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Objective To observe the expression and localization of group Ⅰ metabotropic glutamate receptors (mGluR1/ 5) in rat superior cervical ganglion (SCG) and the effect of chronic intermittent hypoxia (CIH) on mGluR1/ 5 protein level. Methods Twelve male SD rats were randomly divided into control group(Ctrl)and CIH group(CIH), 6 rats in each group. After 6 weeks of modeling, the effect of CIH on mGluR1/ 5 protein level was detected by Western blotting, the expression and distribution of mGluR1/ 5 in SCG were detected by immunohistochemistry and double-immunofluorescent staining. Results mGluR1/ 5 was expressed in rat SCG. mGluR1 was distributed in neurons and small intensely fluorescent (SIF) cells, but not in satellite glial cells (SGCs), nerve fibers and blood vessels, whereas mGluR5 was mainly distributed in nerve fibers and a little in neurons, but not in SGCs, SIF cells and blood vessels. CIH increased the protein levels of mGluR1/ 5 (P<0. 01) in rat SCG. Conclusion Both mGluR1 and mGluR5 are expressed in the rat SCG, but their distribution are different, and the increased protein levels of both may be involved in CIH-induced hypertension.
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OBJECTIVE@#To investigate the expression and localization of metabotropic glutamate receptors 7 and 8 (mGluR7/8) in rat superior cervical ganglion (SCG) and their changes in response to chronic intermittent hypoxia (CIH).@*METHODS@#We detected the expressions of mGluR7 and mGluR8 in the SCG of 8-week-old male SD rats using immunohistochemistry and characterized their distribution with immunofluorescence staining. The expression of mGluR7 and mGluR8 in the cytoplasm and nucleus was detected using Western blotting. A 6-week CIH rat model was established by exposure to intermittent hypoxia (6% oxygen for 30 s followed by normoxia for 4 min) for 8 h daily, and the changes in systolic blood pressure, diastolic blood pressure and mean arterial pressure were measured. The effect of CIH on expression levels of mGluR7 and mGluR8 in the SCG was analyzed using Western blotting.@*RESULTS@#Positive expressions of mGluR7 and mGluR8 were detected in rat SCG. mGluR7 was distributed in the neurons and small fluorescent (SIF) cells with positive staining in both the cytoplasm and nuclei, but not expressed in satellite glial cells (SGCs), nerve fibers or blood vessels; mGluR8 was localized in the cytoplasm of neurons and SIF cells, but not expressed in SGCs, nerve fibers, or blood vessels. Western blotting of the nuclear and cytoplasmic fractions of rat SCG further confirmed that mGluR7 was expressed in both the cytoplasm and the nucleus, while mGluR8 exists only in the cytoplasm. Exposure to CIH significantly increased systolic blood pressure, diastolic blood pressure and mean arterial pressure of the rats (all P < 0.001) and augmented the protein expressions of mGluR7 and mGluR8 in the SCG (P < 0.05).@*CONCLUSION@#mGluR7 and mGluR8 are present in rat SCG but with different localization patterns. CIH increases blood pressure of rats and enhanced protein expressions of mGluR7 and mGluR8 in rat SCG.
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Male , Animals , Rats , Rats, Sprague-Dawley , Superior Cervical Ganglion , Receptors, Metabotropic Glutamate , HypoxiaABSTRACT
Objective:To evaluate the role of bilateral superior cervical sympathetic ganglia (SCG) in myocardial ischemia-reperfusion (I/R) injury in mice and the relationship with NOD-like receptor protein 3 (NLRP3) inflammasomes.Methods:Thirty-two healthy SPF male C57BL mice, aged 8-10 weeks, weighing 25-30 g, were divided into 4 groups ( n=8 each) by the random number table method: sham operation group (NS group), myocardial I/R group (NIR group), bilateral SCG excision group (SCGx group) and bilateral SCG excision + myocardial I/R group (SCGx+ IR group). The myocardial I/R injury model was prepared by ligating the anterior descending branch of the left coronary artery for 30 min followed by 24 h reperfusion in isoflurane-anesthetized mice. Bilateral superior cervical sympathectomy was performed at 3 days before reperfusion. Blood samples were collected from the inferior vena cava at 24 h of reperfusion for examination of pathological changes (by HE and WGA staining) and for measurement of serum creatine kinase isoenzymes (CK-MB) activity, cardiac troponin I (cTnI) concentration, norepinephrine (NE) concentration and lactic dehydrogenase (LDH) activity (by enzyme-linked immunosorbent assay), superoxide dismutase (SOD) activity (by colorimetric method), myocardial reactive oxygen species (ROS) level (by DHE method), myocardial infarct size(by TTC method), and expression of interleukin-1beta (IL-1β), IL-6, IL-10, tumor necrosis factor-alpha (TNF-α), NLRP3 mRNA (by quantitativepolymerase chain reaction ), and expression of tyrosine hydroxylase (TH), IL-1β, TNF-α, NLRP3, atrial natriuretic peptide (ANP)and brain natriuretic peptide (BNP) (by Western blot). Results:Compared with NS group, the NE concentration was significantly decreased, and TH expression was down-regulated in SCGx group, and the serum CK-MB activity, concentrations of cTnI and NE, LDH activity and myocardial ROS level were significantly increased, SOD activity was decreased, the expression of IL-1β, TNF-α, NLRP3, ANP and BNP was up-regulated, and the expression of IL-1β, IL-6, TNF-α and NLPR3 mRNA was up-regulated in NIR group ( P<0.05). Compared with SCGx group, the serum CK-MB activity, concentrations of cTnI and NE, LDH activity and myocardial ROS levels were significamtly increased, SOD activity was decreased, the expression of IL-1β, TNF-α, NLRP3, ANP and BNP was up-regulated, and the expression of IL-1β, IL-6, TNF-α and NLPR3 mRNA was up-regulated in SCGx+ NIR group ( P<0.05). Compared with NIR group, the serum CK-MB activity, cTnI concentration, LDH activity and myocardial ROS level were significantly decreased, SOD activity was increased, the expression of IL-1β, TNF-α, NLRP3, ANP and BNP was down-regulated, the expression of IL-1β, IL-6, TNF-α and NLPR3 mRNA was down-regulated, and myocardial infarct size was decreased in SCGx+ NIR group ( P<0.05). Conclusions:The mechanism by which bilateral SCG excision attenuates myocardial I/R injury is associated with decreased NLRP3 inflammatory inflammasome activation and inhibition of inflammatory responses in mice.
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Objective:To evaluate the effect of superior cervical ganglion block (SCGB) on cardiac function and nucleotide like receptor protein 3 (NLRP3) signaling pathway in a rat model of myocardial ischemia-reperfusion (I/R).Methods:Sixty healthy SPF male Sprague-Dawley rats, weighing 250-300 g, aged 2-3 months, were divided into 4 groups ( n=15 each) using a random number table method: sham operation group (sham group), myocardial I/R group (IR group), myocardial I/R + normal saline group (IR+ NS group), and myocardial I/R + SCGB group (IR+ SCGB group). Myocardial I/R model was developed by ligation of the left anterior descending branch of the coronary artery for 45 min followed by restoration of blood flow in anesthetized aninals. IR+ SCGB group received SCGB (0.25% ropivacaine 0.1 ml) at 10 min before reperfusion once a day for 2 consecutive weeks, while 0.9% sodium chloride was given instead of ropivacaine in IR+ NS group. Blood samples were collected at 24 h and 14 days of reperfusion for determination of serum concentrations of norepinephrine (NE), troponin T (TnT), tumor necrosis factor-alpha (TNF-α), interleukin-18 (IL-18) and IL-1β by enzyme-linked immunosorbent assay. Echocardiography was performed before ischemia and at 14 days of reperfusion, and left ventricular short axis shortening rate (FS), ejection fraction (EF), and cardiac output (CO) were measured. The rats were sacrificed at 14 days of reperfusion and the hearts were taken for determination of the contents of norepinephrine (NE) in myocardial tissues in the infarction area (by enzyme-linked immunosorbent assay), percentage of myocardial fibrosis area (by Masson staining), M1 macrophage marker CD68 + cell count in the infarction area (by immunohistochemical method), and expression of NLRP3 and gasdermin D (GSDMD) in myocardial tissues (by Western blot). Results:Compared with Sham group, the serum concentrations of TnT, TNF-α, IL-18 and IL-1β, percentage of myocardial fibrosis area, and NE levels in serum and myocardial tissues were significantly increased, the expression of NLRP3 and GSDMD in myocardial tissues was up-regulated, CD68 + cell count was increased, and EF, CO and FS were decreased in IR group ( P<0.05). Compared with IR group, the serum concentrations of TnT, TNF-α, IL-18 and IL-1β, percentage of myocardial fibrosis area, and NE levels in serum and myocardial tissues were significantly decreased, the expression of NLRP3 and GSDMD in myocardial tissues was down-regulated, CD68 + cell count was decreased, and EF, CO and FS were increased in IR+ SCGB group ( P<0.05), and no statistically significant changes were found in the parameters mentioned above in IR+ NS group ( P>0.05). Conclusions:SCGB can improve the cardiac function in a rat model of myocardial I/R, and the mechanism may be related to the inhibition of NLRP3 signaling pathway.
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Objective To observe the expression and localization of β-site amyloid precursor protein cleaving enzyme 1 (BACEl) in rat superior cervical ganglion and the effect of chronic intermittent frypoxia (CIH) on BACEl level. Methods The expression and distribution of BACEl in superior cervical ganglion were detected by RT-PCR, Western blotting and immunohistochemistry. Totally 16 male SD rats were randomly divided into control group and CIH group, 8 rats in each group. After 2 weeks of modeling, the effect of CIH on BACEl and peroxisome proliferators activated receptor gamma coactivator 1 alpha (PGC-la) mRNA level was detected by RT-PCR. Results BACEl was expressed in rat superior cervical ganglion, and mainly distributed in satellite glial cells and nerve fibers, but not in blood vessels, neurons and small intesely fluorecent(SIF) cells. CIH down-regulated BACEl mRNA level, but up-regulated PGC-la mRNA level ( P < 0.01). Conclusion BACEl is located in satellite glial cells and nerve fibers in the superior cervical ganglion of rats. The decreased level of BACEl ma)' be involved in the regulation of CIH-induced synaptic plasticity of superior cervical ganglion.
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BACKGROUND: In modern societies, sleep deprivation is a serious health problem. This problem could be induced by a variety of reasons, including lifestyle habits or neurological disorders. Chronic sleep deprivation (CSD) could have complex biological consequences, such as changes in neural autonomic control, increased oxidative stress, and inflammatory responses. The superior cervical ganglion (SCG) is an important sympathetic component of the autonomic nervous system. CSD can lead to a wide range of neurological consequences in SCG, which mainly supply innervations to circadian system and other structures. As the active component of Curcuma longa, curcumin possesses many therapeutic properties; including neuroprotective. This study aimed to evaluate the effect of CSD on the SCG histomorphometrical changes and the protective effect of curcumin in preventing these changes. METHODS: Thirty-six male rats were randomly assigned to the control, curcumin, CSD, CSD + curcumin, grid floor control, and grid floor + curcumin groups. The CSD was induced by a modified multiple platform apparatus for 21 days and animals were sacrificed at the end of CSD or treatment, and their SCGs removed for stereological and TUNEL evaluations and also spatial arrangement of neurons in this structure. RESULTS: Concerning stereological findings, CSD significantly reduced the volume of SCG and its total number of neurons and satellite glial cells in comparison with the control animals ( P < 0.05). Treatment of CSD with curcumin prevented these decreases. Furthermore, TUNEL evaluation showed significant apoptosis in the SCG cells in the CSD group, and treatment with curcumin significantly decreased this apoptosis ( P < 0.01). This decrease in apoptosis was observed in all control groups that received curcumin. CSD also changed the spatial arrangement of ganglionic neurons into a random pattern, whereas treatment with curcumin preserved its regular pattern. CONCLUSIONS: CSD could potentially induce neuronal loss and structural changes including random spatial distribution in the SCG neurons. Deleterious effects of sleep deprivation could be prevented by the oral administration of curcumin. Furthermore, the consumption of curcumin in a healthy person might lead to a reduction of cell death.
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Animals , Male , Rats , Sleep Deprivation/pathology , Sleep Deprivation/drug therapy , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Superior Cervical Ganglion/drug effects , Curcumin/pharmacology , Rats, Sprague-DawleyABSTRACT
BACKGROUND: A stellate ganglion block (SGB) causes increased blood flow in the maxillofacial region, exhibiting the potential for regenerative effects in damaged tissue. The focus of this study was to understand the efficacy of SGB for regenerative effects against nerve damage. A rat model of the superior cervical ganglion block (SCGB) was created instead of SGB, and facial blood flow, as well as sympathetic nervous system function, were measured. METHODS: A vertical incision was made on the left side of the neck of a Wistar rat, and a 5-mm resection of the superior cervical ganglion was performed at the back of the bifurcation of the internal and external branches of the left common carotid artery. Blood flow in the skin at the mandibular angle and mean facial temperature were measured using a laser-Doppler blood flow meter and a thermographic camera, respectively, over a 5-week period after the block. In addition, the degree of ptosis and miosis were assessed over a period of 6 months. RESULTS: The SCGB rat showed significantly higher blood flow at the mandibular angle on the block side (P < 0.05) for 3 weeks, and significantly higher skin temperature (P < 0.05) for 1 week after the block. In the SCGB rat, ptosis and miosis occurred immediately after the block, and persisted even 6 months later. CONCLUSIONS: SCGB in rats can cause an increase in the blood flow that persists over 3 weeks.
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Animals , Rats , Carotid Artery, Common , Horner Syndrome , Miosis , Models, Animal , Neck , Regional Blood Flow , Skin , Skin Temperature , Stellate Ganglion , Superior Cervical Ganglion , Sympathetic Nervous System , ThermographyABSTRACT
Objective To investigate the effect of recombinant botulinum neurotoxin serotype A heavy chain (BoNT/A heavy chain)on local proteins which are related to nerve growth after spinal cord injury in rats,and to get some experimental evidence to explain the mechanism of BoNT/A heavy chain in stimulating neuritogenesis. Methods Recombinant botulinum neurotoxin serotype A heavy chain was applied locally or intrathecally to rats with ipsilateral semi-dissociated lumbar spinal injury. Local spinal tissue was extracted for general protein expression by two dimension electrophoresis plus nitrate silver staining after different time period of injury. Based on the results of 2-D gel electrophoresis,growth-associated protein 43(GAP-43)and of superior cervical ganglion 10(SCG 10)were selected to examine the changes of their expression and distribution features under BoNT/A heavy chain administration using SDS-PAGE,western blot and immunofluorescence. Results (1)The model of spinal cord injury(SCI)in this study was an ipsilateral semi-dissociated lumbar SCI in rat. The rats showed obvious motor and sensory dysfunction in the ipsilateral hind limb.(2)The results from 2-D gel electrophoresis plus nitrate silver staining showed that the administration of BoNT/A heavy chain based on SCI altered the local protein expression pattern. The decrease or increase in the expression of some protein dots /dots group was clearly seen after single SCI. However, these changes were transformed by BoNT/A heavy chain treatment,which appeared as a reversed pattern turning toward that in control group or further increased expression upon SCI,such as the dots located respectively at 35-45 kDa and 18-25 kDa level,pI between 5-7. In addition,the expression of the two dots located at the level as above increased after SCI only, and showed further increase in their expression with BoNT/A heavy chain intervention.(3)The changes of selective GAP-43 and SCG 10 expression and distribution by western blot and immunofluorescence indicated that the administration of BONT/A heavy chain based on SCI amplified the expression of GAP-43 and SCG 10(P < 0.05). Meanwhile,the positive immuonfluorescent staining for both GAP-43 and SCG 10 mainly distributed nearby the proximal area of injury, both cytoplasm and neuronal processes were positively stained. Conclusions Intrathecal delivery of BoNT/A heavy chain increases the expression of growth-associated proteins GAP 43 and SCG 10 after SCI in rats.
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Nitric oxide (NO) participates in neuronal lesions in the digestive form of Chagas disease and the proximity of parasitised glial cells and neurons in damaged myenteric ganglia is a frequent finding. Glial cells have crucial roles in many neuropathological situations and are potential sources of NO. Here, we investigate peripheral glial cell response to Trypanosoma cruzi infection to clarify the role of these cells in the neuronal lesion pathogenesis of Chagas disease. We used primary glial cell cultures from superior cervical ganglion to investigate cell activation and NO production after T. cruzi infection or lipopolysaccharide (LPS) exposure in comparison to peritoneal macrophages. T. cruzi infection was greater in glial cells, despite similar levels of NO production in both cell types. Glial cells responded similarly to T. cruzi and LPS, but were less responsive to LPS than macrophages were. Our observations contribute to the understanding of Chagas disease pathogenesis, as based on the high susceptibility of autonomic glial cells to T. cruzi infection with subsequent NO production. Moreover, our findings will facilitate future research into the immune responses and activation mechanisms of peripheral glial cells, which are important for understanding the paradoxical responses of this cell type in neuronal lesions and neuroprotection.
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Animals , Chagas Disease/immunology , Lipopolysaccharides/pharmacology , Macrophages, Peritoneal/parasitology , Neuroglia/parasitology , Nitric Oxide/biosynthesis , Trypanosoma cruzi/immunology , Chagas Disease/etiology , Fluorescent Antibody Technique , Mice, Inbred BALB C , Macrophages, Peritoneal/drug effects , Macrophages, Peritoneal/immunology , Neuroglia/drug effects , Neuroglia/immunologyABSTRACT
Objective To investigate the expression of histamine in the cardiac sympathetic fibers from the guinea pig superior cervical ganglion and its coexistence with norepinephrine so as to provide morphological evidence for histamine as a cardiac sympathetic neurotransmitter.Methods Biotinylated dextranamine(BDA) anterograde tracing and immunofluorescence histochemical staining for histamine/norepinephrine were applied.Results After injection of BDA into the superior cervical ganglion,BDA labeled sympathetic fibers in the left and right atria and ventricle were observed.Meanwhile,the tracing fibers proved histamine-like immunoreactive or both histamine and norepinephrine-like immunoreactive.Conclusion Histamine is expressed in the cardiac sympathetic fibers from the guinea pig superior cervical ganglion and coexisted with norepinephrine.
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AIM: To explore the influence of different concentration midazolam on the macroscopic voltage gated potassium currents and to discuss the relationship between potassium currents and inhibitory effect of clinical relevant concentration midazolam on sympathetic nervous system. METHODS: Superior sympathetic ganglion neurons were dissociated enzymatically from 7 to10 day old rat. Experiments were performed about 5 h after plating at room temperature (20- 24 ℃ ). Appropriate solution was chosen to separate the K + current from the other transmembrane currents. 1 ?mol?L -1 TTX was applied to the extracelluar solution to block the Na + current. Midazolam was also resolved in extracelluar solution to get various concentration ( 0.1 , 0.3 ,3,10,50,100 ?mol?L -1 ). Currents were recorded with the patch clamp technique in whole cell configuration using glass electrodes with a tip resistance of 2- 4 M . Potassium currents were evoked by test pulse from -100 mV to +30 mV with holding potential -80mV. Data were analyzed using Clampfit 6.0 and Oringih 5.0 software. Whole cell current records were corrected for leakage and capacitance by using the P/5 protocol. RESULTS: Midazolam dose dependently inhibited the whole cell potassium currents. Clinical relevant concentration midazolam ( 0.3 ?mol?L -1 ) only reduced the peak currents by 3.89 %(P= 0.88 ). The concentration required to produce 50% current inhibition(IC 50 ) was 76.065 ?mol?L -1 . CONCLUSION: Midazolam inhibits the whole cell potassium current significantly and dose dependently, but clinical relevant concentration midazolam has minor effect on the potassium currents, indicating that the inhibitory effect of midazolam on potassium current is not related to the suppression of activity of sympathetic system.
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BACKGROUND AND OBJECTIVES: Recently, nitric oxide (NO) has been considered to be a neurotransmitter or a signaling molecule in a number of distinct subpopulation of neurons in the central and peripheral nervous systems. This study attempted to define the distribution patterns and quantitative participation according to the origin of nitrergic innervation in the canine laryngeal ventricles of eight adult dogs. MATERIALS AND METHODS: The nitrergic innervation in the intralaryngeal, superior cervical and nodose ganglion to the laryngeal ventricle were investigated by using double labelled neuronal NO synthase (nNOS) immunocytochemistry combined with a retrograde tracer, cholera toxin subunit B-conjugated horseradish peroxidase (CTB-HRP). RESULTS: NO is suggested to participate in parasympathetic, sympathetic and sensory innervation. Intralaryngeal ganglion is the main source of nitrergic innervation in the canine laryngeal ventricle. The proportions of the nitrergic innervation in the intralaryngeal ganglion, superior cervical ganglion, and nodose ganglion to the canine laryngeal ventricle were 63.1%, 37.7%, 4.9% respectively. CONCLUSION: NO originating from the intralaryngeal ganglion in a canine laryngeal ventricle may play an important role in controlling the laryngeal gland secretion and in regulating the blood flow by modulating the classical parasympathetic cholinergic neurotransmitter as like a neuronal messenger or comediator. NO also may participate in the same role through the sympathetic innervation of superior cervical ganglion: however, NO originating from intralaryngeal ganglion may play more important role than that from superior cervical ganglion. Many neurons of nodose ganglion have demonstrated to have nNOS, but might be less involved in the ventricular sensory innervation.
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Adult , Animals , Dogs , Humans , Cholera Toxin , Ganglion Cysts , Horseradish Peroxidase , Immunohistochemistry , Neurons , Neurotransmitter Agents , Nitric Oxide , Nitric Oxide Synthase , Nitric Oxide Synthase Type I , Nodose Ganglion , Peripheral Nervous System , Superior Cervical GanglionABSTRACT
Objective To study the effect of substance P (SP), calcitonin gene-related peptide (CGRP) on the blood flow and the function of endolymphatic sac (ES) in guinea pigs to clarify the pathogenesis of some inner ear diseases further.Methods The guinea pig model of superior cervical ganglion (SCG) resection was set up. The ESs of the model animals were stained by SP and CGRP immunocytochemically. The staining images were analysed by the computer. The ESBF was measured with the biologic microphere method.Results Compared with the control group, the staining of SP decreased sharply in the model group, however, the staining of CGRP remained unchanged. In the model animals, the ESBF was decreased either.Conclusion SP and CGRP could take part in the regulation of ESBF to affect the function of ES further.
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AIM:To investigate the inhibitory effect of dihydro-?-erythroidine on nicotine induced-current in cultured superior cervical ganglion of neonatal rats.METHODS:Pneumatic pressure administration of drug and whole-cell recording techniques were performed to compare induced-current amplitude.RESULTS:Dihydro-?-erythroidine competitively antagonized nicotinic effect,and EC50 was about 0.015mmol/L.CONCLUSION:Dihydro-?-erythroidine is a competitive antagonist of nicotinic receptors in sympathetic neurons.
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On one hand this paper used co-culture method of rat normal or injuried sciatic nerves with newborn rat superior cervical ganglia (SCG) to observe that the neurite outgrowth of SCG induced by the nerve, on the other hand we made normal or injuried sciatic nerve extracts in order to observe their neurite-promoting effects on PC12 cells to various dilutions of nerve extracts. The results show that normal and injuried sciatic nerves contain neurite-promoting factors (NPFs) for SCG sympathetic neurons. However, the NPF activity of injuried nerve is higher than that of normal nerve and has no significant differences from 1-41 days postlesion. We have also observed the neurite-promoting effects of normal or injuried sciatic nerve extracts on PC12 cells. There is a maximal effect with the injuried nerve extract prepared at 4 days post-lesion. The neurite-promoting activity of injuried (12 hours to 42 days post-lesion) nerve extracts remain constant. The rate of neurite elongation in PC12 cells relate to the dilution of nerve extracts. Experimental analysis suggests that the nerve NPFs may be not the single but two or more factors which may be produced and released by Schwann cells.
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Objective To examine the cardiac primary afferents passing through the superior cervical ganglion which the sensory neurons are located in the vagal ganglion. Methods Retrograde tracing transport combined with immunohistochemistry. Results After injecting the horseradish peroxidase(HRP) into the superior cervical ganglion in the rat, the small number of retrogradely labeled neurons consistently appeared in the upper local portion of the nodose ganglion. The same injecting of fluorogold(FG) followed by immunohistochemical staining with SP, it was found that the double\|labeled neurons with FG/SP were approximately 20% occupied the total population of the SP positive neurons in the nodose ganglion. Conclusions The present results, associated with previous reports, suggest that the pathway of the vagal afferent conveying cardiac pain information which contains SP pass through the superior cervical ganglion.\;[
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The purpose of this research work is to find out the longitudinal distribution of the preganglionic neurons which project to the superior cervical sympathetic ganglion (SCSG). Experiments were performed on 12 adult rabbits and a monkey. Under sodium pentobarbital anesthesia, 20 microliters of 10% HRP were injected slowly into the rabbit's SCSG. In the monkey, 20 microliters of 15% HRP was injected.After a postoperative survival time of 3～6 days, the animals were perfused through,the ascending aorta with a cold fixative mixture composed of 2% paraformaldehyde and 1.25% glutaraldyhyde in 0.1mol phosphatebuffer at pH 7.4. The spinal cord segments C_1～L_3 were cut serially in transverse plane on a cryostat at 48 micra.The HRP reaction product was demonstrated according to Mesulam's (1976) benzidine blue reaction method, and counterstained with neutral red.HRP labeled neurons in the spinal cord were located exclusively on the side ipsilateral to the injected SCSG. The total number of labeled cells were 7908 in 12 rabbits, but the number of labeled cells varied from animal to animal. The highest amount was 1690 (423~#) and the lowest amount was 71 (425~#). The longitudinal distribution of the labeled cells in 12 rabbits was 12 segaments of the spinal cord (C_6～T_9), but the largest proportion (86.18%) of them was concentrated from T_1 to T_4, especially at the level of T_2 and T_3 (56.22%), and with a peak at T_2 (29.10%).In cross section of the spinal cord. HRP-labeled cells were concentrated in four cell groups, they are: nucleus intermediolateralis pars principalis (ILp), nucleus intermediolateralis pars funicularis (ILf), nucleus intercalatus (IC) and nucleus intercalatus pars paraependymalis (ICpe). The latter is subdivided into dorsal portion and ventral portion. HRP positive cells were mainly located in the ILp, In 12 rabbits about 92.99% cells were located in it. A small portion of labeled cells(6.25%) were seen in the ILf. A few labeled neurons could be detected within,the IC (0.68%) and ICpe (0.08%). Furthermore, occasionally, very few labeled cells were found at the dorsol portion of the anterior horn.In the monkey, generally speaking, the pattern of the distribution of labeled cells was the same as the rabbit.