Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0007570 (celiac disease)
 13,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A form of polycystic ovary (PCO) resembling some aspects of the human PCO syndrome can be induced in rats by a single injection of estradiol valerate (EV). An increase in sympathetic outflow to the ovary precedes, by several weeks, the appearance of cysts, suggesting the involvement of a neurogenic component in the pathology of this ovarian dysfunction. The present study was carried out to test the hypotheses that this change in sympathetic tone is related to an augmented production of ovarian nerve growth factor (NGF), and that this abnormally elevated production of NGF contributes to the formation of ovarian cysts induced by EV. Injection of the steroid resulted in increased intraovarian synthesis of NGF and its low affinity receptor, p75 NGFR. The increase was maximal 30 days after EV, coinciding with the elevation in sympathetic tone to the ovary and preceding the appearance of follicular cysts. Intraovarian injections of the retrograde tracer fluorogold combined with in situ hybridization to detect tyrosine hydroxylase (TH) messenger RNA-containing neurons in the celiac ganglion revealed that these changes in NGF/p75 NGFR synthesis are accompanied by selective activation of noradrenergic neurons projecting to the ovary. The levels of RBT2 messenger RNA, which encodes a beta-tubulin presumably involved in slow axonal transport, were markedly elevated, indicating that EV-induced formation of ovarian cysts is preceded by functional activation ofceliac ganglion neurons, including those innervating the ovary. Intraovarian administration of a neutralizing antiserum to NGF in conjunction with an antisense oligodeoxynucleotide to p75 NGFR, via Alzet osmotic minipumps, restored estrous cyclicity and ovulatory capacity in a majority of EV-treated rats. These functional changes were accompanied by restoration of the number of antral follicles per ovary that had been depleted by EV and a significant reduction in the number of both precystic follicles and follicular cysts. The results indicate that the hyperactivation of ovarian sympathetic nerves seen in EV-induced PCO is related to an overproduction of NGF and its low affinity receptor in the gland. They also suggest that activation of this neurotrophic-neurogenic regulatory loop is a component of the pathological process by which EV induces cyst formation and anovulation in rodents. The possibility exists that a similar alteration in neurotrophic input to the ovary contributes to the etiology and/or maintenance of the PCO syndrome in humans.
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PMID:An increased intraovarian synthesis of nerve growth factor and its low affinity receptor is a principal component of steroid-induced polycystic ovary in the rat. 1069 82

Immunoreactivity for galanin was examined in the sympathetic preganglionic neurons in the spinal cord, adrenal glands, sympathetic ganglia, and some sensory ganglia of the filefish Stephanolepis cirrhifer. Galanin-immunoreactive neurons were found only in the rostral part, but not in the caudal part of the central autonomic nucleus (a column of sympathetic preganglionic neurons of teleosts). Many galanin-immunoreactive nerve terminals were found in contact with neurons in the celiac ganglia and the cranial sympathetic ganglia on both sides of the body. Most neurons encircled by galanin-immunoreactive nerve fibers were negative for tyrosine hydroxylase. Galanin-immunoreactive nerve fibers were very sparse in the spinal sympathetic paravertebral ganglia. No galanin-immunoreactive nerve fibers were found in the adrenal glands. No sensory neurons of the trigeminal, vagal, or spinal dorsal root ganglia were positive for galanin-immunoreactivity. These results suggest that galanin-immunoreactive sympathetic preganglionic neurons have distinct segmental localization and might project specifically to a population of non-adrenergic sympathetic postganglionic neurons in the celiac and cranial sympathetic ganglia.
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PMID:Distinct localization and target specificity of galanin-immunoreactive sympathetic preganglionic neurons of a teleost, the filefish Stephanolepis cirrhifer. 1069 44

Neurotrophin-4 (NT-4) is perhaps the still most enigmatic member of the neurotrophin family. We show here that NT-4 is expressed in neurons of paravertebral and prevertebral sympathetic ganglia, i.e., the superior cervical (SCG), stellate (SG), and celiac (CG) ganglion. Mice deficient for NT-4 showed a significant reduction (20-30%) of preganglionic sympathetic neurons in the intermediolateral column (IML) of the thoracic spinal cord. In contrast, neuron numbers in the SCG, SG, and CG were unchanged. Numbers of axons in the thoracic sympathetic trunk (TST) connecting the SG with lower paravertebral ganglia were also reduced, whereas axon numbers in the cervical sympathetic trunk (CST) were unaltered. Axon losses in the TST were paralleled by losses of synaptic terminals on SG neurons visualized by electron microscopy. Furthermore, immunoreactivity for the synaptic vesicle antigen SV2 was clearly reduced in the SG and CG. Levels of catecholamines and tyrosine hydroxylase immunoreactivity were dramatically reduced in the SG and the CG but not in the SCG. Despite this severe phenotype in the sympathetic system, blood pressure levels were not reduced and displayed a pattern more typical of deficits in baroreceptor afferents. Numbers of IML neurons were unaltered at postnatal day 4, suggesting a postnatal requirement for their maintenance. In light of these and previous data, we hypothesize that NT-4 provided by postganglionic sympathetic neurons is required for establishing and/or maintaining synapses of IML neurons on postganglionic cells. Impairment of synaptic connectivity may consequently reduce impulse flow, causing a reduction in transmitter synthesis in postganglionic neurons.
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PMID:Lack of neurotrophin-4 causes selective structural and chemical deficits in sympathetic ganglia and their preganglionic innervation. 1131 92

The present study showed neurons immunoreactive for choline acetyltransferase (ChAT) in the cranial sympathetic ganglia lying close to the trigeminal-facial nerve complex of the filefish. In these ganglia, less than 1% of ganglion cells were positive for choline acetyltransferase. Choline acetyltransferase-positive neurons were significantly larger than the randomly sampled neurons in this ganglion. The majority of choline acetyltransferase-positive neurons were negative for tyrosine hydroxylase, but many of them were positive for galanin (GAL). Some neurons were positive for both choline acetyltransferase and tyrosine hydroxylase, but these neurons were rarely immunoreactive for dopamine beta hydroxylase, suggesting that they are not adrenergic. In the cranial sympathetic ganglia and the celiac ganglia, many nerve fibers immunoreactive for galanin were seen, and varicose terminals were in contact selectively with neurons negative for both choline acetyltransferase and tyrosine hydroxylase, but not with those positive for choline acetyltransferase or tyrosine hydroxylase. Nerve fibers immunoreactive for choline acetyltransferase were found to be present in contact with the deep layer of chromatophores, which was observed only in the labial region. These results suggest that cholinergic postganglionic neurons are present in the filefish cranial sympathetic ganglia, and that they also contain galanin. As few cholinergic sympathetic neurons express tyrosine hydroxylase and none express dopamine beta hydroxylase, they are unlikely to synthesize noradrenaline or adrenaline.
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PMID:Choline acetyltransferase immunoreactive sympathetic ganglion cells in a teleost, Stephanolepis cirrhifer. 1217 Dec 54

We studied the effect of thyrotropin-releasing hormone (TRH) applied centrally on the sympathetic activity of the ovary in female rats. Intracerebroventricular (i.c.v.) administration of a dose of 25 ng/kg weight produced an increase in noradrenaline (NA) content at the ovary after 5 days of hormone administration. However, higher doses in a range up to 500 ng/kg weight decreased NA content at the ovary. At the celiac ganglia (where the cell bodies of sympathetic neurons projecting to the ovary originate) there was an accumulation of NA in spite of a decrease in tyrosine hydroxylase activity (T-OH). After cold exposure, opposite effects on T-OH activity and no effects on NA in ganglia and in ovary were obtained. Besides, i.v. injection of TRH only induced a decrease in ovarian NA. In contrast to the increase in T(3) plasma levels obtained after the cold-stress procedure, none of the i.c.v. doses of TRH used produced changes in T(3) plasma levels, strongly suggesting that the effect on sympathetic activity is mediated by a central effect of TRH acting as a putative activator of ovarian sympathetic nerves.
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PMID:Thyrotropin-releasing hormone as a mediator of the central autonomic pathway controlling ovarian function. 1276 27

The present study tested the hypothesis that, in normal male rats, chronic changes in salt intake alter the levels of tyrosine hydroxylase and the norepinephrine transporter in sympathetic ganglia. Increasing dietary salt (from 0.02% to 1%, 4% or 8% NaCl in rat chow) decreased (p<0.05) the mRNA levels of tyrosine hydroxylase and the norepinephrine transporter in the adrenal gland, superior cervical ganglia and celiac ganglia. In addition, tyrosine hydroxylase and norepinephrine transporter protein levels were decreased (p<0.05) in the adrenal gland. To test the hypothesis that NaCl acts directly on postganglionic neurons to suppress the expression of these proteins, it was determined if increases in NaCl concentrations, of a magnitude achieved during increases in dietary salt in vivo, suppress expression of tyrosine hydroxylase and the norepinephrine transporter in cultured sympathetic neurons in vitro. Increased dietary salt increased plasma NaCl concentrations each by up to 4-6 mEq l(-1) (p<0.05), with the greatest increases occurring at night when the rats consume most of their food. In addition, NaCl added to cultured neurons decreased tyrosine hydroxylase and norepinephrine transporter protein and mRNA levels, and norepinephrine uptake; however, the NaCl concentration increases required were 15-30 mEq l(-1). These data suggest that increased dietary salt can influence the activity of the sympathetic nervous system by suppressing the levels of tyrosine hydroxylase and the norepinephrine transporter. While increased NaCl levels can act directly on neurons to suppress these proteins, this action may occur in vivo only in severe pathophysiological states, but not during increases in dietary salt without the synergistic effect of other factors.
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PMID:Ganglionic tyrosine hydroxylase and norepinephrine transporter are decreased by increased sodium chloride in vivo and in vitro. 1296 19

The present study investigated the chemical coding of neurons in the celiac-superior mesenteric ganglion complex supplying the normal (n=4) and inflamed (n=4) ileum (chemically-induced inflammation) in juvenile pigs using retrograde tracing combined with immunohistochemistry. Ileum-projecting neurons (IPN) were predominantly distributed in the left and right superior mesenteric pools of the ganglion. The majority of them were adrenergic (tyrosine hydroxylase-positive) and also contained neuropeptide Y, somatostatin or galanin. No clear-cut differences in the distribution and chemical coding of IPN were found between normal and inflamed pigs. However, in the inflamed group, the density of peptidergic, IPN-associated nerve fibres was higher than that found in the control group.
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PMID:The distribution and chemical coding of neurons in the celiac-superior mesenteric ganglion complex supplying the normal and inflamed ileum in the pig. 1547 66

The abdominal sympathetic system is unique in that its postganglionic axons do not directly innervate gastrointestinal smooth muscle layers but exert their effects through the enteric nervous system. The purpose of the present study was to examine the ability of neurons in abdominal sympathetic ganglia to regenerate after axonal injury and to determine whether reinnervation occurs after the removal of ganglia. Axons from the celiac ganglion and superior mesenteric ganglion complex (CG/SMG) of adult female BALB/c mice were crushed or the ganglion complex was removed. Immunohistochemistry, western blotting and in situ hybridization were performed to examine the changes in tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP-43) in the duodenum and the sympathetic ganglia. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling and injection of the tracer dye, fluorogold were also performed. After crushing the nerve, TH in the duodenum disappeared and reappeared within 90 days. In the CG/SMG, TH decreased and increased as in the duodenum, while the expression of GAP-43 changed in the opposite direction. Nerve crushing caused cell death to limited number of neurons in the CG/SMG. The removal of CG/SMG decreased TH in the duodenum and stomach, but 180 days later TH-positive innervation was recovered. Fluorogold injection revealed that the inferior mesenteric ganglion reinnervated the stomach. Therefore, postganglionic sympathetic nerves in the abdomen are able to regenerate and reinnervation occurs even after the removal of sympathetic ganglia.
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PMID:Regeneration of the abdominal postganglionic sympathetic system. 1642 93

Diabetes is the major cause of autonomic neuropathy in humans. Sympathetic neurons from the celiac/superior mesenteric ganglia (CG/SMG) develop neuropathic changes in diabetes whereas sympathetic superior cervical ganglion (SCG) neurons do not. Glucose-induced oxidative stress is proposed as a major factor in the development of diabetic neuropathy. The aim of this study was to investigate whether sympathetic neurons that develop neuropathy in diabetes are more susceptible to oxidative stress. Explants of CG/SMG and SCG from control adult rats were cultured in media free of serum and NGF, exposed to menadione for 48 h to induce oxidative stress and assessed for neuronal viability, TUNEL-positive nuclei and tyrosine hydroxylase- (TH)-immunoreactivity. TH-immunoreactivity was also assessed in ganglia from control and 8 week streptozotocin-diabetic rats. Menadione caused a concentration-dependent loss of neuronal viability and increase in TUNEL staining in both ganglia. However, at low concentrations, menadione had a significantly greater effect (p<0.01) on CG/SMG neurons than SCG neurons. At 1 nM, menadione caused a significant increase (p<0.05) in the number of CG/SMG neurons containing intense TH-immunoreactivity without affecting SCG neurons. Similarly, 8 weeks streptozotocin-induced diabetes resulted in a significant increase (p<0.05) in intensely fluorescent TH-containing CG/SMG neurons but not SCG neurons. This is the first demonstration that oxidative stress in vitro causes the same accumulation of TH in CG/SMG neurons as is observed following streptozotocin-induced diabetes in vivo. Furthermore, the selective vulnerability of CG/SMG neurons to diabetes is reflected by increased sensitivity to oxidative stress.
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PMID:Selective susceptibility of different populations of sympathetic neurons to diabetic neuropathy in vivo is reflected by increased vulnerability to oxidative stress in vitro. 1697 73

The neurotransmitter composition of neurons in the cranial cervical ganglion (CCG) and celiac ganglia (CG) in rats of different ages (neonatal, 10, 12, 30, and 60 days) was studied by immunohistochemical methods. The results showed that most neurons in these sympathetic ganglia contain tyrosine hydroxylase (TH). Most TH-positive neurons were also neuropeptide Y (NPY)-positive. In all ganglia, the proportions of neurons containing NPY increased from the moment of birth to the end of the first month of life. In the CG, NPY was present in a significantly greater proportion of neurons than in the CCG. Substance P, vasoactive intestinal peptide, and choline acetyltransferase were present in occasional neurons in the CCG and CG from birth. There was no change in the proportion of this type of neuron with age. Definitive establishment of the neurotransmitter composition in the sympathetic ganglia studied here occurred by the end of the first month of life.
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PMID:Neurotransmitter composition of neurons in the cranial cervical and celiac sympathetic ganglia in postnatal ontogenesis. 2003 2


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