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Nodose ganglion extract has a stimulating effect on the in vitro proliferation of tongue epithelium basal cells. Neurotrophic control of these target cells can be realized by mitogen-like chemical factors which are probably synthesized in sensory neurons, secreted from afferent nerve terminals and stimulate the proliferation of competent cells.
The motor and sensory connections of the cervical vagus nerve and of its inferior ganglion (nodose ganglion) have been traced in the medulla oblongata of 32 adult cats with the neuroanatomical methods of horseradish peroxidase (HRP) histochemistry and amino acid autoradiography (ARG). In 14 of these subjects, an aqueous solution of HRP was applied unilaterally to the central end of the severed cervical vagus nerve. In 13 other cases, HRP was injected directly into the nodose ganglion. Three of these 13 subjects had undergone infranodose vagotomy 6 weeks prior to the HRP injection. A mixture of tritiated amino acid was injected into the nodose ganglion in five additional cats. The retrograde transport of HRP yielded reaction product in nerve fibers and perikarya of parasympathetic and somatic motoneurons in the medulla oblongata. Furthermore, a tetramethyl benzidine (TMB) method for visualizing HRP enabled the demonstration of anterograde and transganglionic transport, so that central sensory connections of the nodose ganglion and of the vagus nerve could also be traced. The central distribution of silver grain following injections of tritiated amino acids in the nodose ganglion corresponded closely with the distribution of sensory projections demonstrated with HRP, thus confirming the validity of HRP histochemistry as a method for tracing these projections. The histochemical and autoradiographic experiments showed that the vagus nerve enters the medulla from its lateral aspect in multiple fascicles and that it contains three major components--axons of preganglionic parasympathetic neurones, axons of skeletal motoneurons, and central processes of the sensory neurons in the nodose ganglion. Retrogradely labeled neurons were seen in the dorsal motor nucleus of X(dmnX), the nucleus ambiguus (nA), the nucleus retroambigualis (nRA), the nucleus dorsomedialis (ndm) and the spinal nucleus of the accessory nerve (nspA). The axons arising from motoneurons in the nA did not traverse the medulla directly laterally; rather, all of these axons were initially directed dorsomedially toward the dmnX, where they formed a hairpin loop and then accompanied the axons of dmnX neurons to their points of exit. Afferent fibers in the vagus nerve reached most of the subnuclei of the nTS bilaterally, with the more intense labeling being found on the ipsilateral side. Labeling of sensory vagal projections was also found in the area postrema of both sides and around neurons of the dmnX. These direct sensory projections terminating within the dmnX may provide an anatomical substrate for vagally mediated monosynpatic reflexes. Following deefferentiation by infranodose vagotomy 6 weeks prior to HRP injections into the nodose ganglion, a number of neurons in the dmnX were still intensely labeled with the HRP reaction product. The axons of these HRP-labeled perikarya may constitute the bulbar component of the accessory nerve.
The effects of the neonatal administration of capsaicin on substance P (SP) immunoreactivity of the vagal sensory ganglion (nodose ganglion) and the CNS site of termination of vagal afferents (nucleus of the solitary tract-NTS) were evaluated with immunocytochemistry and radioimmunoassay. The SP content of the nodose ganglion was reduced by 58%, and a loss of immunoreactive cell bodies was found in capsaicin treated rats. Regional differences were found in the effects of capsaicin treatment on the SP immunoreactivity in the NTS. Whereas the SP in the medial portions of the nucleus was not altered, a reduction of SP immunoreactivity in the lateral portions of the nucleus was shown with immunocytochemistry and with radioimmunoassay. The data confirm that at least a portion of the vagal afferent cell bodies of the nodose ganglion and their projections to the brainstem are capsaicin sensitive. The finding that the SP in the lateral NTS is depleted by capsaicin administration may be of importance in the use of capsaicin in functional studies, particularly of the role of SP containing vagal afferents in respiration.
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The nodose ganglion contains the cell bodies of afferent nerves which convey predominantly sensory information from the viscera to the central nervous system (CNS). Autoradiographic studies show binding sites for beta-adrenoceptor ligands are present on sections of the rat nodose ganglion and also on the corresponding inferior vagal ganglion in humans, indicating the presence of beta-adrenoceptors in these ganglia. Since prolonged stimulation of beta-adrenoceptors in rats with the nonselective beta-adrenoceptor agonist isoprenaline (400 micrograms kg-1 day-1 s.c.) for 14 days results in desensitisation and/or down-regulation of receptors in peripheral tissues, such as heart, kidney and blood vessels, the effects of this treatment on the beta-adrenoceptor population on the nodose ganglion have been examined. Using [125I]-pindolol as a radioligand, autoradiographic studies revealed that specific binding was reduced by 74% in ganglia from isoprenaline-pretreated rats compared to that in ganglia from vehicle-pretreated rats, demonstrating down-regulation of receptors by isoprenaline. [125I]-Pindolol binding was sensitive to inhibition by ICI 118.551 (selective beta 2-adrenoceptor antagonist) but not to atenolol (selective beta 1-adrenoceptor antagonist), indicating receptors are predominantly of the beta 2-adrenoceptor subtype. No change in binding was apparent over the vagus nerve. The nodose ganglion appears to be an additional site at which beta 2-adrenoceptors may be down-regulated in vivo, possibly interfering with normal baro-, chemo- and sensory reflexes.
The nodose ganglion contains placode-derived visceral sensory neurons of the vagus nerve. Previous study showed that axotomy-induced deafferentation reduced the number of tyrosine hydroxylase-immunoreactive and increased the number of vasoactive intestinal peptide-immunoreactive neurons in the ganglion. The present study was conducted to determine whether the changes in neuropeptide/neurotransmitter enzyme content are associated with changes in the expression of tyrosine hydroxylase and vasoactive intestinal peptide messenger RNAs in the nodose ganglion. We used in situ hybridization histochemistry with 35S-labeled oligonucleotide probes for tyrosine hydroxylase and vasoactive intestinal peptide precursor messenger RNAs. Peripheral axotomy of visceral afferent inputs reduced tyrosine hydroxylase messenger RNA and increased vasoactive intestinal peptide messenger RNA expression in neurons of the nodose ganglion of the rat. The number of tyrosine hydroxylase messenger RNA-containing neurons was significantly reduced at three, seven and 14 days after axotomy-induced deafferentation compared with intact and sham-operated controls. Labeling density of tyrosine hydroxylase messenger RNA-containing neurons was significantly reduced at three and seven days. Conversely, the number of vasoactive intestinal peptide messenger RNA-containing neurons increased significantly at three, seven and 14 days, while the labeling density of vasoactive intestinal peptide messenger RNA-containing neurons also increased at one, three, seven and 14 days. The results of the present study indicate that the axotomy-induced down-regulation of tyrosine hydroxylase and up-regulation of vasoactive intestinal peptide in the neurons of the nodose ganglion are associated with changes in their messenger RNAs in response to axotomy-induced deafferentation.
The nucleoli of rat nodose ganglion were investigated during a 24-h span (light span 07.00-19.00 h). The mean volume of nucleoli and that of their components, especially fibrillar centers considered to be the interphasic counterpart of nucleolus-organizing regions, were determined by stereological analysis. The quantitative data showed that (1) nucleoli volumes of rat nodose ganglion neurons did not oscillate diurnally but that (2) there were diurnal dimensional changes in the volume of their fibrillar centers which strongly suggest an ultradian rhythmicity. These results are different from those obtained in studies of superior cervical ganglion neurons, in which nucleoli and nucleolar components followed a circadian rhythm with peak values during daily periods of darkness. Although the nucleoli of these 2 kinds of neurons involved in autonomic nervous system reactions do not show the same behavioural patterns, the present data bring to light a new example of circadian fluctuation in nucleoli and describes their organization in this respect.
The sensory neurons of the nodose ganglion are the classic example of a population of peripheral nervous system neurons that do not require nerve growth factor (NGF) for survival during development but are dependent on other neurotrophins. We have re-examined this assertion by studying the development of the nodose ganglion of mice that have a null mutation in the NGF gene. Compared with wild-type embryos, the number of neurons undergoing apoptosis was elevated in NGF -/- mice, resulting in a significant reduction in the total number of neurons in the ganglion by the end of embryonic development. TrkA, the NGF receptor tyrosine kinase, was expressed in the nodose ganglion throughout development and there was a marked decrease in TrkA mRNA expression in the nodose ganglion of NGF -/- embryos. Although the in vitro survival of the majority of nodose neurons was promoted by brain-derived neurotrophic factor (BDNF), a minor proportion was supported by NGF in cultures established over a range of embryonic stages. These results clearly demonstrate that a subset of nodose ganglion neurons depends on NGF for survival during development. The finding that the expression of tyrosine hydroxylase (TH) mRNA was unaffected in the nodose ganglia of NGF-deficient embryos indicates that this NGF-dependent subset is distinct from the subset of catacholaminergic neurons in the nodose ganglion.
The present study was attempted to examine if mu-opioid receptor (MOR) might be transported by axonal flow peripherally through peripheral axons of somatic sensory ganglion neurons. After unilateral ligation of the sciatic nerve or the vagus nerve distal to the dorsal root ganglion (DRG) or nodose ganglion (NG), MOR-like immunoreactivity (MOR-LI) of neuronal cell bodies in the DRG of the fourth and fifth lumbar nerves, NG, ambiguus nucleus (Amb) and dorsal motor nucleus of the vagus nerve (DMV) on the side of the ligation was apparently reduced within 1 week after the nerve ligation. However, within 24 h after the nerve ligation, a transient enhancement of MOR-LI was observed in cell bodies of DRG neurons, sciatic nerve stump proximal to the ligature, and cell bodies of NG neurons on the side of the ligation; such a transient enhancement of MOR-LI was not detected in the Amb and DMV. The results suggest that MOR undergoes centrifugal axonal flow in peripheral axons of somatic and visceral sensory ganglion neurons, and that MOR synthesis in sensory ganglion neurons is vulnerable to damage of the peripheral axons.
The calcium current components of acutely dissociated nodose ganglion neurons were characterized using the whole-cell variation of the patch-clamp technique. Many neurotransmitters regulate neuronal calcium currents via GTP binding (G) proteins and in some cases affect calcium current components selectively. To determine whether G proteins regulated these current components in the absence of ligand binding, recording pipettes contained 0.1 mM GTP, guanosine 5'-O-(thiodiphosphate) (GDP-beta-S), or guanosine 5'-O-(thiotriphosphate) (GTP-gamma-S). Nodose ganglion neurons had three calcium current components, similar to T, N, and L current components found in other sensory neurons. Isolated T currents did not diminish in magnitude during a 20-min recording, but there was a progressive loss of currents containing the N and L current components. The reduction of current magnitude was primarily dependent on the extent of intracellular dialysis and not on the holding potential (Vh) or stimulus frequency. When GDP-beta-S was substituted for GTP in the pipette solution, there was no change in the T current or in the rate of run-down of N and L current components. Substitution of GTP-gamma-S for GTP in the pipette solution resulted in a moderate (approximately 40%) loss of isolated T current. This effect was most evident on T currents evoked at relatively positive clamp potentials (Vc, -30 to -15 mV) and occurred relatively late (approximately 10 min) in the recording. In the presence of GTP-gamma-S, currents evoked from Vh = -80 mV, containing the N and L current components, were reduced 40-60%, with a lesser effect on those currents evoked from Vh = -40 mV, containing primarily the L current component. The average time to peak current (Ip) was increased 3-4-fold in the presence of GTP-gamma-S, and the Vc at which the maximal peak current was evoked was shifted +10 to 20 mV. These effects were evident within 2-5 min after initiation of the whole-cell recording. Pretreatment of neurons with pertussis toxin attenuated or blocked the effects of GTP-gamma-S. We conclude that nodose ganglion neurons have T-, N-, and L-type calcium current components, which had different stability during whole-cell recording. Activation of G proteins with GTP-gamma-S reduced N greater than T much greater than L currents, effects reduced in the presence of pertussis toxin. Thus, the calcium current components of nodose ganglion neurons were regulated by cytosolic constituents and by Gi- or Go- type G proteins.
To understand the dependence of primary sensory neurons on neurotrophic factors, we examined the distribution and colocalization of mRNAs for receptors of nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) family ligands in dorsal root ganglion (DRG) and nodose ganglion (NG) neurons of adult rats by in situ hybridization (ISH) histochemistry using serial sections. About 35, 10, and 20% of the lumbar DRG neurons expressed trkA, trkB and trkC mRNAs, respectively. Messenger RNA signals for c-ret, a common signaling receptor of GDNF family ligands, were seen in about 60% of DRG neurons, and some of these neurons expressed trkA, trkB, or trkC mRNAs. Most (97%) of the DRG neurons observed were positive to at least one of these four mRNAs. About 50, 20, and 20% of DRG neurons expressed GDNF family receptor alpha1 (GFR alpha1), GFR alpha2, and GFR alpha3 mRNAs, respectively, and most of these neurons were positive to c-ret mRNA. Interestingly, GFR alpha2 and GFR alpha3 mRNA signals were frequently seen in the same neurons, which lack GFR alpha1 mRNA signals. On the other hand, 98% of NG neurons expressed trkB mRNA and 30-40% of NG neurons co-expressed c-ret and GFR alpha1 mRNAs. However, mRNA signals for other receptors (TrkA, TrkC, GFR alpha2, GFR alpha3) were seen in only a few NG neurons. These findings suggest that all the DRG neurons in adult rats depend on at least one of the NGF and GDNF family ligands, and that some DRG neurons depend on two ligands or more. In contrast, NG neurons were suggested to be divided into two major groups; one group depends on brain-derived neurotrophic factor (BDNF)/neurotrophin-4/5 (NT-4/5), and the other depends on both BDNF/NT-4/5 and GDNF.
Placode-derived general visceral afferent neurons of the nodose ganglion transmit visceral sensory information from specialized sensory endings of the vagus nerve and its branches to the nucleus of the solitary tract. These neurons are critical in relaying information such as elevations in blood pressure, changes in blood oxygenation, passage of contents through the esophagus and intestines, and distention of the heart, stomach, and lungs to the CNS for reflex maintenance of visceral functions. Multiple neurotransmitters, neuropeptides, calcium binding proteins, and other neuroactive substances are associated with neurons of the nodose ganglion. Many neurons colocalize 2 or more neuroactive substances creating the potential for complex interactions of neurochemical signals in the NTS. Neurons of the nodose ganglion also contain a variety of receptors which respond to transmitters, inflammatory mediators, and neurotrophic factors. The contents of these neurochemicals and receptors are not static as alterations in their expression are noted in response to epigenetic influences. Although not yet well understood, potential factors and mechanisms regulating neurochemical events in the nodose ganglion neurons are discussed.
The ability of angiotensin II (A II) and 5-hydroxytryptamine (5-HT) to depolarise the rat isolated nodose ganglion preparation was examined. 5-HT depolarised the nodose ganglion, both at room temperature (20-24 degrees C) and at 35-37 degrees C. However, A II depolarised the nodose ganglion only under the latter condition, and these responses were blocked by the A II receptor antagonist saralasin. This study extends previous findings which have demonstrated A II binding sites on the nodose ganglion and axon, and identifies the rat nodose ganglion as a sensitive preparation in which to study the interactions between neuronal A II receptor activation and its blockade by A II receptor antagonists.
In the rabbit, as in various other species, the presence of a cholinergic vagal afferent contingent has been demonstrated previously using biochemical and immunohistological approaches at the nodose ganglion level, where vagal afferent cell bodies are located. This structure is completely devoid of synaptic contacts. In the present study, somatic acetylcholine release is demonstrated on different types of in vitro rabbit nodose ganglion preparations (fragments of nodose tissue or isolated cell bodies) using chemiluminescent detection. Acetylcholine endogenous content was measured and was shown to be greater in the right nodose ganglion compared to the left. This difference was also observed when spontaneous and potassium chloride-evoked acetylcholine release was measured in extracellular fluid after a 15-min incubation of nodose ganglion fragments. Calcium removal totally blocked this somatic release. A kinetic study of acetylcholine release was also performed by placing the samples (nodose ganglion fragments or isolated cell bodies) directly in front of the photomultiplier, allowing the direct monitoring of (acetylcholine + choline) and choline effluxes. The net acetylcholine release was then deduced by subtraction. Identical kinetics was obtained with the two different nodose ganglion preparations used. This somatic release is calcium-dependent. The occurrence of acetylcholine release at the nodose ganglion level is discussed in comparison with the events occurring in the cholinergic nerve endings. These mechanisms could be implicated in the premodulation of the vagal afferent messages conveyed from the periphery to the central nervous system.
Morphometric studies were carried out on the chick nodose ganglion between day 5 of incubation and 2 weeks after hatching. Previous findings showed that ablation of the nodose placode, the locus of precursor cells of nodose ganglion sensory neurons, results in abnormal cardiac function, and that these precursors can be induced to migrate abnormally to the heart and express abnormal phenotypes there, following cardiac neural crest ablation. These results prompted us to investigate further the normal development of nodose ganglion neurons. We find that the major period of neuron generation from placodal precursor cells in the ganglion occurs prior to day 5 of incubation. The loss of more than half of these neurons takes place between embryonic days 5 and 20, while neuron and ganglion sizes increase dramatically. Myelination is not seen at day 12 of incubation, but is present on day 15. Neurons continue to develop after hatching (day 21), reaching their adult size by 2 weeks after hatching. Unexpectedly, we found that the number of neurons increases after hatching, reaching the adult level of 62% more than embryonic day-20 numbers by 2 weeks after hatching. The mechanisms underlying the increase in neuron number after hatching are unexplained and require further investigation.
Previous work showed that axotomy-induced deafferentation of the placode-derived visceral afferent neurons of the nodose ganglion altered their expression of some neuropeptides and tyrosine hydroxylase. The present studies were designed to selectively evaluate the loss of axonal transport on the numbers of vasoactive intestinal polypeptide, tyrosine hydroxylase, and calcitonin gene-related peptide mRNA-containing and immunoreactive neurons in the nodose ganglion of the adult rat. Vinblastine (0.15 mM) application to the cervical vagus nerve was used to block axonal transport between ganglionic perikarya and peripheral targets. In situ hybridization histochemistry with 35S-labeled oligonucleotide probes was used to both quantify the number of mRNA-containing neurons and to assess the density of mRNA expression per neuron, and immunocytochemistry was used to visualize the number of immunoreactive neurons. The efficacy of vinblastine to inhibit axonal transport was verified by evaluating the build-up of calcitonin gene-related peptide immunoreactive in the vagus nerve immediately rostral to the site of drug application. The absence of vinblastine-induced neuronal damage was verified by the relative absence of degenerating nerves in the vagus nerve caudal to the site of drug application. Vinblastine treatment of the vagus nerve increased the numbers of vasoactive intestinal peptide mRNA-containing neurons and vasoactive intestinal peptide-immunoreactive neurons in the nodose ganglion at three, seven and 14 days, and increased the numbers of calcitonin gene-related peptide mRNA-containing and calcitonin gene-related peptide-immunoreactive neurons in the nodose ganglion at one, three and seven days. The average labeling density of vasoactive intestinal peptide mRNA-containing neurons was also increased following vinblastine treatment. Vinblastine treatment of the cervical vagus nerve, however, led to the appearance of low-labeling density calcitonin gene-related peptide mRNA-neurons and resulted in reduction of the average labeling density for calcitonin gene-related peptide mRNA-containing neurons. In contrast, application of vinblastine to the cervical vagus nerve, decreased the number of tyrosine hydroxylase mRNA-containing and tyrosine hydroxylase-immunoreactive neurons in the nodose ganglion. In summary, inhibition of the axoplasmic transport between the periphery and the visceral sensory perikarya appeared to alter vasoactive intestinal peptide, calcitonin gene-related peptide, and tyrosine hydroxylase expression and content in visceral sensory neurons of the nodose ganglion. These data suggest the presence of an axonally transported influence on the regulation of neuropeptide and neurotransmitter enzyme synthesis in mature placode-derived visceral sensory neurons.
The nodose ganglion is the distal cranial ganglion of the vagus nerve which provides sensory innervation to the heart and other viscera. In this study, removal of the neuronal precursors which normally populate the right nodose ganglion was accomplished by ablating the right nodose placode in stage 9 chick embryos. Subsequent histological evaluation showed that in 54% of lesioned embryos surviving to day 6, the right ganglion was absent. Most embryos surviving to day 12, however, had identifiable right ganglia. In day 12 embryos, the right ganglion which developed was abnormal, with ganglion volume and ganglion cell diameter reduced by 50% and 20%, respectively, compared to control ganglia. To investigate the source of the neuron population in the regenerated ganglion, we combined nodose placode ablation with bilateral replacement of chick with quail "cardiac" neural crest (from mid-otic placode to somite 3). These cells normally provide only non-neuronal cells to the nodose ganglion, but produce neurons in other regions. At day 9, quail-derived neurons were identified in the right nodose ganglia of these chimeras, indicating that cardiac neural crest cells can generate neurons in the ganglion when placode-derived neurons are absent or reduced in number. On the other hand, we found that "sympathetic" neural crest (from somites 10 to 20) does not support ganglion development, suggesting that only neural crest cells normally present in the ganglion participate in reconstituting its neuronal population. Our previous work has shown that right nodose placode ablation produces abnormal cardiac function, which mimics a life-threatening human heart condition known as long QT syndrome. The present results suggest that the presence of neural crest-derived neurons in the developing right nodose ganglion may contribute to the functional abnormality in long QT syndrome.