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School of Medical Sciences, Royal Melbourne Institute of Technology University, Bundoora 3083, Melbourne, Victoria, Australia
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Hypertonic saline (HTS; 1.7 M) infused intravenously into conscious rats increases the production of Fos, a marker of cell activation, in the hypothalamic paraventricular nucleus (PVN). The parvocellular PVN contains subpopulations of neurons. However, which subpopulations are activated by HTS is unknown. We determined whether PVN neurons that innervate the rostral ventrolateral medulla (RVLM) or the spinal cord (important autonomic sites) expressed Fos following HTS. Experiments were performed 24-96 h after chronic implantation of an intravenous cannula. HTS significantly increased the number of Fos-positive cells. In the parvocellular PVN, the maximum number of Fos-positive cells occurred rostral of the anterior-posterior level at which the number of neurons that projected to the medulla or spinal cord peaked. Compared with controls, HTS did not significantly increase the number of double-labeled neurons. These findings demonstrate that an elevation in plasma osmolality activates PVN neurons but not the subgroups of PVN neurons with projections to the RVLM or to the spinal cord.
hypothalamic paraventricular nucleus; spinal cord; rostral ventrolateral medulla; hypertonic saline; Fos immunoreactivity
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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DISTURBANCES IN BODY FLUID osmolality will elicit hormonal, neural, and behavioral effects that are designed to counteract the disturbance. Although the central pathways involved are not entirely understood, several regions in the brain are likely to contribute to the reflexes (8, 14, 16). Of particular interest is the paraventricular nucleus (PVN) in the hypothalamus, which may be an important site integrating the hormonal and neural components of the response.
The PVN contains magnocellular and parvocellular neurons distributed into distinct subdivisions (24). Immunohistochemical studies, using antibodies to the protein Fos, a marker of neuronal activation, have highlighted a marked activation of neurons in the PVN following stimuli that increase plasma osmolality (15, 16). Both the magnocellular and parvocellular regions of the PVN contained activated neurons. Magnocellular neurons produce vasopressin or oxytocin, and both peptides are released in response to an osmotic challenge (11, 18, 22). Thus the presence of Fos in those neurons within the PVN following an intravenous infusion of hypertonic saline is in agreement with their known function. However, many parvocellular neurons within the PVN also exhibited Fos following the same osmotic stimulus.
The parvocellular PVN neurons project to different brain regions including central nervous system nuclei that are known to be important in the regulation of the sympathetic nervous system (2, 6, 9, 21, 23, 24). The PVN directly projects to the intermediolateral cell column of the thoracolumbar spinal cord, where the sympathetic preganglionic motoneurons are located (10, 13). The PVN has additional direct connections to the rostral ventrolateral medulla (RVLM), an important autonomic site, that also projects to the sympathetic preganglionic motoneurons and from where the tonic generation of sympathetic nerve activity is believed to originate (19).
PVN neurons that project to the spinal cord or to the RVLM have been previously described, (3, 4, 17, 19). When we compared the distribution of those neurons with the distribution of Fos that has been reported following an intravenous infusion of hypertonic saline, there appeared to be considerable overlap within the PVN. However, whether the PVN neurons that project to the spinal cord or to the RVLM are activated following hypertonic saline infusion has never been examined. Furthermore, their distribution, and that of Fos after the stimulus, has not been compared in detail in the one study.
The aims of the present study were 1) to describe the rostral-caudal distribution of Fos production in the PVN in response to an intravenous infusion of hypertonic saline and 2) to determine whether parvocellular neurons that projected either to the RVLM or to the spinal cord were activated by the osmotic challenge. In this work, we used the production of the protein product Fos as a marker of neuronal activation combined with neuroanatomic tract tracing techniques (3, 4, 7, 19, 20).
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Male Sprague-Dawley rats (200-250 g) obtained from Monash University Animal Services were used for these studies. The experimental protocols were approved by RMIT University Animal Ethics committee and conform to the "Guiding Principles For Research Involving Animals and Human Beings" (1) by the American Physiological Society and the National Health and Medical Research Council of Australia. All efforts were made to minimize animal discomfort and to reduce the number of animals used. All surgical procedures were performed under general anesthesia (pentobarbital sodium 60 mg/kg ip) or a mixture of ketamine HCl (100 mg/kg ip) and xylazine (5 mg/kg ip) with additional supplementation of ketamine HCl (30 mg/kg ip) if necessary. Buscopan Compositum [consisting of a mixture of hyoscine-N-butyl bromide (12.5 mg/kg) and dipyrone (0.1 mg/kg), Boehringer Ingelheim, Australia] was administered subcutaneously to prevent excessive salivation. The antibiotic oxytetracycline (200 mg/kg sc) and the analgesic buprenorphine HCl (15 µg ip) were administered routinely at the conclusion of each surgical procedure.
Surgical Preparations
Injections of retrogradely transported tracer into the RVLM. Thirty-six rats were used. Under general anesthesia, the right femoral artery was cannulated to enable blood pressure monitoring, and the head of the rat was placed into a Kopf stereotaxic apparatus so that lambda and bregma were positioned on the same horizontal plane. A burr hole, ~4 mm in diameter, was made in the occipital bone on the left side of the skull (coordinates 2.0 mm lateral of midsagittal suture and 3.0 mm caudal of lambdoid suture at that lateral level). The pressor region of the left RVLM was located with microinjections of L-glutamate (25-50 nl, 0.1 M) by using a glass micropipette (tip diameter 50-70 microns). Typical coordinates were 1.8-2.2 mm lateral of the midsagittal suture, 2.5-3.5 mm caudal of the lamdoid suture, and 8.9 mm ventral from the brain surface. After locating the pressor region, the pipette was withdrawn, filled with rhodamine-tagged microspheres (LumaFluor, diluted 1:1 in 0.9% sterile saline or Molecular Probes), and then reinserted into the RVLM pressor site. Two-hundred to two-hundred-fifty nanoliters of the tracer were pressure-injected over 5-10 min. The micropipette was removed 5-10 min after the completion of the injection and the muscle and skin wounds were closed. Finally, the cannula was removed from the femoral artery and the animals were subsequently given the antibiotic and the analgesic.
Injections of retrogradely transported tracer into the spinal cord. Under general anesthesia, 12 rats had the retrogradely transported tracer rhodamine-tagged microspheres injected into the spinal cord. The head of the rat was positioned in a Kopf stereotaxic apparatus, a midline incision was made in the upper back, and the spinal cord was exposed between the first and second thoracic vertebrae. The first thoracic vertebra was identified by its large dorsal protuberance. A fine glass micropipette (tip diameter 50-70 microns) filled with the retrogradely transported tracer was inserted into the right side of the spinal cord ~0.7 mm below the surface. The tip of the electrode was aimed at the intermediolateral cell nucleus by using the dorsolateral sulcus as the surface landmark. Three injections of the tracer were made into separate anterior-posterior sites; each injection was ~200 nl. After the final injection, the muscles overlying the cord were sutured together and the wound was closed (3, 5, 19). The sites of the spinal injections were verified histologically at the end of the experiment.
Chronic Cannulation of Femoral Vein
After the injections of the neuroanatomic tracer, at least 2 wk elapsed before the rats were cannulated for intravenous infusion of hypertonic saline (1.7 M NaCl) or normal saline. Under general anesthesia, a small bore cannula, filled with 5,000 U/ml of heparin, was inserted into the left femoral vein, tied in place, and the free end was tunnelled subcutaneously and subsequently exposed at the back of the rat and tied in place between the two scapulae. The experiments were performed between 24 and 96 h after the completion of the surgery. The number of animals in each group at the different times is shown in Table 1.
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Experimental Day
On the day of the experiment, the rats were brought to the experimental room and left to acclimatize for ~60 min. Hypertonic saline (1.7 M NaCl) was infused for 60 min at a rate of 0.83 ml/h. In preliminary experiments in four rats, we observed that this rate of infusion of hypertonic saline did not affect mean arterial blood pressure over the observation period (average change in pressure = 3.2 ± 4.0 mmHg). Normal saline (0.15 M NaCl) was infused instead of hypertonic saline in control rats. Thirty minutes after the end of the infusion, the rats were deeply anesthetized and perfused transcardially with isotonic saline followed by 4% paraformaldehyde in phosphate buffer (300 ml, pH = 7.2). In six animals (3 administered hypertonic saline and 3 administered normal saline), a blood sample was taken before perfusion to determine plasma osmolality.Detection of Fos By Immunohistochemistry
The brains were postfixed for ~3 h and then left overnight in phosphate buffer containing 20% sucrose. Sections of the hypothalamus (40-micron thick) were cut on a freezing microtome, and alternate serial sections were taken and processed immunohistochemically to detect the protein Fos (3, 4). In brief, the procedure involved incubating the sections for 60 min in 10% normal horse serum (NHS), followed by a 24-h incubation with a primary antibody raised in rabbit against a conserved region of the human Fos (Ab5, 1:20,000 in 2% NHS containing 0.3% Triton X; Oncogene Science). After washes in phosphate buffer, the sections were incubated for 60 min with a biotinylated anti-rabbit secondary antibody that was raised in the goat (1:600, Sigma-Aldrich). After further washes with phosphate buffer, the sections were incubated for 60 min using ExtrAvidin (1:400, Sigma-Aldrich). Subsequently, the sections were washed in Tris buffer (0.05 M, pH 7.6) and incubated for 10 min in a mixture of 0.05% 3,3'-diaminobenzidine hydrochloride and 0.04% nickel ammonium sulphate in Tris buffer. Finally, the reaction was begun by the addition of 5 µl of 30% H2O2 and was terminated by washes with Tris buffer.Analysis
Fos-positive cell nuclei were identified under normal bright field illumination, retrogradely labeled cells were detected by using a fluorescent light source, and retrogradely labeled cells containing a Fos-positive cell nucleus were detected by rapidly switching between the two light sources. Labeled cells and Fos-positive cell nuclei were counted on one side of the brain in 15 sections (processed in 5 lots of 3), which represented the rostrocaudal extent of the PVN. In each lot, the data were expressed as the average number per section at each level. The mean values for each group of animals were calculated, and comparisons between hypertonic saline and the respective control group were performed by using Student's unpaired t-test. For comparisons over time, a one-way ANOVA was used with subsequent post hoc analysis between groups using Bonferroni's modification.Plasma osmolality was determined by using freezing-point depression and compared between the groups using Student's unpaired t-test.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Effects of Hypertonic Saline on Fos Production
The infusion of hypertonic saline increased the production of Fos dramatically in all rats studied. In the PVN, this occurred in both the magnocellular and parvocellular regions (Fig. 1).
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Effects of Hypertonic Saline on Fos in Rats with Injections of Tracer into the RVLM
In rats that had the retrogradely transported tracer injected into the RVLM, the number of Fos-positive cell nuclei in the parvocellular PVN, following the infusion of hypertonic saline, was significantly elevated by two- to threefold compared with the respective control group at each time point examined (P < 0.05 at 24 h and P < 0.005 at 48 and 96 h; Fig. 2).
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The increase in the production of Fos occurred throughout the
anterior-posterior extent of the PVN. The maximum number of Fos-positive cell nuclei was found predominantly in the rostral to
midanterior-posterior levels of the PVN (Figs.
3 and 4,
B and C). Similar distribution patterns of
Fos-positive cell nuclei, in response to the infusion of hypertonic
saline, were observed in the animals in which the experiments were
performed 24, 48, or 96 h after the femoral vein was cannulated.
Within the parvocellular PVN, Fos was found in the dorsal, medial, and
lateral parvocellular subregions of the PVN.
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The number of Fos-positive cell nuclei present appeared to decrease as the time between the experimental day and the day of the femoral vein cannulation increased (Fig. 2). This reduction with time was significant in the control animals only (F = 4.406, df = 16, 2; P < 0.05 1-way ANOVA). Post hoc analysis showed that there were significantly less Fos-positive cell nuclei in the 96-h control group than in the 24-h control group (Fig. 2) (P < 0.05 with Bonferroni correction).
In the magnocellular compartment of the PVN, a two- to threefold
increase in the number of Fos-positive cell nuclei was observed in
response to the infusion of hypertonic saline. This was significantly different from the respective control groups at each time point examined (Table 2). Within the treatment
groups, there was no significant difference between the time points.
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RVLM-Projecting Neurons in the PVN
RVLM-projecting neurons were observed in the dorsal, medial, and lateral parvocellullar PVN. The number of neurons in the PVN, with projections to the RVLM, was similar between the control and hypertonic saline-infused groups (Fig. 2). The main concentration of the RVLM-projecting neurons in the PVN was predominantly in the mid to caudal anterior-posterior levels of the PVN, and this was somewhat caudal to the level in which the maximum number of Fos-positive cell nuclei was observed (Fig. 3).RVLM-Projecting Neurons That Contained Fos
In the hypertonic saline-infused groups and the control groups examined 48 and 96 h after the cannulation of the femoral vein, there were virtually no RVLM-projecting neurons that contained Fos in the PVN (Fig. 2). In contrast, in the groups that had been cannulated 24 h before the experimental day, there were considerable numbers of RVLM-projecting neurons that contained Fos (Figs. 2 and 5). In the hypertonic saline-infused group, these neurons represented ~15% of the RVLM-projecting neurons counted in the PVN, whereas in the control group, they represented ~8% of the RVLM-projecting neurons. There was no statistically significant difference in the number of RVLM-projecting neurons that contained Fos between these two groups at this time point. However, both of these groups had significantly greater numbers of double-labeled cells than their respective counterparts in which the experiment was performed 48 or 96 h after the cannulation (Fig. 2) (P < 0.05).
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In the rats that had the experiment performed 24 h after the cannulation, the RVLM-projecting neurons that contained Fos were present throughout the parvocellular PVN including the dorsal, medial, and lateral regions (Fig. 5). The maximum number of those neurons was at the mid to caudal anterior-posterior levels of the PVN.
Effects of Hypertonic Saline on Fos in Rats with Injections of Tracer into the Spinal Cord
Intravenous infusion of hypertonic saline also dramatically increased the production of Fos in both the magnocellular (which we did not quantify in this series) and parvocellular regions of the PVN in rats that had been injected with the retrogradely transported tracer into the spinal cord. In the parvocellular PVN, the increase in the number of Fos-positive cell nuclei was approximately fourfold (Fig. 6). Fos immunoreactivity was present in the dorsal, medial, and lateral parvocellular subregions of the PVN and the number of Fos-positive cell nuclei present peaked in the rostral-midanterior-posterior levels of the PVN (Fig. 6).
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A typical example of the distribution of Fos-positive cell nuclei
within the PVN following the infusion of hypertonic saline is shown in
Fig. 7, left.
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Spinally Projecting Neurons in the PVN
Neurons in the PVN with projections to the spinal cord averaged 25 cells per section overall in the group infused with hypertonic saline and 23 cells per section in the control group. These cells were distributed throughout the PVN, and there was a similar anterior-posterior distribution of those cells in both groups. The maximum number of spinally projecting neurons was found in the mid to caudal anterior-posterior levels of the PVN, slightly caudal to the level at which the number of Fos-positive cell nuclei peaked (Figs. 6 and 7).Spinally Projecting Neurons That Contained Fos
In control animals, there were very few spinally projecting neurons that also contained a Fos-positive cell nucleus (Figs. 6 and 7). After the infusion of hypertonic saline, there was no significant increase in the number of spinally projecting neurons that contained Fos. These neurons represented 1.4% of all the spinally projecting neurons counted in the PVN.Plasma osmolality in animals administered the hypertonic saline was 350 ± 4 mosmol/kgH2O, which was significantly greater than in the control group (322 ± 5 mosmol/kgH2O, P < 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present study provided three important and novel findings. First, intravenous infusion of hypertonic saline increased Fos production primarily in the mid to slightly rostral anterior-posterior levels of the PVN. Second, the distribution of Fos-positive cell nuclei following hypertonic saline infusion occurred in the medial, dorsal, and lateral PVN and was similar to the distribution of PVN neurons that projected to the RVLM or to the spinal cord in those regions. However, there was a difference in the anterior-posterior PVN levels in which the maximum number of Fos-positive cell nuclei was found, compared with the levels that contained the maximum number of retrogradely labeled neurons. Third, PVN neurons with projections to the RVLM and PVN neurons with projections to the spinal cord were not activated by the hypertonic saline infusion.
In the present study, we found that Fos production was increased in the PVN in response to hypertonic saline infusion, confirming previous reports (16). However, for the first time, we quantified the anterior-posterior distribution of Fos-positive cell nuclei in the parvocellular PVN in detail and found that it was maximal in the mid and midrostral PVN. Magnocellular neurons in the PVN were also activated following the hypertonic saline stimulus, and this agrees with the functional role of these neurons in the release of vasopressin and oxytocin that occurs in response to that stimulus (11, 18).
We also found that the increase in Fos production occurred in all the parvocellular subregions of the PVN. These regions contained neurons that projected to the RVLM or to the spinal cord. However, within the PVN, we found that there was a difference in the anterior-posterior distribution of the Fos-positive cell nuclei compared with the distribution of the RVLM-projecting neurons or the distribution of the spinal cord-projecting neurons. The maximum number of Fos-positive cell nuclei elicited by the infusion of hypertonic saline occurred rostral of the level containing the peak number of RVLM- or spinal cord-projecting neurons. This has not been reported earlier, probably because such a detailed analysis of the rostral-caudal distribution has not been performed previously.
The most important finding of the present work is that PVN neurons with projections to the RVLM were not activated following the intravenous infusion of hypertonic saline when the experiment was performed at least 48 h after the cannulation of the vein. This suggests that those neurons were not activated by elevations in plasma osmolality. However, it does not preclude a role of the PVN neurons that project to the RVLM in the central pathways used by intravenous hypertonic saline because those neurons could have been inhibited by the stimulus. It could also be argued that not all neurons may express Fos following their activation. However, Fos expression is increased in PVN neurons that project to the RVLM, or to the spinal cord, following various stimuli (3-5, 19). Furthermore, in the present study, we found that PVN neurons projecting the RVLM expressed Fos when the experiment was performed 24 h after cannulation of the femoral vein.
Interestingly, 15% of the PVN neurons with projections to the RVLM were found to express Fos following the hypertonic saline infusion, if the cannulation procedure occurred within 24 h of the experimental day. We suspect that the stimulus activating these neurons was not hypertonic saline per se but perhaps related to some nonspecific postsurgical recovery sequelae, although the rats used 24 h postcannulation appeared normal. An influence of the surgery on the production of Fos is also suggested by the observation that in the control group, which was used 24 h postcannulation, there was a significantly greater number of double-labeled neurons than in the control groups examined 48 and 96 h after cannulation. Additionally, the number of Fos-positive cell nuclei present in the PVN of control animals declined as the time between the cannulation day and the experimental day increased, further suggesting some influence of surgery on the number of Fos-positive cell nuclei detected.
In the present study, we also examined the distribution of spinally projecting neurons and Fos-positive cell nuclei following intravenous infusion of hypertonic saline. These experiments were performed 96 h after cannulation. The distribution of Fos-positive cell nuclei in these animals was similar to that observed in the other groups of animals. In these experiments, we also found that the PVN neurons with spinal projections did not show an increase in the production of Fos in response to the infusion of hypertonic saline. Thus, the findings of the present study suggest that PVN neurons with projections to the RVLM or to the spinal cord were not activated by an increase in plasma osmolality.
Thus, the projections of the parvocellular neurons that were activated in response to the infusion of hypertonic saline are still to be determined. These may include neurons that project to areas like the dorsomedial medulla, lamina terminalis, and the median eminence, which are known to receive strong projections from neurons in the parvocellular PVN. Local interneurons may also be among those activated by the stimulus. Future studies will be required to investigate whether such pathways are activated.
Perspectives
Functional significance. The RVLM-projecting neurons and the spinally projecting neurons in the PVN are likely to contribute to the changes in sympathetic nerve activity that can be elicited by activating the PVN (2). However, the physiological role of those neurons is not clearly understood. In previous work, we found that the PVN neurons with projections to the RVLM or to the spinal cord were activated by hemorrhage (3, 4), and electrophysiological data indicate that the spinally projecting neurons are inhibited by increases in blood volume (12). These reports suggest that PVN neurons projecting to the RVLM or spinal cord may be activated by a decrease in blood volume. Thus, taken together with the present observations, it appears that a functional specificity exists in the way different subpopulations of parvocellular PVN neurons respond to disturbances in body fluid homeostasis.
Although our present findings suggest that the PVN neurons with projections to the RVLM or to the spinal cord were not activated by hypertonic saline administered intravenously, this does not rule out that they may be involved in the responses evoked by that stimulus. Indeed, it is quite possible that they may be inhibited. Intravenous hypertonic saline can elicit marked changes in sympathetic nerve activity including reductions in renal and splanchnic nerve activity (26). In this regard, it is interesting to note that microinjection of the GABA antagonist into the rat PVN elicits increases in renal sympathetic nerve activity that involve the RVLM (25). Thus, these PVN neurons appear to be under tonic inhibition in the rat. It is tempting to speculate that intravenously administered hypertonic saline may lead to further inhibition of these PVN neurons and a resultant reduction in renal nerve activity. In conclusion, we described the rostral-caudal distribution of Fos production in the hypothalamic PVN and compared it with the distribution of PVN neurons with projections to the RVLM and the spinal cord. In response to an intravenous infusion of hypertonic saline, Fos production occurred in areas of the PVN in which neurons with projections to the RVLM and the spinal cord were present. However, the maximum number of Fos-positive cells occurred rostral of the level in the PVN in which the PVN neurons with medullary and spinal projections were maximal. Despite the marked increase in Fos production following hypertonic saline infusion, there was no significant increase in the number of activated PVN neurons that projected to the RVLM or to the spinal cord when the experimental day was performed at least 48 h after the final surgical procedure. When this time was reduced to 24 h, there was a significant increase in Fos production in the PVN neurons projecting to the RVLM in both the hypertonic saline-infused group and in the control group. Both of these groups had significantly greater numbers of activated PVN neurons with RVLM projections than the respective groups in which the experiments were conducted between 48 and 96 h after cannulation. We hypothesize that hypertonic saline administered intravenously does not activate the PVN neurons with projections to the RVLM or to the spinal cord. The findings also indicate that caution needs to be taken when Fos is used as a marker of neuronal activation and that surgery 24 h before the experimental day may confound the results.| |
ACKNOWLEDGEMENTS |
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The work was supported by the National Health and Medical Research Council of Australia and the National Heart Foundation of Australia.
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FOOTNOTES |
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Address for reprint requests and other correspondence: E. Badoer, School of Medical Sciences, RMIT Univ., PO Box 71, Bundoora 3083, Melbourne, Victoria, Australia (E-mail: emilio.badoer{at}rmit.edu.au).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/ajpregu.00536.2002
Received 4 September 2002; accepted in final form 6 November 2002.
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RESULTS
DISCUSSION
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, Data from
conscious rats administered an infusion of intravenous HTS;
, data from rats infused with isotonic saline
(control). Data were obtained from animals in which the experiments
were performed 96 h after surgery to insert a cannula into a
femoral vein.
