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Objective:To observe the changes of leptin receptor-tyrosine kinase Janus2 （JAK2）/signal transducer and activator of transcription 3 （STAT3） pathway and the regulatory effect of Xiaoyaosan on the hypothalamic arcuate nuclei of rats with chronic mild unpredictable stress model （CUMS）. Method:Sixty male sprague-dawley rats were randomly divided into normal group， model group， Xiaoyaosan group， and fluoxetine group. After one-week adaptive feeding， the rats in model group， Xiaoyaosan group and fluoxetine group were uesd to replicate the chronic psychological stress rat model through mild unpredictable stimulation. Meanwhile ， they were simultaneously administered the corresponding drugs， Xiaoyaosan 19.27 g·kg-1·d-1， Fluoxetine 2 mg·kg-1·d-1 （based on the average adult body weight of 60 kg）， the rats in the normal group and the model group were given the same volume of normal saline for 6 weeks. The body weight， food intake， sucrose consumption ratios， and the experimental behavior in the open field test （OFT） of the groups were observed. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were used to detect the expressions of ob-R， JAK2， and STAT3 in the arcuate nucleus of rat hypothalamus. Result:Compared with the normal group， the body weight and food intake of the model group were significantly decreased （P<0.05， P<0.01）， the sucrose consumption ratios ， the total behavioral distance of the experimental field and the total distance of the central area were significantly reduced， the protein and mRNA expressions of ob-R， JAK2， STAT3 in the arcuate nucleus of hypothalamus in rats increased significantly （P<0.05， P<0.01）. Compared with the model group， the body weight of Xiaoyaosan group increased significantly on the 7th， 14th， 21st and 28th days （P<0.05， P<0.01）， the food intake of rats increased significantly on the 21st and 35th days of the experiment （P<0.05）， and the sucrose consumption ratios， the total distance of the experimental behavior in the open field test （OFT） and the total distance of the central area were significantly improved. Xiaoyaosan had a corresponding regulatory effect on the protein and mRNA expressions of ob-R， JAK2， STAT3 in the arcuate nucleus of hypothalamus in model rats （P<0.05， P<0.01）. Conclusion:Xiaoyaosan regulates the body weight， appetite， and energy metabolism of chronically mild and unpredictable stress rats， which may be related to the ob-R-JAK2/STAT3 pathway in the hypothalamic arcuate nucleus.
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OBJECTIVE@#To observe the effect of electroacupuncture (EA) on the expressions of growth arrest-specific protein 7 (Gas7) and nerve growth factor (NGF) in arcuate nucleus (ARC) of rats with focal cerebral ischemia and explore the potential action mechanism of EA in treatment of focal cerebral ischemia.@*METHODS@#A total of 50 SD rats were randomized into 4 groups, named a normal group ( =12), a sham-operation group ( =12), a model group ( =14) and an EA group ( =12). In the model group and the EA group, the thread embolization method was adopted to duplicate the model of the right middle cerebral arterial embolism. In the sham-operation group, the skin of the neck was opened and sutured without any other intervention. In the EA group, EA was applied to "Baihui" (CV 20) and "Zusanli" (ST 36) on the left side, once a day, 30 min each time, consecutively for 21 days, while there was no any intervention in the normal group, the sham-operation group and the model group. Using the immunohistochemistry (IHC) method and Western blot method, the expressions of Gas7 and NFG of ARC on the ischemic side were determined. Using Nissle staining, the morphological changes in ARC neurons were observed.@*RESULTS@#The results of Nissle staining showed that there was no significant change in the morphology of ARC neurons in the normal group and the sham-operation group. In the model group, the volume of neuron cells was atrophied obviously and the cells were arranged irregularly. In the EA group, the morphology of ARC neuron was similar to the normal group. The results of IHC and Western blot indicated that the expressions of immunoreactive neurons and protein of Gas7 and NGF in ARC of the rats in the model group were increased obviously as compared with the normal group and the sham-operation group and the expressions in the EA group were further enhanced as compared with the model group (all <0.05).@*CONCLUSION@#Gas7 and NGF may be participated in the compensatory process of partial protection of the body in the patients with focal cerebral ischemia. EA up-regulates the expressions of Gas7 and NGF in ARC, which may be one of the neuroprotective mechanisms of EA in treatment of cerebral ischemia.
Subject(s)
Animals , Humans , Rats , Brain Ischemia , Metabolism , Therapeutics , Cerebral Infarction , Metabolism , Therapeutics , Electroacupuncture , Nerve Growth Factor , Metabolism , Nerve Tissue Proteins , Metabolism , Rats, Sprague-DawleyABSTRACT
Objective:This study aimed to explore the effects ofnesfatin-1 on gastric distension (GD)-sensitive neurons in the basomedial amygdala (BMA) and the potential mechanism for nesfatin-1 to regulate gastric motility through the arcuate nucleus (Arc).Methods:The projection of nerve fiber and expression of nesfatin-1 were observed by retrograde tracing and fluo-immunohistochemistry staining;The nuclei microinjection and nuclei electrical stimulation,extracellular discharges of single unit neuron were used to observe the effects ofnesfatin-1 on the GD neurons;Gastric motility recording in vivo were used to monitor the effects ofnesfatin-1 on the amplitude of constriction and frequency of gastric motility in conscious rats.Results:NUCB2/Nesfatin-1/fluorogold-double labeled neurons were from ARC to BMA;Nesfatin-1 could excited the firing rate of most of the GD-E neurons (4.25± 1.02 Hz vs.5.32± 1.17 Hz,P＜0.01) and decreased the firing rate of most of the GD-I neurons (3.73± 0.92 Hz vs.2.64± 0.86 Hz,P＜0.01),inhibited the gastric motility,amplitude and frequency,SHU9119 could weaken the responses induced by nesfaton-1;Electrical stimulation of the Arc,the firing rate of nesfatin-1-induced GD-response neurons (GD-E:5.14± 1.32 Hz vs.6.75± 1.84 Hz,P＜0.05;GD-I:2.84± 0.86 Hz vs.4.05± 1.12 Hz,P ＜0.05) and the gastric amplitude and frequency were increase.Conclusion:It was suggested that nesfatin-1 in the BMA plays an important role in decreasing gastric motility and the Arc may be involved in this regulation process.
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AIM:To observe the expression of tyrosine hydroxylase (TH), ionized calcium binding adapter molecule 1 (Iba1) and pro-opiomelanocortin (POMC) in rat arcuate nucleus (Arc) of hypothalamus induced by substantia nigra (SN) lesion with 6-hydroxydopamine (6-OHDA).METHODS:According to the random number table, 20 SD rats were randomly divided into 6-OHDA group and control group.6-OHDA was injected into the bilateral SN of the rats in 6-OHDA group, and the same volume of saline was injected into the same position of the rats in control group.After 6 weeks, the rats were sacrificed and the brains were obtained.Immunofluorescence staining and Western blot were used to detect TH expression in the SN, and TH, Iba1 and POMC expression in the Arc.RESULTS:Compared with control group, no significant change of body weight in 6-OHDA group was observed, but the weight of retroperitoneal fat decreased from (7.550±0.670) g to (3.895±0.465) g (P<0.01).The number of TH immunoreactive neurons in SN decreased from 56±5 to 14±2 (P<0.05), and the TH protein level decreased from 0.75±0.11 to 0.41±0.09 (P<0.01).In the Arc, the number of TH immunoreactive neurons decreased from 21±2 to 10±3 (P<0.05), the number of Iba1 immunoreactive neurons increased from 12±2 to 30±5 (P<0.05), and the number of POMC immunoreactive neurons increased from 16±4 to 31±2 (P<0.05).In the hypothalamus, the TH protein level decreased from 0.35±0.05 to 0.21±0.02 (P<0.01), the Iba1 protein level increased from 0.23±0.06 to 0.51±0.04 (P<0.01), and the POMC protein level increased from 0.37±0.05 to 0.65±0.03 (P<0.01).CONCLUSION:The changes of TH, Iba1 and POMC expression in Arc of 6-OHDA-treated rats may involved in the fat loss in Parkinson's disease.
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The neuronal and hormonal regulations of food intake expand our knowledge about energy balance .The cen-tral nervous system integrates endocrine signals to regulate food intake and energy consumption .The nervous system and endo-crine system interact with each other to regulate feeding behavior .This paper was a review of the neuronal and endocrine regu-lation of food intake ,and offered a revealing insight for the study and treatment of metabolic disorders .
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Objective To investigate the role of 2B subunits-containing N-methyl-D-aspartate receptors (NR2B) in the arcuate nucleus in the development of inflammatory pain (IP) in rats.Methods One hundred and eight male Sprague-Dawley rats, aged 9 weeks, weighing 200-250 g, were randomly divided into 4 groups using a random number table: sham operation group (group S, n =47);group IP (n =47);dimethyl sulfoxide control group (group DMSO, n =7);selective NR2B antagonist Ro25-6981 group (group Ro25-6981, n=7).IP was induced by injecting complete Freund's adjuvant (CFA) 0.1 ml into the plantar surface of the left hindpaw.Ro25-6981 400 pmol was injected into the arcuate nucleus at 3 days after CFA injection.Seven rats in each group were selected for measurement of the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) at 1 day before CFA injection (T1) and at 2 days after CFA injection (T2), at 30 min before administration on 3rd day (T3) , at 30 min after administration on 3rd day (T4) , and on 5th day (T5).In S and IP groups, The rats were sacrificed at T1-3 and T5 , and the arcuate nucleus of the hypothalamus was removed for determination of NR2B mRNA expression (by real-time reverse transcriptase polymerase chain reaction) and NR2B and phosphorylated NR2B (p-NR2B) expression (by Western blot).Conclusion Compared with group S, the MWT was significantly decreased, and the TWL was shortened at T2-5 in IP, DMSO and Ro25-6981 groups, and the expression of p-NR2B was up-regulated at each time point (P＜0.05) , and no significant change was found in NR2B protein and mRNA expression in group IP (P＞0.05).Compared with group IP, the MWT was significantly increased, and the TWL was prolonged at T4in group Ro25-6981 (P＜0.05) , and no significant change was found in MWT and TWL at each time point in group DMSO (P＞0.05).Conclusion The activation of NR2B in the arcuate nucleus is involved in the development of IP in rats.
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Mounting research evidence demonstrates a significant negative impact of circadian disruption on human health. Shift work, chronic jet lag and sleep disturbances are associated with increased incidence of metabolic syndrome, and consequently result in obesity, type 2 diabetes and dyslipidemia. Here, these associations are reviewed with respect to liver metabolism and disease.
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Binge alcohol drinking during adolescence has been associated with neurotoxicity and increased risk for the development of alcohol use disorders. There is evidence that acute and chronic ethanol administration alters c-fos expression, an indirect index of cellular activity, in different brain regions in adult rats. We evaluate here if a binge-like pattern of ethanol exposure during adolescence has a relevant impact on basal and/or ethanol-stimulated regional c-fos activity during adulthood. For that aim, Sprague-Dawley rats PND 25 were saline pre-treated, (SP group) or binge-ethanol pre-treated (BEP group) for twoconsecutive days, at 48-h intervals, over a 14-day period (PND 25 to PND 38). At adult stage (PND 63) and following 25 ethanol-free days, we evaluated c-fos immunoreactivity in response to saline or acute ethanol (1.5 or 3.0 g/kg) in the hypothalamus and amygdala. We found that acute ethanol administration dose-dependently increased c-fos activity in the the Paraventricular nucleus of the hypothalamus (PVN). Interestingly, binge-ethanol exposure during adolescence significantly reduced basal c-fos activity during adulthood in the Central nucleus of the amygdala (CeA) and the Arcuate nucleus of hypothalamus (Arc). We conclude that binge-like ethanol administration during adolescence causes long-term disturbances in basal neural activity in brain areas critically involved with ethanol consumption.
El consumo en atracón durante la adolescencia está asociado con neurotoxicidad y con el riesgo de desarrollar un trastorno en el uso de alcohol. Diversos estudios muestran que la administración aguda y crónica de alcohol en ratas adultas altera la expresión de c-fos, un marcador indirecto de actividad celular, en diferentes áreas cerebrales. Nosotros evaluamos si el patrón de consumo de alcohol en atracón durante la adolescencia tiene un impacto en la actividad basal de c-fos en esas regiones activadas por el alcohol. Utilizamos ratas Sprague-Dawley en su día post-natal 25 (PND25) tratadas con suero salino (grupo SP) o con etanol tipo atracón (grupo BEP) durante dos días consecutivos, en intervalos de 48 h, durante 14 días (PND25- PND38). En la edad adulta (PND63) y después de 25 días sin etanol, evaluamos la inmunorreactividad para c-fos en respuesta a una administración aguda de suero salino o etanol (1,5 ó 3,0 g/kg) en diferentes regiones cerebrales. La administración de alcohol incrementó de manera dosis-dependiente la actividad de c-fos en el núcleo paraventricular del hipotálamo. Además la exposición a etanol tipo atracón durante la adolescencia disminuyó la actividad basal de c-fos en la adultez en el núcleo central de la amígdala y en el núcleo arqueado del hipotálamo. Concluimos que el consumo de alcohol en atracón durante la adolescencia causa problemas a largo plazo en la actividad basal de regiones cerebrales implicadas en el consumo de alcohol.
Subject(s)
Animals , Rats , Paraventricular Hypothalamic Nucleus/drug effects , Arcuate Nucleus of Hypothalamus/drug effects , Proto-Oncogene Proteins c-fos/drug effects , Ethanol/administration & dosage , Central Amygdaloid Nucleus/drug effects , Immunohistochemistry , Age Factors , Ethanol/pharmacologyABSTRACT
Current estimates suggest that over 1 billion people are overweight and over 300 million people are obese. Weight gain is due to an imbalance between energy expenditure and dietary intake. This review discusses the hypothalamic control of appetite and highlights key developments in research that have furthered our understanding of the complex pathways involved. Nuclei within the hypothalamus integrate peripheral signals such as adiposity and caloric intake to regulate important pathways within the central nervous system controlling food intake and energy expenditure. Firmly established pathways involve the orexigenic NPY/AgRP and the anorexigenic POMC/CART neurons in the arcuate nucleus (ARC) of the hypothalamus. These project from the ARC to other important hypothalamic nuclei, including the paraventricular, dorsomedial, ventromedial and lateral hypothalamic nuclei. In addition there are many projections to and from the brainstem, cortical areas and reward pathways, which modulate food intake.
As estimativas atuais sugerem que mais de 1 bilhão de pessoas apresentam sobrepeso e 300 milhões são obesas. O ganho de peso representa um desequilíbrio entre o gasto energético e o consumo alimentar. Esta revisão discute o controle hipotalâmico do apetite e destaca os pontos-chave no desenvolvimento de pesquisas para ampliar o nosso entendimento dos complexos mecanismos envolvidos nesta regulação. Núcleos situados no hipotálamo integram uma série de sinais com o sistema nervoso central controlando a ingestão alimentar e o gasto energético. As vias mais estabelecidas envolvem os neurônios orexigênicos NPY/AgRP e os neurônios anorexigênicos POMC/CART no núcleo arqueado (ARC) do hipotálamo. Esses neurônios se projetam do ARC para outros importantes núcleos hipotalâmicos, tais quais: paraventricular, dorsomedial, ventromedial e lateral. Além disso, existem várias projeções que vão e vem do tronco cerebral, das áreas corticais e das vias de retroalimentação que modulam o consumo alimentar.
Subject(s)
Humans , Appetite Regulation/physiology , Feeding Behavior/physiology , Hypothalamus/physiology , Obesity/physiopathology , Arcuate Nucleus of Hypothalamus/physiology , Gastrointestinal Hormones/physiology , Obesity/metabolism , Obesity/therapyABSTRACT
@#Objective To study the relationships among leptin, leptin receptor (OB-R) gene in arcuate nucleus and type 2 diabetes mellitus, and the effect of acupuncture on them. Methods Obese rats due to diet were injected in abdomen with small dosage streptozotocin to induce type 2 diabetes mellitus model, and were divided into acupuncture, glibenclamide and model group. Normal rats were in control. After treatment for 4 weeks, fasting blood sugar (FBS), fasting insulin (FINS), leptin, OB-R mRNA expression in arcuate nucleus were evaluated. Height, weight were measured and Lee's index were calculated before and after treatment. Results The FBS and FINS were higher in model group ［(15.79±1.87) mmol/L, (37.20±3.92) mIU/L］ than in control ［(5.16±0.13) mmol/L, (23.57±1.63) mIU/L］, but decreased in acupuncture group ［(5.46±0.20) mmol/L, (20.87±1.80) mIU/L］ and glibenclamide group ［(5.26±0.13) mmol/L, (28.10±1.86) mIU/L］. Leptin was lower in model ［(0.95±0.15) ng/ml］ than in control ［(1.32±0.15) ng/ml］, but was higher in glibenclamide group ［(1.83±0.23) ng/ml］ than in control. Weight and Lee's index decreased in model, acupuncture and glibenclamide groups after treatment. OB-R mRNA expression in arcuate nucleus in model wasn't different from control, acupuncture or glibenclamide group, nor between acupuncture and control, but was lower in glibenclamide group than in control. Conclusion Leptin decreased in type 2 diabetes mellitus rats when they became thin. Leptin resistance appears when treated with glibenclamide. Acupuncture may improve the OB-R mRNA expression in arcuate nucleus to some extent.
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Administração de glutamato monossódico (MSG) em ratos neonatos causa lesão no núcleo arqueado (NA), seguido por uma síndrome de disfunção neuroendócrina caracterizada por obesidade e reduzida atividade simpática. O objetivo da presente investigação foi examinar a resposta da glicogenólise hepática a agonistas adrenérgico em ratos tratados com MSG. Ratos Wistar machos receberam injeções subcutâneas de MSG (4 mg g-1 de peso corporal) ou salina equimolar (controles) durante cinco dias após o nascimento. Noventa dias após o tratamento, os fígados de ratos-MSG ou controles foram perfundidos in situ com epinefrina e agonistas alfa- e beta-adrenérgico. Isoproterenol, fenilefrina e epinefrina aumentaram a glicogenólise em ratos-MSG, comparados aos controles (50 ± 2,8 Vs 17 ± 0,89 µmol min-1 g-1 de fígado, p < 0,0001; 64 ± 0,15 Vs 37 ± 0,39, p < 0,0001; 35 ± 2,48 Vs 27 ± 0,98, p < 0,05, respectivamente). Concluiu-se que a lesão do NA aumentou o catabolismo do glicogênio aos agonistas adrenérgicos, possivelmente devido à reduzida atividade do eixo simpático - medula adrenal.
Administration of MSG to neonate rats causes lesions in the arcuate nucleus (AN), followed by a syndrome of neuroendocrine dysfunction characterized by obesity and decreased sympathetic activity. The aim of the present investigation was to examine the responses of hepatic glycogenolysis to alpha and beta-adrenergic agonists in rats? treatment with MSG. Male Wistar rats received subcutaneous injections of MSG (4 mg g-1 body weight) or hyperosmotic saline (controls) during five days after birth. Ninety days after treatment, the livers of the MSG or controls rats were perfused in situ with epinephryne and alpha- and beta-adrenergic agonists. Epinephryne, Isoproterenol and phenylephrine increased glycogenolysis in the MSG-treated rats, compared to the controls (50 ± 2.8 Vs 17 ± 0.89 µmol min-1 g-1 of liver, p < 0.0001; 64 ± 0.15 Vs 37 ± 0.39, p < 0.0001; 35 ± 2.48 Vs 27 ± 0.98, p < 0.05, respectively). Results indicated that the lesion in the AN increased glycogen catabolism to adrenergic agonists, possibly, due to the reduced activity of the sympathetic-adrenal axis.
Subject(s)
Animals , Rats , Adrenergic Agonists , Glycogenolysis , Sodium Glutamate , Arcuate Nucleus of Hypothalamus , ObesityABSTRACT
These experiments were performed to investigate the effect of saline, melatonin, stress, stressedmelatonin on TH immunoreactivity in rat brain. The animals were injected with melatonin (1 mg/kg, i.p.) after electric shocks for 15days. The results were as follows; 1. TH immunoreactive neurons in brain (the number of staining neuron & the stain intensity in LC and parietal cortex, the stain intensity in arcuate nucleus and median eminence of cerebral cortex) were significantly increased in stressed group compared with all the other groups. 2. TH immunoreactive neurons in brain (the number of staining neuron & the stain intensity in LC and parietal cortex, the stain intensity in arcuate nucleus and median eminence of cerebral cortex were significantly decreased in stressed-melatonin treated group compared with stressed group but were significantly increased compared with the other groups. These experiments indicate that its increase is inhibited by melatonin treatment even though, stress increases TH immunoreactivity in LC and Par.
Subject(s)
Animals , Rats , Arcuate Nucleus of Hypothalamus , Brain , Cerebral Cortex , Median Eminence , Melatonin , Neurons , Rabeprazole , ShockABSTRACT
This study was aimed to investigate the changes of orexin-A (OXA) and neuropeptide Y (NPY) expression in the hypothalamus of the fasted and high-fat diet fed rats. For the experiments, the male Sprague-Dawley (SD) rats were used as the model of high-fat diet-induced obesity. The mean loss of body weight (MLBW) did not show the linear pattern during the fasting; from 24 h to 84 h of fastings, the MLBW was not significantly changed. The numbers of OXA-immunoreactive (IR) neurons were decreased at 84 h of fasting compared with those in other five fasting subgroups. The NPY immunoreactivities in the arcuate nucleus (ARC) and the suprachiasmatic nucleus (SCN) observed at 84 h of fasting were higher than that observed at 24 h of fasting. The number of OXA-IR neurons of the LHA (lateral hypothalamic area) in the high-fat (HF) diet fed group was more increased than that of the same area in the normal-fat (NF) diet fed group. The NPY immunoreactivities of the ARC and the SCN were higher in HF group than those observed in the same areas of NF group. Based on these results, it is noteworthy that the decrease of the body weight during the fast was not proportionate to the time-course, implicating a possible adaptation of the body for survival against starvation. The HF diet might activate the OXA and the NPY in the LHA to enhance food intake.
Subject(s)
Animals , Male , Rats , Adaptation, Physiological/physiology , Arcuate Nucleus of Hypothalamus/metabolism , Dietary Fats , Eating , Fasting/physiology , Hypothalamic Area, Lateral/metabolism , Hypothalamus/metabolism , Immunohistochemistry/veterinary , Intracellular Signaling Peptides and Proteins/metabolism , Neuropeptide Y/metabolism , Neuropeptides/metabolism , Obesity , Rats, Sprague-Dawley/physiology , Suprachiasmatic Nucleus/metabolismABSTRACT
Objective: To investigate the effect of electroacupuncture (EA) on rat with diet induced obesity (DIO) and to explore the possible neurochemical mechanisms using the technique of immumohistochemisty. Methods:To establish DIO rat model by feeding the animals with high fat diet for 14 weeks. DIO rats were randomly divided into 4 groups: (1) 2Hz EA group, (2) 100Hz EA group, (3) restrain control group,(4) diet resistance (DR) group,(5) DIO group and (6) normal control group. EA treatment: (1) The acupoints used were Zusanli and Sanyinjiao on both legs. (2) The intensities of stimulation were 0.5, 1.0 and 1.5mA for 10 mins each. EA treatment was administered 3 times per week. Food intake and body weight were measured daily for 4 weeks. (3) The changes of the expression of ? melanocyte stimulating hormone (? MSH) in the hypothalamic arcuate nucleus (ARC) were measured with immunohistochemical semiquantitative analysis. Results: (1) The food intake and body weight of 2 Hz EA group and 100 Hz EA group were decreased significantly compared with the restrain control group and DIO group. (2) The number of ? MSH positive cells in hypothalamic ARC in 2 Hz EA and 100 Hz EA group was significantly higher than that in restrain control group and DIO group. The number of ? MSH positive cells in hypothalamic ARC in DIO group is significantly lower than those in DR group or normal control group. Conclusion: A decrease of ? MSH level in hypothalamus may be associated with diet induced obesity. The therapeutic effect on obesity produced by EA may be accounted for by the stimulation of pro opio melanocortin neurons in hypothalamic ARC to release ? MSH, which inhibits food intake , resulting in a decrease of body weight.
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AIM: To investigate the effects of D-galactose on ultrastructure of rats' hypothalamic arcuate nucleus.METHODS: 12 rats at age of 6 months were divided into two groups at random,the control and D-galactose group.Rats of control group were treated with saline solution by sc,and rats of D-galactose group were treated with D-galactose by sc at dose of 100(mg?kg~(-1)). Three months later the rats were killed by exsanguinating from heart.After being infused into the left ventricle with 2%-(2.5)% polyformaldehyde at the dose of 50(mg?kg~(-1)),the brains were taken and immerged in(2.5)% polyformaldehyde,then the arcuate nucleus was taken according to the atlas of brain,the tissues taken were made into ultrathin sections to be observed under electron microscope.RESULTS: comparing to rats in control group,neurons of the arcuate nucleus of rats in D-galactose group appeared aging,the number of organelle in plasma decreased,but the number of lipochromesome in plasma increased significantly,and the size of neurons decreased also.Furthermore the apoptosis neuron was observed,the chromosome of which congregated around the nucleus' membrane,the typical aging neuron was also observed,the neuraxon of which was atrophying.But there were no obvious changes observed in neurons of the arcuate nucleus of rats in control group,plenty of organelles were observed under electron microscope clearly.CONCLUSION:D-galactose can cause neurons of rats' arcuate nucleus aging,the neurons appeared atrophying and apoptosis.
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The rat model of obesity was induced by high fat diet and in situ hybridization was performed with oligonucleotide probes.The results showed that expressions of leptin receptor mRNA and neuropeptide Y mRNA were significantly increased, suggesting that these increments might be related to leptin resistance.
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Effect of scalding on secretory function of beta-endorphin neuron in the arcuate nucleus of the rat hypothalamus was studied semiquantitatively using immunocytochemistry and image analysis. The results showed that the number of beta-endorphin neurons and area of positive products reduced significantly (P
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6-OHDA was injected into the third cerebroventricle of rats.24 hours later,thanimals were sacrificed and the degeneration of catecholaminergic (CA) nerve term-inals were studied by electron microscopic cytochemical method.The results showedthat there were a number of degenerated nerve terminals in the arcuate nucleus.Thecharacteristics of these terminals were as follows:enhanced axoplasmic electron opa-sity,destroyed mitochondria and synaptic vesicles and the formation of dense bodies.The multilocular forms were commonly encountered.Most of degenerated terminalswere surrouded by processes of glial cells.The degnerated perikarya of the neuronsin arcuate nucleus with decreased RER,destroyed mitochondria and dense bodieswere also observed.Based on the characteristics of degenerated features the authorsbelieved that these damaged terminals should mainly belong to DA fibers.Theymight regulate or control the function of the arcuate nucleus by means of differentkinds of synaptic mechanisms.The source of DA nerve fibers may originate from A_(12)A_(14) or A_(15) cell groups of the hypothalamus.
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The distribution of neurotensin (NT) and neuropeptide Y (NPY) in the rat hypothalamic arcuate nucleus has been studied ultrastructurally by means of double labeling preembedding immunoelectron microscopic PAP technique. First, the NPY immunoreaction was demonstrated by chromogen DAB, and second, the NT immunoreaction was demonstrated by ammonium molybdate-TMB method. After being stabilized by DAB-cobalt chloride, the vibratome sections were processed for electron microscopic study. The results showed that in the arcuate nucleus the NPY immunoreactive products appeared as high electron-dense granular or flocculent materials deposited diffusely in the organelles and matrix of perikaryon, around the dendritic microtubules and axonic small clear vesicles. Whereas the NT immunoreactive products were dense needle- or mass-like deposits distributed dispersively in the perikaryon, dendrites and axon terminals. They can easily be distinguished although being intermingled together. The NPY-containing dendrites and axons formed synaptic connections with immuno-negative axon terminals, NT-containing somata and dendrites formed also synaptic conections with negative axon terminals. In addition, NPY-positive axon terminals formed symmetrical axodendritic synapses with NT-positive dendrites. The present results provided another new ultrastructural evidence for the peptidergic synaptic regulation of NT neurons in hypothalamus.
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The distributions of neurotensin(NT) and substance P(SP) in the arcuate nucleus of rat hypothalamus have been studied by means of double labeled pre-embedding immunoelectron microscopic technique. It was observed that there were SP- and NT-containing dendrites, perikarya and axons in the arcuate nucleus. SP- and NT-containing dendrites and axons received asymmetric afferent synapses from immunonegative axons. SP-positive axonal terminals established symmetric axo-somatic and axo-dendritic synapses with immunonegative perikarya and dendrites as well as symmetric axo-somatic synapses with NT-positive perikarya. The results of this study directly indicate for the first time that the NT-ergic neurons in rat arcuate nucleus receive innervation from SP-ergic neurons, and provided an ultrastructural evidence for the synaptic regulation of the neuroendocrine of the hypothalamus.