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Objective:To investigate the regulation of orexinergic pathway from the lateral hypothalamic area (LHA) to the nucleus accumbens (NAc) on gastric function and reward feeding.Methods:(1)Forty-eight rats were randomly selected and divided into six groups: normal saline (NS) group, 1 μg orexin-A group, 5 μg orexin-A group, 10 μg orexin-A group, 20 μg orexin receptor antagonist (SB334867) group, 20 μg SB334867 + 5 μg orexin-A group with eight in each group according to the random number table. The gastric motility of rats was observed by injecting orexin-A and SB334867 into NAc. (2)Thirty-two rats were randomly selected and divided into four groups according to the random number table, with eight in each group. They were divided into NS + sham stimulation (SS) group, NS + electrical stimulation (ES) group, SB334867(20 μg) + SS group, and SB334867(20 μg) + ES group. The gastric motility of rats were observed by electro-stimulation of rat LHA and rat NAc injection of SB334867. (3)In order to observe the feeding-behavior related conditioned place preference (CPP) and gastric function (such as gastric emptying and gastric secretion), thirty-two rats were randomly divided into four groups with eight in each group by using the method of NAc injection of orexin-A and SB334867 according to the random number table: NS group, orexin-A(5 μg), SB334867(20 μg), SB334867(20 μg) + orexin-A(5 μg). (4)Thirty-two rats were randomly selected in accordance with the random number table and divided into four groups with eight in each group: NS + SS group, NS + ES group, SB334867(20 μg) + SS group, SB334867(20 μg) + ES group, using electro-stimulation of rat LHA and rat NAc injection of SB334867, observing the feeding-behavior related CPP and gastric function (such as gastric emptying and gastric secretion).Results:(1)In the gastric motility experiment, both the NAc microinjection of orexin-A and electrical stimulation of the LHA significantly increased the amplitudes and frequencies of gastric contraction in rats, and these effects could be blocked by the pre-administration of SB334867 (10 min after administration of orexin-A: 10 μg orexin-A group (60.78±5.67)% vs NS group (7.35±1.08)%; t=26.18, P<0.05). (2)The results of gastric emptying showed that the rates of gastric emptying were significantly increased by the NAc microinjection of orexin-A and electrical stimulation of LHA, which were blocked by the SB334867 pretreatment (after electrical stimulation of LHA: NS + SS group (71.18±17.78)% vs NS+ ES group (132.23±31.18)%; t=4.81, P<0.05). (3)Orexin-A microinjection in the NAc and electrical stimulation of the LHA significantly increased gastric acid secretion, and these effects could be blocked by pre-injection of SB334867 in NAc (90 minutes after administration of orexin-A: orexin-A group(100.18±23.23) vs NS group (39.23±7.69); t=7.05, P< 0.05) in the gastric secretion experiment.(4)The results of CPP showed that the rats were kept in the chocolate compartment for a longer time after the NAc microinjection of orexin-A and electrical stimulation of the LHA, which could be blocked by the SB334867 pretreatment in NAc (after LHA was electrically stimulated: NS+ SS group (36.23±6.23)% vs NS+ ES group (53.36±6.66)%; t=5.31, P<0.05). Conclusion:There is an orexinergic pathway from LHA to NAc that may regulate gastric function and food reward.
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Objective@#To investigate whether γ-aminobutyric acid (GABA) receptor signaling pathway is involved in the regulation of thalamic undefined (ZI)-nucleus accumbens (NAc) neural pathways on gastric distraction (GD)-sensitive neuronal firing activity and the impact on food intake, the number of times and the frequency in rats.@*Methods@#Six rats were randomly selected and the neural pathway between ZI and NAc in rat thalamus was observed by fluorescent gold (FG) retrograde tracing method.Eighty-two rats were randomly selected, and the gastric balloon was placed in gastric cavity, the microelectrode was placed in the NAc, and the stimulating electrode was placed in the ZI. The single-cell discharge recording method was used to observe the effect of electrical stimulation ZI on the excitability of GD-sensitive neurons in rat NAc.Eighteen rats were randomly selected and were divided into three groups according to the random number table. They were NS group, GABA group, GABA + GABA receptor antagonist bicuculline (BIC) group with 6 in each group, and the rat NAc was used to embed the cannula. The method of GABA and BIC was injected to observe the changes of cumulative food intake in rats for 4 h. Eighteen rats were randomly selected and randomly divided into three groups: sham stimulation (SS) group, 50 μA electrical stimulation group, 50 μA electrical stimulation + BIC group with 6 in each group. The 4 h cumulative food intake of rats was observed by electro-stimulation of rat ZI and rat NAc injection of BIC.@*Results@#Fluorescent gold retrograde tracking combined with fluorescent immunohistochemical staining showed that there were visible GABA and fluorescent gold double labeled neurons in ZI. Electrical stimulation of ZI, the frequency of GABA-sensitive GD neurons in rat NAc increased significantly (GD-E increase: (78.8±8.4)%, GD-I increase: (89.3±9.2)%, P<0.01), but the inhibitory effect was antagonized by BIC (GD-E increase: (113.8±13.6)%, GD-I increase: (121.8±14.2)%, P<0.01). Microinjection of GABA in rat NAc significantly increased the cumulative food intake for 4 h ((155.72±18.84) kcal, t=3.41, P<0.05), which was antagonized by partial BIC (123.43±15.11) kcal, t=3.28, P<0.05). Electrical stimulation of ZI significantly increased the food intake in rats ((39.07±11.27) kcal, t=2.96, P<0.05), and this effect can be partially antagonized by BIC ((34.17±10.85)kcal, t=2.33, P<0.05).@*Conclusion@#The ZI-NAc neural pathway regulates the discharge activity of rat gastric distension (GD)-sensitive neurons and the feeding status of rats, and the GABA receptor signaling pathway may be involved in mediating the process.
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Objective To investigate whether γ-aminobutyric acid (GABA) receptor signaling pathway is involved in the regulation of thalamic undefined (ZI)-nucleus accumbens (NAc) neural pathways on gastric distraction (GD)-sensitive neuronal firing activity and the impact on food intake,the number of times and the frequency in rats.Methods Six rats were randomly selected and the neural pathway between Zl and NAc in rat thalamus was observed by fluorescent gold (FG) retrograde tracing method.Eighty-two rats were randomly selected,and the gastric balloon was placed in gastric cavity,the microelectrode was placed in the NAc,and the stimulating electrode was placed in the ZI.The single-cell discharge recording method was used to observe the effect of electrical stimulation ZI on the excitability of GD-sensitive neurons in rat NAc.Eighteen rats were randomly selected and were divided into three groups according to the random number table.They were NS group,GABA group,GABA + GABA receptor antagonist bicuculline (BIC) group with 6 in each group,and the rat NAc was used to embed the cannula.The method of GABA and BIC was injected to observe the changes of cumulative food intake in rats for 4 h.Eighteen rats were randomly selected and randomly divided into three groups:sham stimulation (SS) group,50 μA electrical stimulation group,50 μA electrical stimulation + BIC group with 6 in each group.The 4 h cumulative food intake of rats was observed by electro-stimulation of rat ZI and rat NAc injection of BIC.Results Fluorescent gold retrograde tracking combined with fluorescent immunohistochemical staining showed that there were visible GABA and fluorescent gold double labeled neurons in ZI.Electrical stimulation of ZI,the frequency of GABA-sensitive GD neurons in rat NAc increased significantly (GD-E increase:(78.8±8.4) ％,GD-I increase:(89.3±9.2) ％,P＜0.01),but the inhibitory effect was antagonized by BIC (GD-E increase:(113.8 ± 13.6)％,GD-I increase:(121.8± 14.2)％,P＜0.01).Microinjection of GABA in rat NAc significantly increased the cumulative food intake for 4 h ((155.72± 18.84) kcal,t=3.41,P＜0.05),which was antagonized by partial BIC (123.43± 15.11) kcal,t =3.28,P＜ 0.05).Electrical stimulation of ZI significantly increased the food intake in rats ((39.07± 11.27) kcal,t =2.96,P＜0.05),and this effect can be partially antagonized by BIC ((34.17 ± 10.85) kcal,t =2.33,P＜ 0.05).Conclusion The ZI-NAc neural pathway regulates the discharge activity of rat gastric distension (GD)-sensitive neurons and the feeding status of rats,and the GABA receptor signaling pathway may be involved in mediating the process.
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Objective To investigate the effects of orexin-A on firing activity of gastric distensionsensitive (GD) neurons in the basomedial amygdala (BMA) and food intake in diet-indaced obese rats.Methods Healthy male Wistar rats were selected,and the diet-induced obesity (DIO) rat model and dietinduced resistant (DR) rat model were established by high-fat diet.The effects of orexin-A and an opioid receptor antagonist naloxone on BMA GD neurons were observed by recording the extracellular potentials of single neurons.The effects of orexin-A and naloxone on the food intake of different rats were observed by using BMA catheterization.The mRNA expression and protein expression of orexin-1 receptor (OX-1R) and μ opioid receptor were detected by real-time PCR and Elisa,respectively.Results After microinjection of orexinA into the BMA,the firing frequency of GD-sensitive neurons in the normal rats was significantly increased (GD-E:(78.3±6.9)％,GD-Ⅰ:(55.5±4.7) ％,P＜0.01),and this effect was completely blocked by OX-1R receptor antagonist SB334867,and naloxone partially blocked the discharge-promoting effect of orexin-A;Compared with the normal rats,the firing frequency of GD-sensitive neurons in the DIO (GD-E:(91.6±7.1) ％,GD-Ⅰ:(67.9±8.1) ％) and DR(GD-E:(87.9±6.8) ％,GD-Ⅰ:(69.2±5.8) ％) rats was significantly increased after BMA injection of orexin-A (P＜0.05).After administration of orexin-A into the BMA,food intake of the normal rats,DIO rats and DR rats ((2.38±0.34) g,(3.75 ±0.32) g,(4.01 ±0.38) g,respectively) was significantly increased (P＜0.01),and the food intake of DR and DIO rats were significantly higher than that of normal rats (P＜0.05).After BMA was injected with naloxone,the food intake of rats was inhibited,and the food intake of the DIO rats was significantly lower than that of the DR rats (P＜0.05),food intake of the DR rats was significantly lower than that of the normal rats (P＜0.05).The results of real-time PCR showed that the mRNA levels of OX-1R in DIO and DR rats were(5.85±0.45)and (6.03±0.42)were higher than that of normal rats,and the difference was significant (P＜0.05);and mRNA levels of μ-opioid receptors in DIO and DR rats((4.51±0.42) and (8.31±0.41) times) were higher than those in normal rats (P＜0.05).The results of Elisa showed that the protein levels of OX-1R in DIO ((2.98±0.28) ng/μl)and DR rats ((3.05±0.31) ng/μl) were higher than those in normal rats ((1.53±0.31) ng/μl,P＜0.05).The content of μ-opioid receptor protein in DR rats ((4.21±0.35) ng/μl) was higher than that of DIO rats ((2.77±0.27) ng/μl),and higher than that of normal rats((1.48±0.32) ng/μ),the difference was significant (P＜0.05).Conclusion BMA orexin-A promotes the spontaneous discharge of GD-sensitive neurons and food intake in normal rats,DIO rats and DR rats,μ-opioid receptors may be involved in the regulation of this process.
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Objective:This study aimed to explore the Ventromedial Hypothalamic Orexin-1 and Orexin-1 Receptors in Regulation of Gastric Acid Secretion in Conscious Rats.Methods:Rats were anaesthetized and fitted with a stainless steel carmula placed just above the VMH or paracele,after random allocation orexin-A,[Pro34]-peptide YY and [CPP1-7,NPY19-23,Ala31,Aib32,Gln34] -pancreatic polypeptide were injected in the VMH;SB-334867 was intraperitoneal injection;atropine was subcutaneous injection;GR-231118 and CGP-71683 were injected in the paracele.Using pyloric ligation model,tests the effect of different drugs on rat gastric acid secretion and gastric juice volume.Results:OXA induced dose-dependent increase of gastric acid secretion;SB-334867 induced dose-dependent inhibition of gastric acid secretion.The stimulatory effect of OXA on acid secretion was inhibited by SB-334867;atropine induced dose-dependent increase of gastric acid secretion and block the effect of orexin-A on gastric acid secretion;the gastric acid secretion was inhibited by GR-231118 or CGP-71683,and GR-231118 or CGP-71683 were blocked the effect of orexin-A on gastric acid secretion;Intraventromedial hypothalamic injections of [CPP1-7,NPY19-23,Ala31,Aib32,Gln34]-pancreatic polypeptide increased gastric acid secretion.Conclusion:It is suggested that endogenous orexin-A acts on the ventromedial hypothalamus to stimulates acid secretion.This stimulatory effect is probably mediated through orexin receptor,Y1 and Y5 receptor,and the vagus nerve system.
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Objective:To investigate the effects of Orexin peptides on feeding and energy metabolism in mice.Methods:The mice were divided into two groups:feeding group and metabolic group.The feeding group were injected with different doses (1,3 and 10 nmol) of orexin-A and orexin-B to observe their effects on feeding and the activity of tyrosine hydroxylase in liver.We used the metabolic cages and observed the changes of respiration rate and respiration rate of mice were under light condition,dark condition and fasting condition.Results:Compared with the control group,1 nmol and 10 nmol orexin-A significantly stimulated mice to feed (P ＜0.05) within 4 hours after injection,and the effect of 3 nmol orexin-A on feeding was not obvious,but increase the activity of tyrosine hydroxylase.Any dose of orexin-B did not show a stimulating effect on mice feeding.(P ＞0.05).In the light cycle,orexin-A could significantly reduce the respiration rate (RQ),the metabolic rate was significantly increased (P ＜0.05);In the dark cycle,orexin-A had no effect on RQ,but the metabolic rate was significantly rised (P ＜0.05);But the injection of orexin-A in fasting mice induced a brief increase in RQ and a significant increase in metabolic rate (P ＜0.05).Conclusion:Orexins may play an important role in regulating feeding and energy metabolism in mice.
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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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Objective To observe the protective effect of ghrelin on hippocampal injury induced by global cerebral ischemia/reperfusion (I/R) and explore its effect mechanisms.Methods The male Sprague-Dawley (SD) rats were randomly divided into four groups,namely sham group,I/R group,normal saline (NS)+I/R group and Ghrelin+I/R group,with 42 rats in each group.The model of I/R was reproduced by clipping bilateral carotid artery of rats 15 minutes and then releasing them for 60 minutes.There were no challenges for rats in sham group,just exposed their carotid artery.Ghrelin+I/R group and NS+I/R group were challenged by injecting 1 μ.L ghrelin or NS into lateral ventricle before I/R.Some of brain tissue in the rats was harvested after experiment to determine the levels of malonaldehyele (MDA),myeloperoxidase (MPO) and glutathione (GSH) in hippocampus by using chemical colorimetry and observe infarct sizes and histopathology.Single extracellular neuron discharge in other rats was recorded to observe the activity of glutamic sensitive neurons (Glu-N) and γ-aminobutyric acid (GABA) sensitive neurons (GABA-N) in hippocampus CA1 region of rats suffered I/R.Results Compared with sham group,the levels of MDA and MPO in hippocampus of rats in the I/R group were raised markedly,the level of GSH was decreased significantly,the infarct sizes was increased significantly and pycnosis neurons were increased markedly.All sorts of indexes between NS+I/R group and I/R group showed no significantly statistical significance.Compared with NS+I/R group,the levels of MDA and MPO in hippocampus of rats in the Ghrelin+I/R group were decreased significantly [MDA (nmol/g):16.4 ± 4.2 vs.24.5 ± 6.7,MPO (nmol/g):6.4 ± 1.8 vs.10.2 ± 2.9,both P ＜ 0.05],the activity of GSH was risen remarkably (μmol/g:2.65 ± 0.72 vs.1.66 ± 0.50,P ＜ 0.05),the infarct sizes of hippocampus were reduced markedly [(43.9 ± 9.5)％ vs.(77.0 ± 12.7)％,P ＜ 0.01],the number of pycnosis neuron was reduced markedly (cells:36.2±4.5 vs.47.1 ±6.1,P ＜ 0.01).The results of electrophysiology showed that the discharge frequency of Glu-N and GABA-N in hippocampus CA1 region of rats in I/R group increased markedly as compared with sham group,and no significant difference in the discharge frequency of Glu-N and GABA-N between NS+I/R group and I/R group.Compared with NS+I/R group,injected ghrelin could make the discharge frequency of Glu-N in hippocampus CA1 region of rats decreased markedly (Hz:3.81 ±0.67 vs.4.98±0.33 at ischemia,3.01 ±0.37 vs.3.77 ± 0.41 at reperfusion,both P ＜ 0.05),and the discharge frequency of GABA-N increased markedly (Hz:5.62 ± 0.54 vs.3.62±0.39 at ischemia,4.81±0.48 vs.3.71±0.21 at reperfusion,both P ＜ 0.05).Conclusion Ghrelin might protect hippocampal neuron after I/R iniury,and neuron excitability decrease might be related.
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Objective To research the functional role of thyroidal motilin and the effects of electric excitation of the paraventricular nuclei(PVN) on gastric motility and the levels of motilin in thyroid and plasma.Methods The expression of motilin in rat and human thyroid was detected by immunofluorescence staining.A phase Ⅲ-like contraction was recorded before and after thyroidectomy and after PVN excitation.The changes in concentrations of plasma FT3,FT4 and motilin were determined via radioimmunoassay (RIA).c-Fos expression of PVN after thyroidectomy and motilin expression in thyroid after PVN excitation were observed by immunohistochemical staining.Results There were motilin immunoreactive cells in rat and human thyroid.The phase Ⅲ-like contraction and concentration of motilin in plasma decreased significantly when measured on the second and fourth days after thyroidectomy(2d,P＜0.01 ;4d,P＜0.05).The expression of c-Fos in PVN after thyroidectomy was significantly increased(P＜0.05).An electric excitation of PVN could increase the concentration of motilin in plasma and thyroid and increase corresponding gastric motility in rats (P ＜0.05).The increased phase Ⅲ-like contraction by PVN excitation could be partially inhibited by administration of motilin receptor antagonist,GM-109 (P＜0.05).Excitation of PVN in thyroidectomized rats resulted in lower plasma motilin and less intense phase Ⅲ-like contraction of stomach,as compared with the sham operated control group(P＜0.05).Conclusion Motilin from the thyroid may be secreted into the peripheral plasma to affect gastric motility and PVN may modulate gastric motility and motilin expression in the thyroid.
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Objective To investigate the tracking neurofibra pathway from the hippocamlpal neurons to septal nucleus,and to explore the effects and mechanisms of ghrelin on the learning and memory in septal nucleus lesion rats.Methods Retrogradely tracing method was used to observe Fluorogold (FG) reaching sites in hippocampus.The septal nucleus was destructed by direct current using stereotactic technique.Step-down test and morris water maze were used to test the effects of learning and memory ability by means of microinjecting ghrelin into hippocampal CA1 area in rats.Results After injection of FG into septal nucleus,retrogradely labeled neurons and neurofibra were found in the hippocampal neurons with FG.Ghrelin injection of hippocampal CAI area could promoter learning and memory ability in rats.It showed that the escaped latent period was significantly lengthened ( (3.2 ± 0.9) s vs (6.9 ± 1.1 ) s,P ＜ 0.05) and the wrong numbers in 5 min were obviously decreased in escape response test; and the latency of looking for the plat was significantly shorter in morris water maze test ( 1.8 ±0.4vs 0.8 ± 0.1,P ＜ 0.05 ).However the effects above-mentioned on learning and memory was significantly weak after septal nucleus lesioning.It showed that the escaped latent period was markedly shortened ( ( 19.5 ±3.2)s vs ( 10.5 ± 2.1 ) s,P ＜ 0.05 ) and the wrong numbers in 5 min were obviously increased ( ( 3.9 ± 0.8 ) s vs ( 1.8 ±0.5 ) s,P＜0.05 ) in escape response test.The latency of looking for the plat was significantly lengthened in morris water maze (P＜0.05).Conclusion Ghrelin could elevate the learning and memory ability in hippocampus,and the effects may be related to the septal-hippecampus pathway.
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Objective To study the effects of exercises training on the recovery of neurological function and the expression of matrix metalloproteinase-9 (MMP-9) in perihematomal brain tissue after intra cerebral hemorrhage (ICH) in rats. Methods Sixty-four male adult Sprague-Dawley rats were randomly divided into exercises group and control group. ICH model was induced by autobiood injection. The rats in exercises group were given balance, grasping and walking exercises every day. The rats in control group exercised freely in standard cages. Neurological function in both groups was measured at the 3rd, 7th, 14th and 21st d. All the rats were sacrificed and the concentration of MMP-9 was measured with immunohistochemical method and in situhybridization. Results In both groups neurological function scores was lowest at the 3rd d, were highest at the 21st d. There was no significant difference between two groups at the 3rd d, but at the 7th, 14th and 21st d the differences between two groups were significant ( P < 0.05 ). In exercises group, MMP-9 expressed weakly at the 3rd d, and peaked at the 7th d, then declined gradually. In control group, MMP-9 expression peaked at the 3rd d, then decreased slowly. MMP-9 protein expression was in accord with mRNA. MMP-9 expression in exer-cises group was significantly different from control group on the 3rd and 7th d (P < 0.05 ) , but not at the 14th and 21st d ( P > 0.05 ). Conclusions Early exercises can inhibit the expression of MMP-9 that could play a role in protecting neurons. Daily exercises can stimulates the expression of MMP-9 so as to have a positive role in midstage of disease. MMP-9 may be involved in tissue remodelling and vascular repairing, which prompt neu-rofunction recovery.
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Background In recent years,some researches had been conducted on the pathologic changes of the secondary injury of perihematoma in animal experiments,but only a few studies had been done on the dynamic pathologic and ultrastructural changes of the perihematoma in ICH patients. The unique contribution of our study is to investigate the dynamic pathologic and ultrastructural changes of the perihematoma in ICH patients and provide significant insights into how the pathophysiology and ultrastructures changed after ICH.Methods The written informed consents were obtained from the ICH patients or their relatives. 30 patients (the supertentorial hemotoma volume＞30 mi and the cerebellar hemotoma volume ＞10 mi) were divided into 8 groups according to the time passed after ICH:＜6 h (6 patients), 6 ～ 12 h (7 patients), 12 ～24 h (5 patients), 24～48 h (3 patients), 48 ～72 h (3 patients), 3 ～4 days group (3 patients), 5 days group (2 patients) and 8 days group ( 1 patient) and subjected to craniotomy for hemotoma evacuation. During the operation for the hemotoma's evacuation, a small amount of tissues that must be removed, which located at 1 cm near the hematoma, were taken as experimental groups; And the same tissues of 7 patients (＜12 h), which were far from the hemotoma on the operational way, were taken as control group. The pathologic and ultrastructral changes were observed.Results The tissues of the control group were almost normal while the damages of the tissues from the experimental groups were slight in ＜6 h groups, more severe after 6h and got to the maximum between 24 ～48 h , recovered gradually after 72 h, became similar to the 6 ～ 12 h group on 5 th day, got better on 8 th day and resembled the 6 h group.Conclusions The injury of the perihematoma occurred in early stage, reached the peak level between 24 and 48 hours after ICH; which was consistent to the clinical nervous functional deficits in the ICH patients.