Inhibiting effect of vagal nerve stimulation to seizures in epileptic process of rats

Objective Our previous work suggested that sensitivity of hippocampal neurons is changed in process of epileptic activities,and closely parallel to the dynamic characteristic of epileptic activity of the neurons.This study investigated the sensitivity of epileptic brain to vagal nerve stimulation（VNS）in epileptic process.Methods Epileptic model was evoked by penicillin.Left vagal nerves were stimulated to inhibit the seizures induced by penicillin.The electrocorticography（ECoG）and electromyography（EMG）were recorded to analyze inhibiting effect of VNS in epileptic process.Results It was found that VNS could inhibit the seizures caused by penicillin,and the inhibiting effect of VNS to seizures increased as the vagal nerve stimulating time prolonged.It was also found that the inhibiting effect of VNS to seizures decreased in epileptic process.Conclusion The results suggested that the sensitivity of epileptic brain to VNS was different in epileptic process.The inhibiting effect of VNS to seizure decreased as the development of seizures.

Ghrelin and gastric acid secretion

Ghrelin, a novel growth hormone-releasing peptide, was originally isolated from rat and human stomach. Ghrelin has been known to increase the secretion of growth hormone (GH), food intake, and body weight gain when administered peripherally or centrally. Ghrelin is also known to stimulate the gastric motility and the secretion of gastric acid. In the previous studies, the action of ghrelin on acid secretion was shown to be as strong as that of histamine and gastrin in in-vivo experiment. In the studies, the mechanism for the action of ghrelin was also investigated. It was shown that vagotomy completely inhibited the action of ghrelin on the secretion of gastric acid suggesting that vagal nerve is involved in the mechanism for the action of ghrelin on acid secretion. As famotidine did not inhibit ghrelin-in-duced acid secretion in the study by Masuda et al, they concluded that histamine was not involved in the action of ghrelin on acid secretion. However, we have shown that famotidine completely inhibited ghrelin-induced acid secretion and histidine decarboxylase (HDC) mRNA was increased in gastric mucosa by ghrelin injection which is inhibited by vagotomy Our results indicate that histamine is involved in the action of ghrelin on acid secretion. Furthermore synergistic action of gastrin and ghrelin on gastric acid secretion was shown. Although gastrin has important roles in postprandial secretion of gastric acid, ghrelin may be related to acid secretion during fasting period or at night. However, further studies are needed to elucidate the physiological role of ghrelin in acid secretion.

Updates on gastric electrical stimulation to treat obesity: Systematic review and future perspectives

AIM: To evaluate the current state-of-the-art of gastric electrical stimulation to treat obesity. METHODS: Systematic reviews of all studies have been conducted to evaluate the effect of different types of gastric electrical stimulation(GES) on obesity.RESULTS: Thirty-one studies consisting of a total of 33 different trials were included in the systematic review for data analysis. Weight loss was achieved in most studies, especially during the first 12 mo, but only very few studies had a follow-up period longer than 1 year. Among those that had a longer follow-up period, many were from the Transcend(Implantable Gastric Stimulation) device group and maintained significant weight loss. Other significant results included changes in appetite/satiety, gastric emptying rate, blood pressure and neurohormone levels or biochemical markers such as ghrelin or HbA1 c respectively. CONCLUSION: GES holds great promises to be an effective obesity treatment. However, stronger evidence is required through more studies with a standardized way of carrying out trials and reporting outcomes, to determine the long-term effect of GES on obesity.

Blood Pressure Change in Intrafascicular Vagal Activities

Baroreflex plays a significant role in modulating blood pressure for the human body.It is known that activation of the vagal nerve related to baroreflex can lead to reductions of blood pressure.However,how the vagal activities quantitatively relate with blood pressure can hardly be achieved.Here fine carbon nanotube yarn(CNTy)electrodes were adopted for recording intrafascicular vagal activities,synchronized with measurement of arterial blood pressure in a rat.Together with a novel algorithm,the results preliminarily quantified that there were six clusters of neural spikes within recorded vagal activities,and the number of individual vagal spikes correspondingly varied with blood pressure.Especially for Cluster 2,the neural activations decreased with arterial blood pressure increasing.This study can shed lights on the quantified neural mechanism underlying the control of vagal activities on blood pressure,and guide the vagal-nerve neuromodulation for treating hypertension.

Cholinergic anti-inflammatory pathway： a possible approach to protect against myocardial ischemia reperfusion injury

Objective A general review was made of studies involving： （1） the concept and mechanism of the cholinergic anti-inflammatory pathway （CAP）, （2） the important role of inflammatory response in myocardial ischemia reperfusion （I/R） injury and （3） the evidence and mechanisms by which CAP may provide protection against myocardial I/R injury. Data sources The data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1987 to 2009. The search terms were ＂vagal nerve stimulation＂, ＂myocardial ischemia reperfusion injury＂, ＂nicotine acetylcholine receptor＂ and ＂inflammation＂. Study selection （1） Clinical and experimental evidence that the inflammatory response induced by reperfusion enhances myocardial I/R injury. （2） Clinical and laboratory evidence that the CAP inhibits the inflammation and provides protection against myocardial I/R injury. Results The myocardial I/R injury is really an inflammatory process characterized by recruitment of neutrophils into the ischemic myocardium and excessive production of pro-inflammatory cytokines. Because the CAP can modulate the inflammatory response by decreasing the production and release of pro-inflammatory cytokines, it can provide protection against myocardial I/R injury. Conclusions The CAP can inhibit the inflammatory response induced by reperfusion and protect against myocardial I/R injury. It represents an exciting opportunity to develop new and novel therapeutics to attenuate the myocardial I/R injury.