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Biomedical subjects

L C Weaver

Publications and source records attributed to L C Weaver.

At least 55 records · Page 3Linked to original sources

Effect of chromogranin A on central autonomic control of blood pressure.

We investigated the effect of exogenous chromogranin A (CgA) on central autonomic structures involved in the control of blood pressure. Actions of CgA were assessed on neurons in the rostral ventrolateral medulla, the most important brain area for cardiovascular control and for generation of sympathetic activity. Changes in renal sympathetic nerve activity, arterial pressure, heart rate, and somato-sympathetic reflexes were measured after microinjections of chromogranin A into the rostral ventrolateral medulla of anesthetized rats. The sites of microinjection of chromogranin A were determined from well known sympathetic and cardiovascular responses to microinjection of the inhibitory amino acid glycine. Significant decreases in renal nerve activity and arterial blood pressure began 10 min after microinjection of chromogranin A into the rostral ventrolateral medulla, and the maximum effect was observed at 20 min. Moreover, the bulbar component of somato-sympathetic reflexes was depressed 20 min after microinjections of chromogranin A. Our results indicate that chromogranin A can modify the activity of neurons within rostral ventrolateral medulla involved in regulation of cardiovascular autonomic control.

Animals↗

Central sympathetic mechanisms of blood pressure control in hamsters.

The goal of this study was to investigate central vasomotor control of blood pressure in golden hamsters. Electrophysiological experiments demonstrated that tonic and reflex firing of renal nerves was controlled by brainstem and spinal circuits in manner similar to control of these nerves in rats, rabbits and cats. These findings confirmed that autonomic neural circuits for vasomotor control in hamsters are functionally similar to those of other well-studied species.

Animals↗

Spinal cord regulation of sympathetic activity in intact and spinal rats.

Excitatory amino acid (EAA) and cholinergic neurotransmission in the spinal cord of urethan-anesthetized rats was investigated to assess mechanisms regulating sympathetic activity after spinal cord injury. Blockade of EAA transmission by intrathecal injection of kynurenic acid decreased arterial blood pressure by 24 +/- 4 mmHg, heart rate by 15 +/- 10 beats/min, and renal sympathetic nerve activity (RSNA) by 85 +/- 4% in intact rats. In rats with cervical spinal transections, this blockade decreased RSNA by 51 +/- 5% and had no effect on arterial pressure and heart rate. Muscarinic blockade by intrathecal atropine decreased RSNA by 12 +/- 3 and 32 +/- 6% in intact and spinal rats, respectively, and caused no cardiovascular responses in either group. Combined blockade of EAA and muscarinic receptors in spinal rats decreased RSNA by 77 +/- 1%. Intrathecal injections of the EAA agonist D,L-homocysteic acid in spinal rats caused initial increases (335 +/- 28%) in RSNA lasting approximately 3 min and later sustained increases (157 +/- 19%) lasting 36 +/- 8 min. Only the early excitation increased arterial pressure by 17 +/- 3 mmHg, and then pressure returned to baseline values. The EAA agonist kainic acid increased RSNA by 402 +/- 90% in spinal rats, an effect lasting 70 +/- 5 min, and increased arterial pressure by only 8 +/- 2 mmHg for 12 +/- 5 min. These findings suggest that tonic activity of spinal neurons with EAA and cholinergic receptors maintains tonic RSNA after spinal cord transection. However, this activity does not play a major role in maintaining arterial pressure, even if it is increased substantially by EAA receptor stimulation.

Animals↗

GABAB receptor-mediated mechanisms in the RVLM studied by microinjections of two GABAB receptor antagonists.

The cardiovascular effects of microinjections of two gamma-aminobutyric acid (GABA) antagonists specifically acting on GABAB receptors, 2-hydroxy-saclofen (2-OH-S) and CGP-35348, into vasopressor sites of rostral ventrolateral medulla (RVLM) were studied in rats anesthetized with urethan. Bilateral microinjection of 2-OH-S induced significant increases in mean arterial pressure (MAP) and heart rate (HR) in 21 of 26 RVLM vasopressor sites (81%); average increases obtained in the 26 sites studied were +25.2 +/- 3.0 mmHg and +12.7 +/- 2.1 beats/min. Bilateral microinjection of CGP-35348 induced significant increases in MAP and HR in 10 of 12 RVLM sites (83%). Average increases in the 12 sites studied were +27.6 +/- 3.9 mmHg and +14.6 +/- 2.5 beats/min. Sixteen rats received unilateral electrolytic lesions of one RVLM. Microinjections of either 2-OH-S or CGP-35348 into vasopressor sites within the intact RVLM significantly antagonized the depressor responses observed after injections of baclofen (20 pmol) into the same sites, whereas both GABAB antagonists did not affect the depressor response induced by microinjection of muscimol (5 pmol). These results suggest a tonic inhibitory mechanism within the RVLM mediated by GABAB receptors involved in central cardiovascular regulation.

Animals↗

Pontine reticular neurons provide tonic excitation to neurons in rostral ventrolateral medulla in rats.

To determine whether the pontine reticular formation (PRF) is a source of tonic activity for cardiovascular neurons in the rostral ventrolateral medulla (RVLM), the discharge of PRF neurons was inhibited by unilateral microinjections of glycine (1.0 M; 60 nl) while recording the discharge of single neurons in the RVLM in 14 Saffan-anesthetized rats. RVLM units were characterized as cardiovascular if their spontaneous activity was changed by baroreceptor activation and was synchronized to the cardiac cycle. Glycine injection into the ipsilateral PRF eliminated the ongoing activity of six cardiovascular units and reduced the activity of four (mean decrease -91 +/- 4%). Inhibition of these units lasted 20-115 s (mean 59 +/- 9 s). Glycine injection into the PRF had no effect on the discharge of five cardiovascular units. Activity of six noncardiovascular units did not respond to PRF blockade. Glycine injection into the PRF caused decreases in arterial pressure (-28 +/- 5 mmHg), heart rate (-23 +/- 3 beats/min), and renal nerve activity (-42 +/- 7%) that also returned to control values between 25 and 120 s (mean 55 +/- 5 s). These results indicate that PRF neurons provide tonic excitatory drive to some cardiovascular neurons located in the RVLM.

Animals↗

Generation of recombinant herpes simplex virus type 1 to be used for automatic tract tracing.

We generated two insertional beta-galactosidase (lacZ) expressing herpes simplex virus type 1 (HSV-1) with putative mutations in the UL41 or US5 open reading frames. Purified recombinants or wild-type HSV-1 were injected into the left adrenal gland of hamsters. Three days later, virus-infected neurons were visualized with immunohistochemistry in spinal cord sections from all infected hamsters. Neurons were also visualized with X-Gal histochemistry in spinal cord sections from hamsters infected with either of the recombinants but not with the wild-type virus. Insertional mutagenesis of the HSV-1 genome by lacZ did not disrupt the neurotropic properties of the virus. Both recombinant viruses transneuronally labelled the central nervous system (CNS) sympathoadrenal preganglionic neurons and may be useful for the study of synaptic organization of neural circuits. Successful transynaptic transmission of this marker gene into CNS neurons from a peripheral organ suggests that other foreign genes may also be delivered into CNS neurons using HSV-1.

Adrenal Glands↗

Action of propofol on central sympathetic mechanisms controlling blood pressure.

This study was done using Wistar rats to determine if the actions of propofol (22 +/- 1, 40 +/- 2, 64 +/- 3 and 103 +/- 3 mg.kg-1 x hr-1) decreased blood pressure and heart rate through depression of brain stem vasomotor centres. All rats were given atropine to block vagal influences on the heart. Propofol decreased renal nerve activity as well as blood pressure and heart rate in a dose-dependent manner. Infusion of the lowest dose of propofol (22 +/- 1 mg.kg-1 x hr-1) had no effect on blood pressure, heart rate and renal nerve activity. Infusion of propofol at 40 +/- 2 mg.kg-1 x hr-1 decreased renal activity by 22 +/- 4% (mean +/- SEM) and at 64 +/- 3 mg.kg-1 x hr-1 it decreased renal nerve activity by 36 +/- 6%. Finally, infusion of the largest dose of propofol (102 +/- 3 mg.kg-1 x hr-1) decreased nerve activity by 50 +/- 5%. The haemodynamic changes observed in our experiments during the infusion propofol paralleled the changes in sympathetic firing, suggesting that hypotension was caused by central actions of propofol to depress sympathetic firing. In experiments with bolus injections of propofol, the renal nerve activity returned to normal before arterial pressure and heart rate recovered. Because decreases in blood pressure and heart rate were longer-lasting than changes in renal nerve activity, a part of the vasodepression and bradycardia caused by propofol likely resulted from direct actions on blood vessels and the heart. Sympathetic and cardiovascular responses to blocking neurons in the ventrolateral medulla with microinjection of glycine were depressed by propofol.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Distribution of immunoreactivity for enkephalin, substance P and vasoactive intestinal peptide in fibres surrounding splanchnic sympathetic preganglionic neurons in rats.

The distribution of substance P, enkephalin and vasoactive intestinal peptide in fibres and cells was examined in the autonomic nuclei of the lower thoracic and lumbar segments of the rat spinal cord. Attention was focussed on the location of the peptides in sympathetic preganglionic neurons contributing to the greater and lesser splanchnic nerves and in fibres surrounding these neurons. To identify splanchnic preganglionic neurons, Fluoro-Gold was applied to the left splanchnic nerve in anaesthetized rats and some of these animals received intrathecal administration of colchicine at thoracic segments 6, 9 and 12, 24-48 h before perfusion with fixative. Immunoreactivity for substance P, enkephalin and vasoactive intestinal peptide in fibres and cells of the sixth thoracic to second lumbar spinal cord was detected with fluorescent immunocytochemical techniques. Most retrogradely labelled cells (90%) were located in the intermediolateral nucleus and the rest were situated in the nucleus intercalatus and the central autonomic nucleus of the gray matter. Terminals of fibres containing immunoreactivity to all three peptides were found in all autonomic regions. Fibres immunoreactive for substance P and enkephalin were seen projecting in the white matter to the region of the intermediolateral nucleus and extending from this nucleus to the central autonomic nucleus. Terminals containing each of the three peptides were also found surrounding the retrogradely labelled cells in the intermediolateral nucleus. Approximately two cells immunoreactive for vasoactive intestinal peptide were found per section and 80% were located in the autonomic regions. Fewer cells immunoreactive for substance P and enkephalin were observed (approximately one per section) and 70% were outside laminae VII and X. Although cells immunoreactive for substance P, enkephalin and vasoactive intestinal peptide were located in all autonomic regions of the spinal cord, cells doubly labelled with retrograde dye and with the antisera to either of the peptides could not be identified. The data suggest that (i) substance P, enkephalin and vasoactive intestinal peptide are contained in fibres of neurons regulating preganglionic sympathetic control of the abdominal viscera and its vasculature; and (ii) these peptides may not be major transmitters within splanchnic preganglionic neurons.

Animals↗

Proportions of renal and splenic postganglionic sympathetic populations containing galanin and dopamine beta hydroxylase.

Galanin is a 29-amino acid neuropeptide found in rat spinal cord, autonomic ganglia and gastrointestinal tract, as well as in other areas of the nervous system in rats and other species. As part of an overall objective to determine if peptides contribute to target-specific control of visceral function, this study was designed to determine the percentages of populations of renal and splenic postganglionic neurons that contain galanin, and to determine if these neurons were likely to be adrenergic. Retrogradely transported fluorescent dyes were placed on renal and splenic nerves in male Wistar rats anaesthetized with sodium pento-barbital. Four days post-operatively, rats were perfused transcardially with fixative, and T12-L1 thoracolumbar chain ganglia, splanchnic ganglia and the solar plexus were removed. Immunocytochemical methods were then used to determine the proportions of the retrogradely labelled renal and splenic neurons containing galanin-like immunoreactivity and dopamine beta hydroxylase-like immunoreactivity. In seven rats, 24 +/- 3% of 2838 renal neurons were found to contain galanin-like immunoreactivity; in six rats, 32 +/- 5% of 5102 splenic neurons were found to contain galanin-like immunoreactivity. These proportions of the two populations were not significantly different from one another. In three rats, 94 +/- 2% of 684 renal neurons were found to contain dopamine beta hydroxylase-like immunoreactivity, and 95 +/- 2% of 2597 splenic neurons in three rats also showed dopamine beta hydroxylase-like immunoreactivity. These experiments indicate that subpopulations of both renal and splenic postganglionic sympathetic neurons contain the neuropeptide galanin and that these neurons are likely to be adrenergic in function. These findings suggest a role for galanin in control of the kidney and the spleen by the sympathetic nervous system.

Adrenergic Fibers↗

Identification of renal sympathetic preganglionic neurons in hamsters using transsynaptic transport of herpes simplex type 1 virus.

Herpes viruses have been used as retrograde transsynaptic tracers to identify pathways from the CNS to specific target tissues. We used herpes simplex virus to identify central nervous system neurons responsible for control of the kidney. Herpes simplex type 1 or herpes simplex type 2 was injected into rat kidneys and herpes simplex type 1 was microinjected into hamster and guinea pig kidneys. After three to seven days, ganglia, spinal cords and brains were examined using immunohistochemistry to visualize the virus-infected neurons. Our first experiments demonstrated that rats were not susceptible to infection with neurotropic strains of herpes simplex type 1. Injections of a wildtype strain of herpes simplex type 2 into rat kidneys led to nonspecific infection of many central nervous system neurons and glia. In contrast, herpes simplex type 1 injections in hamsters and guinea pigs caused specific infection of limited numbers of neurons in approximately one-third of the animals and the study was continued using hamsters. Sympathetic preganglionic neuron labelling was found in the ipsilateral intermediolateral cell column of the spinal cord as well as the lateral funiculus. Most infected preganglionic neurons were located in the seventh to the ninth thoracic spinal segments. Infected neurons were not found in the dorsal or ventral horn of the spinal gray matter and only one or two cells were found in the brainstem. Sympathetic preganglionic neuron morphology was usually normal, showing detailed dendritic arborizations, and lysis was infrequent. Small infected cells were sometimes observed close to sympathetic preganglionic neurons. Because herpes simplex type 1 virus was not detected immunocytochemically in ganglionic neurons in these same hamsters, the polymerase chain reaction was used in some additional hamsters to detect viral DNA in the T12 and T13 chain ganglia and splanchnic ganglia ipsilateral to the kidney injected with herpes simplex type 1. Finally, the overall distribution of renal postganglionic and splanchnic preganglionic neurons in hamsters was examined for comparison to the number and locations of virus-labelled neurons. Retrograde transport of the fluorescent dye FluoroGold demonstrated that (i) renal postganglionic neurons are distributed in the T10-L1 chain ganglia and in the prevertebral splanchnic ganglion and (ii) splanchnic preganglionic neurons are located in the T3-T12 spinal segments, predominantly in the intermediolateral and funicular spinal autonomic nuclei. In conclusion, herpes simplex type 1 virus infected an exclusive population of "renal" neurons in hamsters without lysis and with little cellular reaction to the infection after a survival period of three days, permitting these neurons to be studied in detail.

Animals↗

Connections between the pontine reticular formation and rostral ventrolateral medulla.

Pontine reticular formation (PRF) neurons provide tonic excitatory drive to sympathetic nerves and are involved in cardiovascular control [K. Hayes and L. C. Weaver. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1567-H1575, 1992]. However, connections between the PRF and the well-known vasomotor region in the rostral ventrolateral medulla (RVLM) are unknown. In propofol (Diprivan)- anesthetized rats we investigated arterial pressure, heart rate, and renal nerve responses to microinjection of glycine (1.0 M, 60 nl) into the PRF before and after injection of the synaptic blocking agent cobalt chloride (4.0 mM, 200 nl) into the RVLM. Glycine injections into the PRF caused decreases in arterial pressure, heart rate, and discharge of renal sympathetic nerves. Synaptic blockade of the RVLM almost eliminated cardiovascular and sympathetic responses to glycine injections into the PRF and blocked somatosympathetic reflexes in the renal nerve. Cobalt injections into the RVLM had very small effects on basal renal nerve firing, arterial pressure, or heart rate. These results suggest that the neurons within the RVLM relay influences from the PRF to sympathetic preganglionic neurons. Because injections of the excitatory amino acid antagonist, kynurenate, into the RVLM also interrupted responses to blockade of the PRF and blocked somatosympathetic reflexes, glutamate is a likely neurotransmitter from the PRF to the RVLM and for somatosympathetic reflexes.

Animals↗

Dorsal root afferent influences on tonic firing of renal and mesenteric sympathetic nerves in rats.

After spinal cord transection in cats and rats, the activity of many sympathetic nerves is not entirely lost, and firing of other nerves continues unabated or is increased. This study was done to evaluate the importance of dorsal root afferent discharge on the generation of tonic sympathetic activity in renal and mesenteric postganglionic nerves in spinal rats and in rats with intact neuraxes. Sympathetic discharge was recorded in anesthetized rats, and peripheral afferent influences were eliminated by dorsal rhizotomy from T4 to L2. Activity of renal and mesenteric nerves was well maintained after high cervical and thoracic (T4) cord transections. Rhizotomy had no effect on sympathetic discharge in rats with intact neuraxes but decreased renal nerve activity significantly (-25%) in spinal rats. Because rhizotomy decreased mesenteric discharge in only three of six spinal rats, mean mesenteric nerve discharge was not decreased significantly. The decreased renal nerve discharge after dorsal rhizotomy could not be attributed to input from any specific spinal segment, and ipsilateral input was no greater than contralateral input. After rhizotomy, both renal and mesenteric nerves had substantial excitatory drive from the transected, deafferented spinal cord. These findings demonstrate that dorsal root afferent influences on spinal neurons can contribute to the generation of tonic discharge in some sympathetic nerves in spinal animals.

Afferent Pathways↗

Somatic and visceral inputs to neurons of the rostral ventrolateral medulla.

Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play an essential role in the generation of basal sympathetic tone and in the reflex regulation of blood pressure. In this study responses of RVLM "cardiovascular" neurons to somatic and visceral afferent stimulation were investigated. The activity of 34 RVLM neurons was recorded in urethan-anesthetized paralyzed and artificially ventilated rats. These neurons were identified as cardiovascular based on their baroreceptor sensitivity and their pulse-synchronous discharge. Electrical stimulation of the sciatic nerve excited 31 of the 34 RVLM units (91%). Renal nerve stimulation inhibited firing of 14 of 22 RVLM neurons tested (64%), not affecting the remaining 8 units. Stimulation of splenic nerves inhibited the discharge of 7 of 12 RVLM neurons tested (58%), whereas the remaining 5 units were not affected. All RVLM units responsive to visceral afferent stimulation were also responsive to sciatic nerve stimulation. These results indicate that RVLM cardiovascular neurons receive somatic and visceral inputs, suggesting an involvement of these units in the integration of homeostatic responses to changes in the internal and external environment.

Animals↗

Comparison of locations and peptide content of postganglionic neurons innervating veins and arteries of the rat hindlimb.

The ganglionic location of hindlimb vasoconstrictor sympathetic neurons in several species is known but the locations of neurons innervating limb arteries or veins, specifically, have not been compared and neurochemical differences between them have not been examined in detail. This study was designed to determine whether neurons innervating arteries and veins are organized as distinct populations and whether neurons innervating arteries, veins or footpads contain the same peptides. Retrograde transport of fluorescent dyes was used to identify, separately, paravertebral postganglionic neurons in the 13th thoracic to 6th lumbar (T13-L6) chain ganglia that innervate the femoral arteries, femoral veins and footpads of the rat hindlimb. The proportions of venous and arterial vasomotor neurons and footpad neurons containing neuropeptide Y- and vasoactive intestinal polypeptide-immunoreactivity (NPY-Ir, VIP-Ir) were then compared. Venous vasomotor neurons were found mostly (62%) in the L1 and L2 ganglia. The majority of arterial vasomotor neurons (81%) were distributed slightly more caudally in L1-L3. Veins and arteries were not innervated by the same cells. Footpad neurons were located mostly in L4-L6. NPY-Ir was identified in 17% of the venomotor neurons, in 94% of arterial neurons and in 24% of footpad neurons. VIP-Ir was found in 3% of the venomotor neurons, 8% of the arterial neurons and in 44% of the footpad neurons. In conclusion, hindlimb venous and arterial vasomotor neurons are anatomically distinct, are mixed randomly within the chain ganglia and differ markedly in their content of NPY, consistent with reported differences in neuromuscular transmission to arteries and veins. The most likely hindlimb postganglionic neurons to contain VIP were those innervating footpads, probably controlling sweat gland function.

Animals↗

Distributions of neuropeptide Y, vasoactive intestinal peptide and somatostatin in populations of postganglionic neurons innervating the rat kidney, spleen and intestine.

Some peripheral peptidergic nerves selectively innervate different types of tissue in abdominal organs. Neuropeptide Y- and vasoactive intestinal peptide-immunoreactive nerve terminals have been identified in the kidney, spleen and intestine and these peptides may have important physiological actions. Somatostatin has been found in sympathetic ganglia, and nerve terminals containing this peptide have been identified in the intestine. We have used fluorescent retrograde tracers to identify renal, splenic and mesenteric postganglionic neurons in rat sympathetic ganglia and then used immunocytochemistry to determine the proportions of these three identified groups of neurons displaying immunoreactivity for neuropeptide Y, vasoactive intestinal peptide and somatostatin. Most renal, splenic and mesenteric neurons were immunoreactive for neuropeptide Y and less than 1% of cells innervating these organs were immunoreactive for vasoactive intestinal peptide. Somatostatin immunoreactivity was present only in a small percentage of mesenteric neurons and not in renal or splenic neurons. The present study demonstrates that (i) the rat kidney, spleen and intestine do not differ in the proportion of innervation by neuropeptide Y-immunoreactive neurons, (ii) the solar plexus, splanchnic ganglion and chain ganglia (T12 and T13) provide very little vasoactive intestinal peptide-immunoreactive inputs to these organs, and (iii) somatostatin-immunoreactive neurons innervate the intestine but not the kidney or spleen.

Animals↗

Spinal stimulation to locate preganglionic neurons controlling the kidney, spleen, or intestine.

The organization of sympathetic preganglionic neurons may be a substrate for selective control of sympathetic outflow to different vascular beds. This study was done to determine the spinal segments containing preganglionic neurons controlling discharge of renal, splenic, and mesenteric postganglionic nerves. In urethan-anesthetized rats, preganglionic neurons were stimulated by microinjecting D,L-homocysteic acid (3 nl, 0.17 M) into the lateral gray matter of the third thoracic (T3) to the fourth lumbar (L4) spinal segments. Responses from all three nerves could be elicited from segments T4-T13. The greatest increases in renal nerve discharge were evoked from segments T8-T12, the largest increase of 59 +/- 9% elicited from T10. Increases in splenic and mesenteric nerve discharge were smaller and were evoked more uniformly from T4-L3. The largest increases in discharge of splenic and mesenteric nerves were 19 +/- 5% (from T5) and 26 +/- 4% (from T10), respectively. The widely overlapping spinal cord segments controlling these three organs suggest that location of the preganglionic neurons in different spinal segments is not part of the mechanism for selective sympathetic control. However, the larger renal nerve responses demonstrate that sympathetic output to these organs can be differentiated at the level of the spinal cord.

Animals↗

Tonic sympathetic excitation and vasomotor control from pontine reticular neurons.

The pontine reticular formation (PRF) was explored for regions providing tonic control of arterial pressure, heart rate, and activity of sympathetic nerves. In Saffan (alfaxalone-alfadolone)-anesthetized rats, discharge of neurons in the PRF or rostral ventrolateral medulla (RVLM) was inhibited by microinjections of glycine (1 M; 65 +/- 2 nl). PRF blockade caused large, short-lasting (116 +/- 17 s) decreases in arterial pressure and equal decreases in renal (-47 +/- 4%) and splenic (-45 +/- 4%) nerve activity, indicating that PRF neurons contribute to resting control of vasomotor discharge. In contrast, RVLM blockade caused long-lasting (41 +/- 3 min) decreases in arterial pressure and unequal decreases in activity of renal (-50 +/- 4%) and splenic (-31 +/- 6%) nerves. The short duration of the responses to PRF blockade could not be attributed to compensation by baroreceptors or by actions specific to glycine. Excitation of PRF neurons with amino acids caused increases as well as decreases in arterial pressure and sympathetic activity, and therefore activated neurons distinct from those that are tonically active. These results identify a source of cardiovascular control in the reticular formation of the pons that provides tonic excitatory drive to sympathetic nerves and that differs from the well-known source in the RVLM.

Animals↗

Distribution of splenic, mesenteric and renal neurons in sympathetic ganglia in rats.

The distribution of postganglionic neurons innervating the spleen, intestine and kidney in paravertebral and prevertebral sympathetic ganglia was studied in rats using retrograde transport of fluorescent dyes. Labelled cells were counted in the thoracolumbar chain ganglia T6-L4, splanchnic ganglia and the solar plexus (fusion of left and right coeliac ganglia and superior mesenteric ganglion). Most splenic neurons were located in the splanchnic ganglion (64%), mesenteric neurons in the solar plexus (96%) and renal neurons in the sympathetic chain ganglia (80%). These three groups of neurons were distributed in overlapping ganglia within the paravertebral chain. Innervation of the spleen and intestine from the chain ganglia was bilateral, whereas innervation of the kidney was almost entirely ipsilateral. In conclusion, the sympathetic postganglionic neurons controlling the spleen, intestine and kidney have their cell bodies in different ganglia. These three groups of neurons are candidates for innervation by different subgroups of preganglionic neurons.

Animals↗