Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Division of the axons of adrenergic neurones by crushing the postganglionic nerve trunks of rat superior cervical ganglia (SCG) at 6 days of age resulted in a permanent atrophy of the SCG reflected by a persistent decrease in the total protein content and in the activities of the enzymes tyrosine hydroxylase and DOPA decarboxylase. Administration of nerve growth factor (NGF) to rats with unilateral axotomy at a dose of 10 mug/g/day for the period 7-21 days of age resulted in hypertrophy of both normal and axotomised SCG. There was a progressive rise in the total protein content and in the activities of the two enzymes till the end of the treatment period in both SCG. After treatment ceased there was a progressive fall in the total protein content and activities of the two enzymes reaching a stable level after 4 weeks. The level reached for treated unoperated SCG remained elevated when compared to untreated control SCG. Axotomised treated SCG had approximately the same biochemical parameters as untreated control SCG and very much elevated over untreated axotomised SCG. These final levels persisted for at least 56 days after treatment had ceased. Animals showed a persistent ptosis after axotomy at 6 days of age but treatment with NGF resulted in a functional recovery by 11 weeks of age. It is suggested that there is normally a retrograde transfer of a factor durind development from the target cell to the perikarya of the neurone permitting survival if the appropriate connections are made. Failure to make such a contact results in cedd death. The cell death occurring normally, and the cell death resulting from axotomy, can both be prevented by NGF treatment leading to an hypertrophy of both SCG. This consistent with the hypothesis than NGF is the retrograde trophic agent for the sympathetic nervous system in the developing animal.
 ...
PMID:The response of adrenergic neurones to axotomy and nerve growth factor. 23 22

Neuroleptic activity in laboratory animals is characterized by a decrease in locomotor activity, ptosis, catalepsy, antagonism of certain amphetamine-induced responses, and inhibition of a conditioned avoidance response. Neuroleptics have also been shown to be potent antagonists of dopamine (DA), cis-5,6-Dimethoxy-2-methyl-3-[2-(4-phenyl-1-piperazinyl)-ethyl]indoline (DHO) has been shown to possess the above described pharmacological profile. However, in contrast to known neuroleptics, DHO has no effect on DA levels, DA turnover rate or DA-stimulated cyclase; nor did it have an effect on tyrosine hydroxylase activity. In addition, DHO did not antagonize apomorphine-induced gnawing or amphetamine-induced stereotyped behavior, both of which have been reported to be DA-dependent. However, the agent decreased the level of norepinephrine in the forebrain. An attempt is made to demonstrate that the "DA-hypothesis" of schizophrenia may not be valid in all cases, and that the biochemistry of the disease state is very complex.
 ...
PMID:Is dopamine antagonism a requisite of neuroleptic activity? 611 Dec 98

In the rat, systemic administration of murine monoclonal antibodies against acetylcholinesterase caused rapid piloerection and ptosis (within 30-60 min after the injection). Using indirect immunohistochemistry the effect of these antibodies on peptides and enzyme expression was studied in the rat adrenal gland. Four days after antibody administration a total disappearance of acetylcholinesterase-immunoreactive fibers was observed. However, groups of acetylcholinesterase-immunoreactive chromaffin cells and intramedullary ganglion cells, both cell types showing acetylcholinesterase immunoreactivity also in the control adrenal medulla, expressed increased immunoreactivity. Analysis revealed that the acetylcholinesterase-immunoreactive chromaffin cell groups lacked phenylethanolamine-N-methyltransferase staining both in controls and treated rats. Antibody administration also affected levels of several peptides present in nerve fibers and chromaffin cells. Thus, the number of cells expressing enkephalin, calcitonin gene-related peptide and galanin was dramatically increased compared to the very few cells observed containing these three peptides in the normal gland. The majority of cells expressing enkephalin after antibody treatment also showed phenylethanolamine-N-methyltransferase immunoreactivity. In contrast, the few chromaffin cells expressing strong enkephalin-like immunoreactivity in controls were phenylethanolamine-N-methyltransferase negative. The sparse networks of calcitonin gene-related peptide- and galanin-positive fibers found in control adrenals were unchanged after the antibody treatment. However, the dense network of enkephalin varicose fibers totally disappeared after the antibody injection. A few substance P- and somatostatin-immunoreactive cells, not present in the normal gland, appeared after administration of the antibodies, whereas no changes were encountered with regard to immunoreactive nerve fibers. No clear differences between normal and treated animals could be observed in chromaffin cells with regard to immunoreactivity for neuropeptide Y or any of the four catecholamine-synthesizing enzymes, tyrosine hydroxylase, aromatic 1-amino acid decarboxylase, dopamine beta-hydroxylase or phenylethanolamine-N-methyltransferase. The present findings demonstrating a disappearance of acetylcholinesterase- and enkephalin-immunoreactive nerve fibers in the adrenal gland after intravenous injection of acetylcholinesterase antibodies support earlier reports showing that these antibodies cause degeneration of preganglionic fibers, and that neuronal decentralization of the adrenal gland induces marked increases in the levels of several peptides in chromaffin cells.
 ...
PMID:Effects of antibodies against acetylcholinesterase on the expression of peptides and catecholamine synthesizing enzymes in the rat adrenal gland. 810 82

Inborn errors of catecholamine biosynthesis are rare but of great interest as they are genetic disorders, and in some, treatment may completely reverse severe neurological abnormalities. They also provide insights into the action of the biogenic amines in the developing brain. We describe the clinical course of an infant with tyrosine hydroxylase (TOH) deficiency over a 30-month period. The parents are consanguineous, and genetic analysis revealed the infant to be homozygous for the common G698A mutation in the TOH gene. TOH deficiency can be seen as a model of pure catecholamine deficiency. Experimental evidence, reports of other disorders of biogenic amines, and our experience with this infant suggest that the symptoms of catecholamine deficiency in infancy can be broadly subdivided. Signs of dopamine deficiency include tremor, hypersensitivity to levadopa (L-dopa) therapy, oculogyric crises, akinesia, rigidity, and dystonia. Manifestations of norepinephrine deficiency include ptosis, miosis, profuse oropharyngeal secretions, and postural hypotension. Hypersensitivity to L-dopa was a particular management problem in this infant.
 ...
PMID:Tyrosine hydroxylase deficiency: clinical manifestations of catecholamine insufficiency in infancy. 1192 Nov 23

When performing anterior colporrhaphy for cystocele, most pelvic surgeons have not considered the neuroanatomy that contributes to urethral function. The aim of the study was to anatomically identify nerve fibers located in the anterior vagina associated with the pathogenesis of incontinence and pelvic organ prolapse. Anterior vaginal specimens were obtained from 17 female cadavers and 33 cases of clinical cystocele by anterior vaginal resection. The specimens were step-sectioned and stained with hematoxylin-eosin, S100 antibody, and tyrosine hydroxylase antibody. As a result, descending nerves 50-200 microm in thickness were identified between the urethra and vagina. They were located more than 10 mm medially from a cluster of nerves found almost along the lateral edge of the vagina and stained with S100 and tyrosine hydroxylase antibody, originated from the cranial part of the pelvic plexus, and appeared to terminate at the urethral smooth muscles. The authors classified the density of S100 positive nerve fibers in the anterior vaginal wall obtained from clinically operated cases of cystocele into three grades (Grade 1, nothing or a few thin nerves less than 20 microm in diameter; Grade 2, thick nerves more than 50 microm in diameter and thin nerves; Grade 3, more than 3 thick nerves in one field at an objective magnification of 40x). Mean urethral mobility (Q-tip) values (28.1 degrees +/-+/- 19.6 degrees ) observed in the Grade 3 cases was significantly lower than those (50.0 degrees +/-+/- 27.4 degrees and 59.4 degrees +/-+/- 19.9 degrees ) in Grade 2 and Grade 1, respectively. In addition, the presence of preoperative or postoperative stress urinary incontinence in the cases of Grade 1 was significantly higher than those of the cases with S100 positive stained nerves. In conclusion, the novel nerve fibers immunohistochemically identified in the anterior vaginal wall are different from those of the common nervous system or the pelvic floor and are associated with the pathogenesis of urethral hypermobility.
 ...
PMID:A clinicoanatomical study of the novel nerve fibers linked to stress urinary incontinence: the first morphological description of a nerve descending properly along the anterior vaginal wall. 1702 34

We describe the development of a novel animal model of acute severe dopamine (DA) deficiency by using genetically altered mice lacking the DA transporter (DAT-KO mice). In the absence of a DAT-mediated recycling mechanism in these mice, striatal DA concentrations become entirely dependent on its de novo synthesis, and acute pharmacologic inhibition of tyrosine hydroxylase induces transient (up to 16 hours) elimination of brain DA. Dopamine-deficient DAT-KO mice (DDD mice) demonstrate a striking behavioral phenotype manifested as severe akinesia, rigidity, tremor, and ptosis. We propose that DDD mice represent a novel acute model of severe DA deficiency that might be used to identify compounds with potential therapeutic use for the treatment of Parkinson's disease (PD). This model is particularly promising as a tool for evaluating the efficacy of compounds that may induce movement independently of DA. The advantages and limitations of DDD mice in comparison to other rodent PD models are discussed.
 ...
PMID:DDD mice, a novel acute mouse model of Parkinson's disease. 1703 Jul 35