No Abstract Available.
Adenylyl Cyclases* ; GTP-Binding Proteins* ; Receptors, Cell Surface*

No abstract available.
GTP-Binding Proteins*

No abstract available.
Eating* ; Melanocortins*

There is increasing evidence demonstrating that reward-related motivational food intake is closely connected with the brain’s homeostatic system of energy balance and that this interaction might be important in the integrative control of feeding behavior. Dopamine regulates motivational behavior, including feeding behaviors, and the dopamine reward system is recognized as the most prominent system that controls appetite and motivational and emotional drives for food. It appears that the dopamine system exerts a critical role in the control of feeding behavior not only by the reward-related circuit, but also by contributing to the homeostatic circuit of food intake, suggesting that dopamine plays an integrative role across the converging circuitry of control of food intake by linking energy state-associated signals to reward-related behaviors. This review will cover and discuss up-to-date findings on the dopaminergic control of food intake by both the reward-related circuit and the homeostatic hypothalamic system.

There is increasing evidence demonstrating that reward-related motivational food intake is closely connected with the brain’s homeostatic system of energy balance and that this interaction might be important in the integrative control of feeding behavior. Dopamine regulates motivational behavior, including feeding behaviors, and the dopamine reward system is recognized as the most prominent system that controls appetite and motivational and emotional drives for food. It appears that the dopamine system exerts a critical role in the control of feeding behavior not only by the reward-related circuit, but also by contributing to the homeostatic circuit of food intake, suggesting that dopamine plays an integrative role across the converging circuitry of control of food intake by linking energy state-associated signals to reward-related behaviors. This review will cover and discuss up-to-date findings on the dopaminergic control of food intake by both the reward-related circuit and the homeostatic hypothalamic system.

The authors experienced a case of plasma cholinesterase variant who received succinylcholine, atracurium and reversal with pyridostigmine, and showed prolonged neuromuscular blockade postoperatively, and was ventilated artificia1ly until complete recovery. The patient and her two children later gave samples of blood. The patients blood revealed very low plasma cholinesterase activity of 0.11 IU/L(normal range; 5-12 IU/L) and dibucaine number of 33. In consideration of her childrens plasma cholinesterase activities and dibucaine numbers, we suggest that she has genetically abnormal plasma cholinesterase and probably her genotype is E E or E E.
Atracurium ; Child ; Cholinesterases ; Dibucaine ; Genotype ; Humans ; Neuromuscular Blockade* ; Plasma* ; Pyridostigmine Bromide ; Succinylcholine

BACKGROUND: The melanocortin 4 receptor (MC4R) is involved in the regulation of homeostatic energy balance by the hypothalamus. Recent reports showed that MC4R can also control the motivation for food in association with a brain reward system, such as dopamine. We investigated the expression levels of MC4R and the dopamine D2 receptor (D2R), which is known to be related to food rewards, in both the hypothalamus and brain regions involved in food rewards. METHODS: We examined the expression levels of D2R and MC4R by dual immunofluorescence histochemistry in hypothalamic regions and in the bed nucleus of the stria terminalis (BNST), the central amygdala, and the ventral tegmental area of transgenic mice expressing enhanced green fluorescent protein under the control of the D2R gene. RESULTS: In the hypothalamic area, significant coexpression of MC4R and D2R was observed in the arcuate nucleus. We observed a significant coexpression of D2R and MC4R in the BNST, which has been suggested to be an important site for food reward. CONCLUSION: We suggest that MC4R and D2R function in the hypothalamus for control of energy homeostasis and that within the brain regions related with rewards, such as the BNST, the melanocortin system works synergistically with dopamine for the integration of food motivation in the control of feeding behaviors.
Amygdala ; Animals ; Arcuate Nucleus ; Brain* ; Dopamine* ; Eating* ; Feeding Behavior ; Fluorescent Antibody Technique ; Homeostasis ; Hypothalamus ; Mice ; Mice, Transgenic ; Motivation ; Obesity ; Receptor, Melanocortin, Type 4* ; Receptors, Dopamine D2* ; Reward ; Ventral Tegmental Area

Corneal and conjunctival squamous epithelial cells have been known to express the mucin MUC1. We attempted to reveal the expression and localizational characteristics of the membrane-spanning mucin MUC1 as a component of the mucous layer in the human corneal epithelium. An antibody to the MUC1 was used to detect the MUC1 on the corneal epithelium by immunohistochemistry and immunofluorescent staining. In situ hybridization was performed to determine the distribution of MUC1 mRNA in the ocular surface. Immunohistochemically, the MUC1 mucin was observed along the apical membranes of the corneal epithelium. According to immunofluorescent staining, cells varied in the amount of mucin MUC1. Expression of MUC1 mRNA was observed in all layers of the corneal epithelium. The MUC1 mucin synthesized by the corneal epithelia exists on the apical membrane of the superficial cells. The amount of MUC1 may vary with the vertical migration and the activity of the cells.
Epithelial Cells ; Epithelium, Corneal* ; Humans* ; Immunohistochemistry ; In Situ Hybridization ; Membranes ; Mucin-1 ; Mucins ; RNA, Messenger

No abstract available.
Chicago

In ischemic strokes, apoptosis is caused by excitotoxicity, ionic imbalance, oxidative/nitrosative stress, and apoptotic-like pathways. Nitric oxide (NO), a free radical, is elevated after ischemic insult. NO, which is generated primarily by neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS), promotes neuronal damage following ischemia. Evidence obtained in recent years has demonstrated that endoplasmic reticulum (ER)-mediated cell death plays an important role in cerebral ischemia. Agmatine is an endogenous substance synthesized from L-arginine by arginine decarboxylase (ADC) and is present in mammalian brain. We had previously reported that agmatine contributes to neuroprotection against ischemic injury. In continuation of our earlier work, we intended to investigate whether agmatine protects brain from transient global ischemia, and also tried to determine the neuroprotective mechanism of agmatine. Twenty minutes of transient global ischemia was induced by 4 vessel occlusion (4-VO). Agmatine (100 mg/kg, IP) was administered simultaneously with reperfusion. Samplings of brain were done at 6, 24, 48, and 72 h after reperfusion to determine the effect of agmatine on ischemic injured hippocampus. ER-damage was also investigated using electron microscope. Results showed that agmatine treatment prevented delayed neuronal cell death in hippocampal CA1 neurons after global cerebral ischemia. It also blocked NOS expression in the rat brain. Agmatine induced the increased expression of glucose-regulated protein 78 (Grp78). These results suggest that agmatine inhibits the production of NO by decreasing the expression of nNOS and iNOS on global forebrain ischemia and the neuroprotective effect of agmatine were concerned with the ER stress-mediated condition.
Agmatine ; Animals ; Apoptosis ; Arginine ; Brain ; Brain Ischemia ; Carboxy-Lyases ; Cell Death ; Electrons ; Endoplasmic Reticulum ; Glycosaminoglycans ; Hippocampus ; Ischemia ; Neurons ; Neuroprotective Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type II ; Prosencephalon ; Rats ; Reperfusion ; Stroke