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Localization of bursicon in CCAP-immunoreactive cells in the thoracic ganglia of the cricket Gryllus bimaculatus

Bursicon is a neuropeptide that induces tanning of the cuticle in freshly moulted insects. In an earlier investigation, we demonstrated that bursicon activity can be detected throughout the ventral nerve cord of the cricket Gryllus bimaculatus. This study aims at identifying the neurosecretory cells within the thoracic ganglia that produce bursicon. When homogenates of anterior pieces of thoracic ganglia were separated using SDS gel electrophoresis, proteins with bursicon activity could be eluted only from a slice of the gel spanning the 28-33 kDa region. In the anterior lateral cortex of the thoracic ganglia, there are two bilaterally paired neurosecretory cells with large vacuoles that project contralaterally to neurohaemal release sites associated with segmental nerves N5 and N6. These cells and their processes in N5 and N6 were labelled using antisera against crustacean cardioactive peptide (CCAP). The cell projecting into N6 showed a Tyndall effect (i.e. appeared opaque under oblique illumination) in older adults, and single isolated somata contained bursicon activity. Homogenates of nerves N5 and N6 also showed bursicon activity, but neither bursicon activity nor CCAP-immunoreactive processes were found in segmental nerve N4. The thoracic connectives, which contain three major CCAP-immunoreactive processes, also showed bursicon activity. Homogenates of posterior pieces of the thoracic ganglia did not contain bursicon activity. Western blots demonstrated that the anti-CCAP serum does not recognize the 30 kDa bursicon-active protein fraction. These results suggest that a CCAP-like neuropeptide and a protein with bursicon activity are co-localized in the anterior lateral neurosecretory cells of the thoracic ganglia and in their segmental homologues in the other ganglia. Additionally, we have shown using western blots that a monoclonal antibody raised against a 56 kDa protein from the housefly Musca domestica, a protein thought to be bursicon, does not label the 30 kDa bursicon-active protein of crickets. However, this antibody does label an unidentified 56 kDa protein isolated from anterior as well as posterior pieces of thoracic ganglia.

Journal Article↗

Anterior cruciate ligament ganglia and mucoid degeneration: coexistence and clinical correlation.

OBJECTIVE: The purpose of our study was to describe the MR appearance and coexistence of anterior cruciate ligament ganglia with mucoid degeneration and to address the clinical significance of these entities. MATERIALS AND METHODS: A database search of 4221 knee MRI examinations over 2 years revealed 90 examinations with reported anterior cruciate ligament ganglion or mucoid degeneration. Imaging criteria for ligament ganglion included fluid signal in the ligament disproportionate to joint fluid showing mass effect on intact ligament bundles. The size, location, complexity, and degree of lobulation of ganglia were recorded. Criteria for mucoid degeneration included ligament bundles poorly seen on T1-weighted and proton density-weighted images but with both bundles seen as intact on T2-weighted images. Intraosseous cysts at the ligament attachments and presence of joint effusion were noted. Clinical assessment of ligament instability was recorded when available. RESULTS: Of 74 examinations that met imaging criteria, 56 (76%) had discrete intraligamentous ganglia, 18 (24%) had mucoid degeneration, and 26 (35%) had features of both. Ganglia were located in the proximal ligament in 16 examinations (22%) and the distal ligament in 10 (14%) and involved the entire ligament in 30 (40%). Ganglia ranged in maximum diameter from 20 to 73 mm (mean, 31 mm). Complexity of ganglia was mild (41%), moderate (39.2%), or marked (19.8%). Intraosseous cysts were noted proximally in 48 examinations (65%) and distally in 20 (27%). Of 52 patients with accessible records, 48 had no clinical evidence of instability. Twelve patients who underwent arthroscopy had an intact anterior cruciate ligament at that time. CONCLUSION: Anterior cruciate ligament ganglia and mucoid degeneration commonly coexist on MRI and are typically not associated with ligament instability.

Adult↗

Development of a reverse transcriptase-polymerase chain reaction assay to detect feline herpesvirus-1 latency-associated transcripts in the trigeminal ganglia and corneas of cats that did not have clinical signs of ocular disease.

OBJECTIVE: To develop a reverse transcriptase-polymerase chain reaction (RT-PCR) assay to detect feline herpesvirus-1 (FHV-1) latency-associated transcripts (LATs) in the corneas and trigeminal ganglia of cats that did not have clinical signs of ocular disease. SAMPLE POPULATION: Corneas and trigeminal ganglia obtained from 21 cats necropsied at the Indiana Animal Disease Diagnostic Laboratory and 25 cats euthanatized at a humane shelter; none of the cats had a recent history of respiratory tract or ocular disease, and all had normal results for ophthalmic examinations. PROCEDURE: Both corneas and both trigeminal ganglia were harvested from each cat. An initial PCR assay detected FHV-1 DNA in the corneas and trigeminal ganglia. The RNA was then isolated from samples positive for FHV-1 DNA, and an RT-PCR assay was used to detect LATs. RESULTS: FHV-1 DNA was detected in 45 of 92 (48.9%) corneas and 38 of 92 (41.3%) trigeminal ganglia. In many samples, the RNA had degraded and RT-PCR assay was not possible. Of the samples subjected to RT-PCR assay, none of the 39 corneas but 4 of 16 trigeminal ganglia had positive results when tested for LATs. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of the results indicated that a high percentage of cats that did not have clinical signs of ocular disease had detectable FHV-1 DNA in their corneas and trigeminal ganglia. This study documents that the RT-PCR assay can successfully identify LATs and may serve as a tool to better understand the biologic characteristics of FHV-1 and its relationship to clinical disease.

Alphaherpesvirinae↗

Detection of HSV-I nucleic acids in rat vestibular ganglia.

Rats were infected with HSV-I through the middle ear. DNA and RNA were extracted from the vestibular ganglia, trigeminal ganglia, cerebrum, cerebellum and brainstem in the productive or latent state after inoculation. DNA and RNA were applied for polymerase chain reaction (PCR) to detect HSV-I genomes. In particular, in the RNA PCR, the latent-associated transcript (LAT) mRNA, which is said to be present in the cervical or trigeminal ganglia at much lower levels during the productive state, was detected. In the productive state, DNA was clearly detected in all samples whereas LAT was detected only in the trigeminal ganglion on the inoculated side, cerebrum and cerebellum. In the latent state, DNA was detected in the vestibular ganglion only on the inoculated side, bilateral trigeminal ganglia, cerebrum, cerebellum and brainstem; LAT was detected in the vestibular ganglion on the inoculated side, the bilateral trigeminal ganglia and brainstem. These data indicate that HSV-I can establish latent infection in the vestibular ganglia in a similar way as in the cervical or trigeminai ganglia.

Animals↗

Contributions of placodal and neural crest cells to avian cranial peripheral ganglia.

The method of embryonic tissue transplantation was used to confirm the dual origin of avian cranial sensory ganglia, to map precise locations of the anlagen of these sensory neurons, and to identify placodal and neural crest-derived neurons within ganglia. Segments of neural crest or strips of presumptive placodal ectoderm were excised from chick embryos and replaced with homologous tissues from quail embryos, whose cells contain a heterochromatin marker. Placode-derived neurons associated with cranial nerves V, VII, IX, and X are located distal to crest-derived neurons. The generally larger, embryonic placodal neurons are found in the distal portions of both lobes of the trigeminal ganglion, and in the geniculate, petrosal and nodose ganglia. Crest-derived neurons are found in the proximal trigeminal ganglion and in the combined proximal ganglion of cranial nerves IX and X. Neurons in the vestibular and acoustic ganglia of cranial nerve VIII derive from placodal ectoderm with the exception of a few neural crest-derived neurons localized to regions within the vestibular ganglion. Schwann sheath cells and satellite cells associated with all these ganglia originate from neural crest. The ganglionic anlagen are arranged in cranial to caudal sequence from the level of the mesencephalon through the third somite. Presumptive placodal ectoderm for the VIIIth, the Vth, and the VIIth, IXth, and Xth ganglia are located in a medial to lateral fashion during early stages of development reflecting, respectively, the dorsolateral, intermediate, and epibranchial positions of these neurogenic placodes.

Animals↗

Immunohistochemical localization of the high-affinity NGF receptor (gp140-trkA) in the adult human dorsal root and sympathetic ganglia and in the nerves and sensory corpuscles supplying digital skin.

BACKGROUND: Nerve growth factor (NGF) is produced in target tissues of sympathetic and neural-crest derived sensory neurons, including skin, to provide them trophic support. The biological effects of NGF on responsive cells are mediated by specific high-affinity receptors. Recently, a protein tyrosine kinase of congruent to 140 kDa molecular weight, encoded by the proto-oncogene trkA, has been identified as the high-affinity NGF receptor (gp140-trkA). The present work was undertaken to study the localization of gp140-trkA-like immunoreactivity (IR) in human peripheral ganglia (sympathetic and dorsal root ganglia), and in glabrous skin. METHODS: Lumbar dorsal root ganglia, para- and prevertebral sympathetic ganglia, and digital glabrous skin were studied immunohistochemically using a rabbit anti-gp140-trkA polyclonal antibody. In order to accurately establish the localization of gp140-trkA IR, the neurofilament proteins and S-100 protein were studied in parallel in: (1) sensory and sympathetic ganglia, to label neuron cell bodies and satellite or supporting cells, respectively; (2) human skin, to label axons, Schwann and related cells within nerves and sensory corpuscles. Moreover, a quantitative study (neuron size, intensity of immunostaining) was carried out on sympathetic and dorsal root ganglia neuron cell bodies. RESULTS: A specific gp140-trkA-like IR was found in: (1) a subpopulation (65%) of primary sensory neuron cell bodies, including most of the large-sized ones but also small- and intermediate-sized ones; (2) most of sympathetic neuron cell bodies (82%); (3) the perineurial cell, Schwann cells, and large axons of the nerve trunks supplying digital skin; (4) the lamellar cells of Meissner corpuscles; (5) the central axon, inner-core, outer-core, and capsule of Pacinian corpuscles. In addition, the occurrence of gp140-trkA-like IR was observed in some non-nervous tissues of the skin, including epidermis (mainly in the basal layer), sweat glands, and arterial blood vessels. CONCLUSIONS: Present results provide evidence for the localization of gp140-trkA-like IR in: (1) nerve cells which are known to be NGF-responsive, and (2) non-nervous cutaneous tissues which are innervated by NGF-dependent peripheral neurons. These findings suggest that, in addition to the well-established role of NGF on sensory and sympathetic neurons, this neurotrophin may be able to regulate some other functions on non-nervous cells which are targets for NGF-dependent peripheral neurons.

Adult↗

Structure, afferent innervation, and transmitter content of ganglia of the guinea pig gallbladder: relationship to the enteric nervous system.

Although a well-developed plexus of nerves and ganglia is known to be present in the wall of the gallbladder, little has previously been learned about the function or organization of this innervation. The current study was undertaken in order to evaluate the hypothesis that the ganglionated plexus of the gallbladder is analogous to elements of the enteric nervous system (ENS). The ganglionated plexus of the gallbladder was found to resemble closely the submucosal plexus of the small intestine in its organization into two irregular anastomosing and interwoven networks of ganglia, in the numbers of neurons per ganglion, and in the manifestation of histochemically demonstrable acetylcholinesterase activity in virtually all ganglion cells. In common with enteric ganglia, laminin immunoreactivity was observed to be excluded from the interiors of gallbladder ganglia, which were surrounded by a periganglionic laminin-immunoreactive sheath. As in the submucosal plexus, intrinsic substance P-, vasoactive intestinal polypeptide (VIP)-, and neuropeptide Y (NPY)-immunoreactive neurons were seen in the ganglionated plexus of the gallbladder. Extrinsic nerves in the gallbladder that degenerated following chemical sympathectomy with 6-hydroxydopamine (6-OHDA), and which contained NPY, tyrosine hydroxylase (TH), and dopamine-beta-hydroxylase (DBH) immunoreactivities, formed a perivascular plexus closely associated with blood vessels. Endogenous catecholamines could also be demonstrated in these perivascular nerves by aldehyde-induced histofluorescence. In addition to perivascular nerves, paravascular nerve bundles were observed that were loosely associated with vessels, did not degenerate following administration of 6-OHDA, and contained NPY immunoreactivity. Other paravascular nerves, probably visceral sensory axons, coexpressed substance P and calcitonin-gene-related peptide (CGRP) immunoreactivities. The ganglionated plexus of the gallbladder resembled enteric ganglia in having intrinsic 5-hydroxytryptamine (5-HT)-immunoreactive cells and highly varicose nerve fibers. The 5-HT-immunoreactive gallbladder axons were, like those of the gut, resistant to 6-OHDA, and separate from fibers that expressed TH immunoreactivity. Differences between the ganglionated plexus of the gallbladder and enteric ganglia of the small intestine included in the gallbladder are 1) the presence of TH-immunoreactive cells that contain an endogenous catecholamine, but not DBH; 2) DBH-immunoreactive neurons, some of which coexpress substance P immunoreactivity, but which contain neither a catecholamine nor TH immunoreactivity; 3) an apparent absence of CGRP-immunoreactive cell bodies.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗

The effect of nerve growth factor and limb regeneration on the spinal and sympathetic ganglia of Triturus.

In Triturus administration of NGF causes hypertrophy of neuronal perikarya of third dorsal root ganglia and post-subclavian sympathetic ganglia. Two classes of neurons were characterized cytologically in the third dorsal root ganglia. Some evidence is presented which indicates that Class I neurons respond more vigorously to NGF. It is suggested that Class I neurons are similar to the medio-dorsal neuroblasts of chick embryos in their response to NGF. Forelimb amputation did not cause neuronal hypertrophy in either third dorsal root ganglia or post-subclavian sympathetic ganglia. The incorporation of (3H)-uridine increases to a highly significant extent in third dorsal root ganglia following NGF treatment or limb amputation. When NGF treatment and limb amputation were combined, no further increase in (3H)-uridine incorporation was noted. This suggests that RNA synthesis is maximally stimulated by either NGF treatment alone or limb amputation alone.

Amputation, Surgical↗

Glial cell line-derived neurotrophic factor stimulates fiber formation and survival in cultured neurons from peripheral autonomic ganglia.

Human recombinant glial cell line-derived neurotrophic factor (GDNF) was tested for its ability to stimulate fiber formation and neuron survival in primary cultures of peripheral ganglia dissected from the chicken embryo. GDNF, first characterized by its actions on central nervous system (CNS) neurons, had a marked stimulatory effect on fiber outgrowth in sympathetic and ciliary ganglia. Weaker responses were evoked in sensory spinal and nodose ganglia and in the ganglion of Remak. In addition, survival of neurons from the sympathetic and ciliary ganglia was stimulated by GDNF at 50 ng/ml. The effects were not mimicked by the distant but related protein transforming growth factor beta 1 (TGF beta 1). The profile of neurons stimulated by GDNF is also distinct from the patterns of stimulation shown by nerve growth factor (NGF), stimulating strongly sympathetic but not ciliary ganglia, and ciliary neurotrophic factor (CNTF), stimulating mainly the ciliary ganglion. Moreover, using in situ hybridization histochemistry, GDNF was demonstrated to be present in the pineal gland in the newborn rat, a target organ for sympathetic innervation. The present results suggest that GDNF is likely to act upon receptors present in several autonomic and sensory neuronal populations. GDNF may serve to support fiber outgrowth and cell survival in peripheral ganglia, adding yet one more trophic factor to the list of specific proteins controlling development and maintenance of the peripheral nervous system.

Animals↗

Differential effects of denervation on acetylcholinesterase activity in parasympathetic and sympathetic ganglia of the frog, Rana pipiens.

The transsynaptic regulation of acetylcholinesterase (AChE) was studied by recording the changes in enzymatic activity following denervation in two types of autonomic ganglia in the frog, Rana pipiens. Opposite effects on AChE were found in the parasympathetic cardiac ganglion and in the sympathetic lumbar ganglion; denervation produced a significant increase in AChE activity in cardiac ganglia but a significant decrease in lumbar ganglia. The relative effects of denervation on intracellular and total AChE were examined by selectively inhibiting extracellular AChE with echothiophate, a poorly lipid-soluble cholinesterase inhibitor. Denervation resulted in a significant increase in intracellular AChE in cholinergic cardiac ganglia but had no effect on intracellular AChE activity in adrenergic lumbar ganglia. Histochemical studies revealed little change in extracellular AChE staining upon denervation in the cardiac ganglion, whereas in the lumbar ganglia there was a loss of AChE-specific reaction product. These results raise the possibility that the transsynaptic control of AChE activity by innervation in the frog is influenced by the transmitter synthetic properties of the postsynaptic ganglion cells.

Acetylcholinesterase↗

Rescue of sensory ganglia that are programmed to degenerate in normal development: evidence that NGF modulates proliferation of DRG cells in vivo.

The dorsal root ganglia (DRG, spinal ganglia) are a metameric series of structures that develop from neural crest cells within the dorsal somitic mesoderm. A striking element of patterning within this meristic series is the disappearance of the five or six most rostral DRG early in the embryonic development of birds and mammals. The transient DRG have been named "Froriep's ganglia" after their 19th century discoverer (reviewed in Lim et al., 1987). The ontogeny of the longest surviving Froriep's ganglion of the chick embryo, DRG C2, has recently been examined in detail (Rosen et al., 1996). At St. 18 (Embryonic Day (E)2.5+), the C2 DRG had the same shape and volume as permanent ganglia C5 and C6. C2's development first diverged from that of normal DRG at St. 19 (E3-), when C2 was observed to be half the size and shaped differently from its neighbors, and its peripheral nerve root began to degenerate. Both lower proliferation and higher apoptosis rates contribute to the reduced size of C2 compared to normal DRG at St. 19-20. One-third fewer C2 cells were found to be in S-phase when compared to neighboring ganglia, and apoptotic cells were more than three times more abundant in C2 than in conventional DRG at this stage. Since growth factors modulate both proliferation and apoptosis, we postulated that these molecules and/or their receptors might be responsible for the difference in fate between C2 and C5. In order to begin to evaluate this hypothesis, we have now treated embryos with nerve growth factor (NGF) in ovo. NGF treatments partially rescued C2, producing a 50% reduction in the normal difference in size between C2 and C5 at St. 23. At least part of this rescue could be accounted for by increased levels of proliferation in the NGF-treated C2 compared to those in control embryos. Proliferation in normal DRG C5 was unaffected by NGF application. NGF treatment rescued DRG cells in both C2 and C5 from cell death. Staining of pycnotic nuclei revealed that NGF dramatically reduced the death in the C2 ganglia. In addition to providing insight into the early patterning of the DRG, our results shed new light on the best-studied neurotrophic factor, NGF. Our finding is the first direct evidence for a role for NGF in control of DRG cell proliferation in vivo.

Animals↗

Distribution of brain-derived neurotrophic factor in cranial and spinal ganglia.

In a previous study we have shown that a subpopulation of primary sensory neurons contain brain-derived neurotrophic factor immunoreactivity. In the present study we investigated the distribution of brain-derived neurotrophic factor and its mRNA in cranial and spinal ganglia at different segmental levels, using immunohistochemical and quantitative reverse transcriptase-polymerase chain reaction techniques. Our results show that there is no significant difference in the percentage of brain-derived neurotrophic factor-immunoreactive neurons in spinal ganglia of different segmental levels. In contrast, more brain-derived neurotrophic factor-immunoreactive neurons were found in placode-derived than neural crest-derived ganglia. The percentage of brain-derived neurotrophic factor-immunoreactive neurons is consistent with the percentage of neurons lost after deletion of brain-derived neurotrophic factor or trkB genes. However, there is no correlation between brain-derived neurotrophic factor mRNA levels and the number of brain-derived neurotrophic factor immunoreactive neurons in these ganglia, suggesting that some neurons synthesize brain-derived neurotrophic factor while others accumulate the factor following its retrograde transport within nerve fibers. In particular, the proportion of brain-derived neurotrophic factor that is derived from extraganglionic sources in the placode-derived ganglia appears greater than that in the neural crest-derived ganglia.

Animals↗

Changes in sorbitol, myo-inositol and lipid inositol in dorsal root and sympathetic ganglia from streptozotocin-diabetic rats.

Sorbitol, fructose, myo-inositol and lipid inositol concentrations were measured in excised dorsal root and sympathetic ganglia from rats with streptozotocin-induced diabetes, both in the acute stage (1 and 2 weeks after the induction of diabetes) and chronically (after 2 months of diabetes). In comparison with age-matched controls, myo-inositol concentrations were decreased by 26-32% after 1 and 2 weeks but had returned to normal levels at 2 months. Lipid inositol concentrations were normal both in the acutely and chronically diabetic animals. Sorbitol was not detectable in ganglia from diabetic or control animals except for a small quantity (0.05 mumol/g wet weight) in dorsal root ganglia at the 2-month stage. Fructose was present in dorsal root ganglia (1.71-3.53 mumol/g wet weight) at all stages and in sympathetic ganglia (2.18 mumol/g wet weight) at the 8-week stage. The differences in these results from those obtained in peripheral nerve trunks are possibly related to the lack of a blood-nerve barrier in sensory and autonomic ganglia.

Animals↗

Proton magnetic resonance spectroscopy of basal ganglia in chronic schizophrenia.

Proton spectra in the regions of the right and left basal ganglia were studied in 14 medicated patients with chronic schizophrenia using proton magnetic resonance spectroscopy (1H MRS). Ratios of N-acetyl-aspartate (NAA) to choline-containing compounds (Cho) were significantly reduced in the bilateral basal ganglia regions compared to normal subjects. The relative level of Cho was increased in the left basal ganglia region in comparison to normal subjects. This finding suggests the presence of disturbances in phospholipid metabolism in the basal ganglia. The level of NAA was decreased in the bilateral basal ganglia regions, which may indicate neuronal dysfunction. The 1H MRS study demonstrated dysfunctions in the basal ganglia regions in medicated patients with chronic schizophrenia.

Adult↗

Projections from the prevertebral and major pelvic ganglia to the ileum and large intestine of the male rat.

The sympathetic innervation of the gut arises from the prevertebral and pelvic ganglia, and to a variable extent, from neurons located in the paravertebral ganglia, the splanchnic and intermesenteric nerves. In this study we have injected retrograde tracers into the wall of the ileum and several regions of the large intestine to determine the proportion of neurons supplying these regions from each of the ganglia and nerves. The sympathetic supply to the ileum arises primarily from neurons in the splanchnic nerves and the paravertebral ganglia T9-T11 (SPL) and the coeliaco-mesenteric ganglion complex (CG/SMG), with a small supply from the proximal intermesenteric nerves (IMN). The distribution of neurons projecting to the proximal colon is very similar, although some labelled neurons are found throughout the length of the IMN and also in the inferior mesenteric ganglion (IMG). The middle colon is primarily supplied by the IMN and the IMG, although this region receives innervation from all the ganglia and nerves investigated, including the major pelvic ganglia (MPG). Neurons located in the distal two-thirds on the IMN and more caudal structures were labelled from the distal colon. The distal colon is the only region of gut to receive a relatively large innervation from the MPG, with approximately one third of labelled neurons in each of the IMN, IMG and the MPG. These studies also compared two retrograde tracers, Fast Blue and Fluorogold. Fluorogold was found specifically to label neurons projecting to each region of intestine injected. However, when injected into the middle colon, Fast Blue labelled neurons that project to this region as well as many neurons that Fluorogold studies indicate project to other regions; Fast Blue should therefore be used only with caution.

Amidines↗

Location of sensory nerve cells that provide calbindin-containing laminar nerve endings in myenteric ganglia of the rat esophagus.

To determine the origin of the calbindin-containing laminar nerve endings in the myenteric ganglia of the rat esophagus, retrograde tracing experiments combined with immunohistochemistry using an antibody for calbindin were carried out. After Fast blue was injected into the cervical portion of the esophagus, labeled neurons were found bilaterally in the nodose ganglion and dorsal root ganglia of C1 to T3. 80% of the total neurons in the nodose ganglion and 20% of those in the dorsal root ganglia showed calbindin immunoreactivity. Moreover, 79% of Fast-blue-labeled neurons found in the nodose ganglion and 18% of those in the dorsal root ganglia were immunoreactive for calbindin. These results suggest that the calbindin antibody we used is useful as a marker for identifying esophageal vagal afferents derived from the nodose ganglion. The calbindin-immunoreactive nerve fibers forming the laminar endings in the myenteric ganglia of the rat cervical esophagus are mainly derived from sensory neurons in the nodose ganglion and partly derived from those in the cervical and upper thoracic dorsal root ganglia. Calbindin-containing laminar nerve endings may be related to mechanoreceptors in the esophagus.

Amidines↗

Noradrenergic innervation of rabbit pancreatic ganglia.

Sympathetic nerve stimulation indirectly regulates pancreatic endocrine and exocrine secretion, in part, through actions on the cholinergic parasympathetic innervation of the secretory tissues. Earlier work identified noradrenergic nerves in pancreatic ganglia and demonstrated the effects of exogenous norepinephrine (NE) on synaptic transmission but no quantitative studies of ganglionic NE content and release exist. Therefore, the distribution and density of catecholamine (CA)-containing nerves in rabbit pancreatic ganglia were studied using paraformaldehyde/glutaraldehyde (FAGLU) staining and HPLC analysis of CA concentrations. Neural release of [3H]NE was measured in ganglia isolated from the head/neck or body regions of the pancreas. CA-containing nerves densely innervated most ganglia (86%) from both regions, while neural and non-neural CA-containing cell bodies were rarely found. Ganglia from the head/neck region contained significantly higher concentrations of NE. Both 40 mM K+ and veratridine evoked Ca2+-dependent [3H]NE release and tetrodotoxin inhibited 80% of veratridine-stimulated release. omega-Conotoxin GVIA alone antagonized veratridine-stimulated release by 40% but the addition of nifedipine or omega-agatoxin IVA caused no further inhibition. There were no apparent regional differences in the Ca2+-dependence or toxin-sensitivity of NE release. In conclusion, ganglia throughout the rabbit pancreas receive a dense, functional noradrenergic innervation and NE release is dependent upon N- but not P/Q- or L-type voltage-dependent Ca2+ channels. These noradrenergic nerves may indirectly regulate pancreatic secretion through actions on ganglionic transmission.

Analysis of Variance↗

Somatotopy in the basal ganglia: experimental and clinical evidence for segregated sensorimotor channels.

Growing experimental and clinical evidence supports the notion that the cortico-basal ganglia-thalamo-cortical loops proceed along parallel circuits linking cortical and subcortical regions subserving the processing of sensorimotor, associative and affective tasks. In particular, there is evidence that a strict topographic segregation is maintained during the processing of sensorimotor information flowing from cortical motor areas to the sensorimotor areas of the basal ganglia. The output from the basal ganglia to the motor thalamus, which projects back to neocortical motor areas, is also organized into topographically segregated channels. This high degree of topographic segregation is demonstrated by the presence of a well-defined somatotopic organization in the sensorimotor areas of the basal ganglia. The presence of body maps in the basal ganglia has become clinically relevant with the increasing use of surgical procedures, such as lesioning or deep brain stimulation, which are selectively aimed at restricted subcortical targets in the sensorimotor loop such as the subthalamic nucleus (STN) or the globus pallidus pars interna (GPi). The ability to ameliorate the motor control dysfunction without producing side effects related to interference with non-motor circuits subserving associative or affective processing requires the ability to target subcortical areas particularly involved in sensorimotor processing (currently achieved only by careful intraoperative microelectrode mapping). The goal of this article is to review current knowledge about the somatotopic segregation of basal ganglia sensorimotor areas and outline in detail what is known about their body maps.

Animals↗