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In order to investigate how the ganglia in ganglionated plexus were distributed throughout the overall region of the gallbladder, the gallbladder was dissected from guinea-pig and washed with Krebs solution via the cystic duct. This gallbladder was distended with 2 ml of the mixed solution of OsO4 and ZnI2 injected with a syringe via the cystic duct and the cystic duct was immediately tied with a thread. The gallbladder was placed in excess of the mixed solution for 7-10 hours. The gallbladder was longitudinally divided into two approximately equal parts and each was prepared for microscopic investigation. The one preparation was the ventral side of the gallbladder and the other preparation was its dorsal side. These preparations were viewed through a photomicroscope. The obtained results were as follows: 1. Ganglia which involved several nerve cells were observed. Ganglia and nerve bundles connecting the fellow ganglia formed an irregular network, that is, the so-called ganglionated plexus. These nerve bundles were connected with the perivascular nerves which ran parallel to and around blood vessels in several places of the wall of the gallbladder. 2. Ganglia were full of variety in size and shape. That is to say, the shape of ganglia is arranged in various patterns such as oval, spherical, triangular, square and so on. When the size of ganglia were shown by surface area of ganglia which were viewed within the sweep of photomicroscope, the size of ganglia were divided into three large groups, the small ganglia in the range of 1,400 microns2-3,500 microns 2, the large ganglia in the range of 3,500 microns2-10,000 microns2 and the extra-large ganglia in the range of 10,000 microns2-38,000 microns2. Per one gallbladder, 240 +/- 41 (n = 3) small ganglia, 263 +/- 28 (n = 3) large ganglia and 8 +/- 1 (n = 3) extra-large ganglia were found. And these ganglia were irregularly scattered all over the wall of gallbladder. Small ganglia were found more numerous than large ganglia in the cervical portion of the gallbladder. On the other hand, small ones were slightly fewer than large ganglia in the remainder portion of the gallbladder. 3. The ganglionated plexus contained 511 +/- 69 (n = 3) ganglia.(ABSTRACT TRUNCATED AT 400 WORDS)
The expression of inducible and constitutive heme oxygenase and biliverdin reductase was studied in normal and cultured peripheral ganglia from adult rats, using immunocytochemistry and in situ hybridization. Dramatic changes were induced by one to two days' culturing of dorsal root ganglia, nodose ganglia, otic ganglia, sphenopalatine ganglia and superior cervical ganglia. An up-regulation of inducible heme oxygenase was found in satellite cells of the cultured nodose ganglia, dorsal root ganglia, sphenopalatine ganglia and otic ganglia, whereas only a few satellite cells in the superior cervical ganglia responded with an increase in inducible heme oxygenase immunoreactivity. In the superior cervical ganglia inducible heme oxygenase also appeared in a subpopulation of macrophages. During culturing, expression of inducible heme oxygenase immunoreactivity also increased in axons and in nerve cell bodies. In situ hybridization corroborated the immunocytochemical findings, revealing a strong up-regulation of inducible heme oxygenase messenger RNA in satellite cells, and less pronounced up-regulation in nerve cell bodies. Constitutive heme oxygenase immunoreactivity was found in most neurons in all of the ganglia studied. No significant changes in constitutive heme oxygenase immunoreactivity could be observed in cultured ganglia. Biliverdin reductase immunoreactivity was barely detectable in any of the normal ganglia; however, after culturing it appeared in axons, single nerve cell bodies and nerve cell nuclei. The results show that inducible heme oxygenase is up-regulated in peripheral ganglia after axonal injury, and suggest a role for carbon monoxide in cellular signaling and a requirement for the antioxidant (bilirubin) during the regeneration process.
The involvement of the basal ganglia in motor functions has been well studied. Recent neurophysiological, clinical and behavioral experiments indicate that the basal ganglia also process non-noxious and noxious somatosensory information. However, the functional significance of somatosensory information processing within the basal ganglia is not well understood. This review explores the role of the striatum, globus pallidus and substantia nigra in nociceptive sensorimotor integration and suggests several roles of these basal ganglia structures in nociception and pain. Electrophysiological experiments have detailed the non-nociceptive and nociceptive response properties of basal ganglia neurons. Most studies agree that some neurons within the basal ganglia encode stimulus intensity. However, these neurons do not appear to encode stimulus location since the receptive fields of these cells are large. Many basal ganglia neurons responsive to somatosensory stimulation are activated exclusively or differentially by noxious stimulation. Indirect techniques used to measure neuronal activity (i.e., positron emission tomography and 2-deoxyglucose methods) also indicate that the basal ganglia are activated differentially by noxious stimulation. Neuroanatomical experiments suggest several pathways by which nociceptive information may reach the basal ganglia. Neuroanatomical studies have also indicated that the basal ganglia are rich in many different neuroactive chemicals that may be involved in the modulation of nociceptive information. Microinjection of opiates, dopamine and gamma-aminobutyric acid (GABA) into the basal ganglia have varied effects on pain behavior. Administration of these neurochemicals into the basal ganglia affects supraspinal pain behaviors more consistently than spinal reflexive behaviors. The reduction of pain behavior following electrical stimulation of the substantia nigra and caudate nucleus provides additional evidence for a role of the basal ganglia in pain modulation. Some patients with basal ganglia disease (e.g., Parkinson's disease, Huntington's disease) have alterations in pain sensation in addition to motor abnormalities. Frequently, these patients have intermittent pain that is difficult to localize. Collectively, these data suggest that the basal ganglia may be involved in the (1) sensory-discriminative dimension of pain, (2) affective dimension of pain, (3) cognitive dimension of pain, (4) modulation of nociceptive information and (5) sensory gating of nociceptive information to higher motor areas. Further experiments that correlate neuronal discharge activity with stimulus intensity and escape behavior in operantly conditioned animals are necessary to fully understand how the basal ganglia are involved in nociceptive sensorimotor integration.
Neuropeptide-like immunoreactivity to antisera raised against Leu- and Met-enkephalin, vasoactive intestinal peptide (VIP), neuropeptide Y (NPY) and substance P (SP) have been studied immunohistochemically in middle cervical and stellate ganglia of dogs. To investigate the relationship of the peptides to one another as well as to preganglionic and postganglionic neurons, intact and chronically decentralized middle cervical and stellate ganglia were studied. Ganglia were processed for immunohistochemistry in unoperated dogs and in dogs two weeks after unilateral ganglionic decentralization. The immunoreactivity for each peptide had a characteristic distribution in the ganglia. These distributions differed from one another and from the distribution of cardiac postganglionic sympathetic neurons. Camera lucida drawings of peptide distributions were made to compare different peptides and counts were made to determine the percentages of cells immunoreactive for a given peptide. The results demonstrated that enkephalin-like immunoreactivity in axons was present in both the stellate and middle cervical ganglia, but was heaviest in the caudal 2/3 of the stellate ganglia. Enkephalin-like immunoreactive fibers formed pericellular baskets around stellate ganglion neurons. VIP-like immunoreactive cell bodies and processes were distributed sparsely, but widely, in the stellate ganglia and to a lesser extent in the middle cervical ganglia. One of two commercial antisera to SP resulted in immunoreactive staining of cell bodies and processes in the stellate ganglia. SP-like immunoreactivity in neurons represented about 10% or less of the cells in the stellate ganglia. At least 80-85% of the neurons in the stellate and middle cervical ganglia were immunoreactive for NPY antisera. Decentralization eliminated enkephalin-like immunoreactive staining in the middle cervical and stellate ganglia, but not the VIP-, NPY- and SP-like immunoreactive staining of neurons in these ganglia. In summary, the enkephalin-like immunoreactive axons in the thoracic autonomic ganglia appear to be derived from extrinsic neurons, most likely from preganglionic spinal neurons. VIP-, SP- and NPY-like immunoreactivity were not significantly affected by decentralization. The results provide anatomical evidence for substrates related to neuropeptidergic synaptic mechanisms in thoracic autonomic ganglia.