopic cats was decreased，notably in layer IV of visual cortex (P＜0．0001)．The pattern of isoform expression varied between normal and strabismic amblyopic cats with decreased numbers of 1-a，1- b and 1-1 isoforms and apparently increased expression of 1-3 P ＜0．0001)，whereas no significant difference was found for the 1-2 and 1-4 isoforms (P＞0．05)． Conclusion Transcriptional inhibition of NMDA-R1 mRNA and of specifie isoforms may underlie the change in receptor expression．Alternatively，preferentialloss of neurones bearing particular NMDA-R1 isoforms and compensation with a proportional increase in cells expressing other isoforms may occurr during the critical period of visual plasticity． (Chin J Ocul Fundus Dis，2000，16：71-138)
Objective To review the biologic characteristics and biologic effect of cholecystokinine (CCK) on the central nervous system. Methods The literatures of recent years on research advancement of cholecystokinine as neurotransmitters/peptides in signal transduction, neuron protection and pain management in the central nervous system are reviewed. Results CCK possesses the ability to suppress the convulsant effects of convulsants. CCK8 is able to reduce the neural damage caused and delay the neural aging. CCK antagonists play an important role in human pain transduction. Conclusion CCK has been proven to be one of the richest neurotransmitters/neuropeptides as well as an important signal factor in the brain, and its important biologic effect is being confirmed.
Objectives To investigate the changes of serum monoamine neurotransmitters and myocardial enzymes in patients with refractory epilepsy (RE), and the possible effects on the cardiovascular system, which would contribute to provide help and guidance to the early warming and prevention to the sudden unexpected death in epilepsy (SUDEP). Methods We collected sixty patients with RE who admitted to Neurological department of First Hospital of Jilin University from December 2015 to December 2016. According to the exclusion criteria, we selected thirty-two patients into the study. The study included 21 males and 11 females patients. Epinephrine (EPI), norepinephrine (NE), dopamine (DA), 5-hydroxytryptamine (5-HT), creatine kinase isoenzyme (CKMB), lactate dehydrogenase (LDH) and hydroxybutyrate dehydrogenase (HBDH) were measured in peri-ictal period and the interictal period in the patients. All the data were analyzed by SPSS17.0 statistical software. Results ① Thirty two patients were eligiblefor this study and the maleto female ratio is 21:11; The age ranged from 15 to 85 years old, with the average age of 50.9±17.6 years old. Twelve (37.5%) were older than 60 years old and 20 (62.5%) were under 60 years old. The epilepsy history ranged from 1 year to 14 years, with an average of 3.75±3.12 years; ② Comparing the levels of monoamine neurotransmitters in peri-ictal period and the interictal period in the patients with RE, we found that the level of EPI and LDH was significantly lower than that in interictal period, while the levels of NE and DA were significantly increased; ③ The results showed that EPI, NE and DA levels in patients under 60 were higher than over 60; ④ Patients were divided into four groups according to the etiology of the disease: idiopathic epilepsy group (10 cases, 31.25%), post-encephalitic epilepsy group (7 cases, 21.88%), post-stroke epilepsy group (9 cases, 28.12%) and epilepsy after brain injury group (6 cases, 18.75%). The results showed that the levels of EPI, NE and DA in the post-strokeepilepsy group were significantly lower than those in the other three groups. The level of CKMB in the idiopathic epilepsy group was higher than that in post-stroke epilepsy and epilepsy induced by brain injury patients. Conclusions RE patients have a higher level of serum NE and DA interictal period, suggesting that seizures may increase sympathetic nervous excitability. The patients under 60 years-old with RE release more catecholamines than young patients, suggesting that the latterwith intractable epilepsy may have higher sympathetic nerve excitability. And it may be associated with the higher incidence of SUDEP in young patients. Post-stroke epilepsyrelease less catecholamine than others, suggesting that the sympathetic nervous excitability is relatively low, and it may have relatively little damage to heart.
External trigeminal nerve stimulation (eTNS) is a new non-invasive physical and electrical stimulation therapy based on the anatomical characteristics of the trigeminal nerve. It can control seizures by regulating epilepsia-related brainstem nuclei and part of forebrain structures, regulating neuroinflammation, improving synaptic plasticity and promoting neurogenesis, which has broad clinical application prospects. It has been approved by the European Union as an adjuvant treatment for drug-resistant epilepsy patients over the age of 9 years old. Therefore, this article mainly reviews the central nervous system regulatory mechanism of eTNS in improving epilepsy, eTNS stimulation mode and parameters.