Gene/Protein Disease Symptom Drug Enzyme Compound
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There have been no works devoted to the study of the influence of (131)I and maternal (131)I-induced hypothyroidism on the state of the C-cells in the thyroid gland of the developing embryos. A study was made on the effect of a dose of 150 microCi (131)I (0.5 Gy) leading to hypothyroidism in rats, on 35 mother rats and 168 newborn pups. The mother rats were divided into control and four treated groups which were injected with (131)I before pregnancy, on gestation days 5, 10, and 16, respectively. Immunohistochemically, the thyroid gland was examined for calcitonin-positive cells. Maternal hypothyroidism induced by (131)I leads to the development of hyperplasia and hyperthrophy of calcitonin-positive cells in the pups at the time of birth. The discovery of separate C-cells in the peripheral zone of the thyroid lobe may be evidence of an unbalance in the development of the medial and lateral source of the thyroid. There is a verifiable increase in the quantity of C-cells per 1 mm(2) field of the localization in the central zone of the gestation days 10 and 16 groups. This might be a compensatory mechanism for regulating the activity of the thyroid gland under induced hypothyroidism. Thus, in cases when there is a breakdown in the normal external regulation of the embryonic morphogenesis, a reduction in the level of maternal thyroid hormones and also direct exposure to (131)I, there is also a change in the foetus' internal regulatory systems. A change in C-cell system could lead to the appearance of endocrinological disorders later in life.
Anat Rec 1999 09 01
PMID:The influence of maternal hypothyroidism and radioactive iodine on rat embryonal development: thyroid C-cells. 1045 80

Several previous studies have described the distribution of neuropeptide Y (NPY)-like and calcitonin gene related peptide (CGRP)-like immunoreactive nerve fibres in the atrioventricular valves of humans and various animals. It has been suggested that peptide-containing nerve fibres might have motor or sensory roles in valvular function. Although there is evidence that diabetic changes occur in the sympathetic (preganglionic and postganglionic), parasympathetic (vagal) and peptidergic nerves of rats, the changes of peptide-containing nerve fibres in the atrioventricular valves of the diabetic rat have not been studied. The distribution, relative density and staining intensity of NPY-like and CGRP-like immunoreactive nerve fibres in the mitral and tricuspid valves were studied in whole mount preparations using confocal microscopy with a computer-assisted image analysis system. Streptozotocin-induced diabetic and control rats were sacrificed at 12 and 24 months. The nerve staining intensity within the tricuspid valve was greater than the mitral valve in both control (P < 0.01) and diabetic (P < 0.001) rats. Nerve density in the anterior leaflet was greater than the posterior leaflet of the mitral valve. However, the anterior leaflet of the mitral and tricuspid valves showed a decreased number of nerve fibres, followed by drastic reduction in the staining intensities for both the peptides studied (P < 0.001) in the long-term diabetic rat. The decrease in the number of nerve fibres that follow the mechanical interruption of nerves raises the possibility that cycles of degeneration may occur. It is suggested that these peptide-containing nerve fibres in the atrioventricular valves may be involved in valvular dysfunction in the diabetic state.
Anat Rec 2000 03 01
PMID:Changes in peptidergic nerves in the atrioventricular valves of streptozotocin-induced diabetic rats: a confocal microscopy study. 1070 48

In order to gain a better understanding of the central and local control of laryngeal blood flow, the vascular innervation to the rat laryngeal muscles was examined. To visualize the vascular network, the animals were perfused with a gelatin/India ink solution. The larynges were removed and fixed. The superior laryngeal, cricothyroid, and inferior laryngeal arteries (all branch off the superior thyroid artery) were dissected in continuity into their respective muscles. Specimens were reacted in toto using immunohistochemical techniques for the presence of neuropeptide-Y (NPY), vasoactive intestinal peptide (VIP), calcitonin gene related peptide (CGRP), and neuronal nitric oxide synthase (NOS-1). Results show that all of the laryngeal vasculature is richly innervated by fibers containing these peptides. Qualitatively, the most prominent of these is NPY in association with the superior and the inferior laryngeal arteries, followed by VIP and NOS-1, and finally CGRP distributed equally on all the vessels. Immunopositive fibers are found along the entire course of the feeding arteries, beginning with the superior thyroid artery and continuing down to small arterioles into the terminal vascular beds. These peptides can act as vasodilators, vasoconstrictors, and/or neuromodulators and may work synergistically or antagonistically with other transmitters in controlling laryngeal blood flow. Their effects are dependent on the specific vascular bed in question, that is, in some areas they are vasodilators, in others vasoconstrictors, and in other neuromodulators. What effects they have on the laryngeal vasculature and how they interact within the larynx have yet to be determined.
Anat Rec 2000 06 01
PMID:Nonadrenergic innervation of the rat laryngeal vasculature. 1082 Mar 20

Lower numbers of neuropeptide-containing fibers in arthritic joints have been found as compared to control joints. This may be the result of fiber depletion, necrosis of fibers, or proliferation of soft tissues without neural sprouting. To discriminate between these possibilities, we studied the relationships between soft tissue proliferation, changes in vascularity of synovial tissues, and changes in joint innervation during arthritis. Arthritis was induced in the knee joint of mice by a single subpatellar injection of methylated bovine serum albumin after previous immunization. Antibodies to protein gene product 9.5, S-100, and growth-associated protein-43 (GAP-43) were used to study the general innervation pattern. Antibodies to calcitonin gene-related peptide (CGRP), vasointestinal polypeptide (VIP), substance P (SP), and tyrosine hydroxylase (TH) were used to localize sensory (SP, CGRP, VIP) and sympathetic (TH) fibers. Blood vessels of the joint were studied with ink perfusion, GAP-43, and a vascular marker (LF1). Directly after the induction of arthritis, the synovial cavity was enlarged and filled with leukocytes. From day 4 onward, small sprouting blood vessels penetrated the avascular mass of cells in the joint cavity. After 1 week, the vascular sprouting activity and GAP-43 immunoreactivity were maximal, and after 2 weeks, vascular sprouting activity diminished. In the subsequent period, the synovia slowly regained their prearthritic appearance and thickness. The most pronounced changes in the general staining pattern of CGRP, SP, VIP, and TH were found in the periosteum. From 2 days to 4 weeks after the induction of arthritis, the layer of SP, CGRP, and VIP fibers in the femoral periosteum was thicker and more irregular. GAP-43 staining showed many terminal varicosities, which suggested sprouting of nerve fibers. From 2 days to 2 weeks after the induction of arthritis, the SP and CGRP fibers in the periosteum showed gradual depletion. In the thickened subsynovial tissues that were revascularized, no ingrowth of neural elements was found. As the total number of nerve fibers in the synovial tissue did not change, large parts of the synovia directly facing the joint cavity were not innervated at 1 week after the induction of arthritis. These results strongly suggest that periosteal SP and CGRP fibers were depleted during arthritis. Synovial proliferation without concomitant fiber growth is the main cause of the reduced number of immunocytochemically detectable fibers in the mouse arthritic knee joint.
Anat Rec 2000 09 01
PMID:Neurovascular plasticity in the knee joint of an arthritic mouse model. 1096 36

The complexity of the neural regulation of the gallbladder is reflected by the variety of neuroactive compounds that are found in the intrinsic and extrinsic nerves of the guinea pig gallbladder. The studies reported here used antisera to test for the presence of gallbladder nerves that are immunoreactive for the neuroactive peptides, pituitary adenylyl activating polypeptide (PACAP), and/or orphanin FQ (OFQ, also known as nociceptin). PACAP immunoreactivity was observed in nerve fibers of the paravascular plexus that were also immunoreactive for calcitonin gene-related peptide. These nerve fibers, which are also immunoreactive for substance P, could be followed into the ganglionated plexus. Within the ganglia, a small proportion of neurons was found to be immunoreactive for PACAP; these neurons were also immunoreactive for vasoactive intestinal peptide and nitric oxide synthase. Immunoreactivity for OFQ was observed in the perivascular plexus in nerve fibers that were also immunoreactive for tyrosine hydroxylase. These nerves were previously shown to be immunoreactive for neuropeptide Y. In the ganglionated plexus, immunoreactivity was observed in all gallbladder neurons, as demonstrated by double staining with antiserum directed against the neuron-specific RNA binding protein, Hu. OFQ immunoreactivity was also present in the small catecholaminergic neurons that are observed in a subset of the ganglia. These results further demonstrate the neurotransmitter diversity of the nerves of the gallbladder, and they provide an incentive for studies of the actions of these compounds in the gallbladder wall.
Anat Rec 2001 01 01
PMID:Chemical coding of intrinsic and extrinsic nerves in the guinea pig gallbladder: distributions of PACAP and orphanin FQ. 1114 33

In normal skeletal muscle, the protein dystrophin is associated with plasma membrane glycoproteins and may be involved in the stabilization of the sarcolemma. Mutant mdx mice are markedly deficient in dystrophin and show muscle fiber necrosis followed by regeneration. Changes in the distribution of acetylcholine receptors (AChRs) have been reported at the neuromuscular junction of mdx mice possibly as a result of alterations in the release or response to neural trophic factors. One such factor is calcitonin gene-related peptide (CGRP), which has been implicated in AChR synthesis and function. In this study, we used rhodamine-alpha-bungarotoxin and anti-CGRP IgG FITC to study AChR and CGRP distribution at the neuromuscular junction of mdx mice. Using laser scanning fluorescence confocal microscopy, it was possible to see that CGRP-like immunoreactivity had a presynaptic distribution, covering the AChRs. Thirty-four percent of dystrophic junctions were found to be labeled with CGRP compared to 80% of control endplates. Since CGRP-positive and -negative fibers showed similar changes in AChR distribution, it is suggested that CGRP is probably not directly involved in the altered pattern of AChR seen in dystrophin-deficient muscle fibers of mdx mice.
Anat Rec A Discov Mol Cell Evol Biol 2004 Aug
PMID:Distribution of calcitonin gene-related peptide at the neuromuscular junction of mdx mice. 1527 51

The role of neural elements in regulating blood flow through the hepatic sinusoids, solute exchange, and parenchymal function is incompletely understood. This is due in part to limited investigation in only a few species whose hepatic innervation may differ significantly from humans. For example, most experimental studies have used rats and mice having livers with little or no intralobular innervation. In contrast, most other mammals, including humans, have aminergic and peptidergic nerves extending from perivascular plexus in the portal space into the lobule, where they course in Disse's space in close relationship to stellate cells (fat storing cells of Ito) and hepatic parenchymal cells. While these fibers extend throughout the lobule, they predominate in the periportal region. Cholinergic innervation, however, appears to be restricted to structures in the portal space and immediately adjacent hepatic parenchymal cells. Neuropeptides have been colocalized with neurotransmitters in both adrenergic and cholinergic nerves. Neuropeptide Y (NPY) has been colocalized in aminergic nerves supplying all segments of the hepatic-portal venous and the hepatic arterial and biliary systems. Nerve fibers immunoreactive for substance P and somatostatin follow a similar distribution. Intralobular distribution of all of these nerve fibers is species-dependent and similar to that reported for aminergic fibers. Vasoactive intestinal peptide and calcitonin gene-related peptide (CGRP) are reported to coexist in cholinergic and sensory afferent nerves innervating portal veins and hepatic arteries and their branches, but not the other vascular segments or the bile ducts. Nitrergic nerves immunoreactive for neuronal nitric oxide (nNOS) are located in the portal tract where nNOS colocalizes with both NPY- and CGRP-containing fibers. In summary, the liver is innervated by aminergic, cholinergic, peptidergic, and nitrergic nerves. While innervation of structures in the portal tract is relatively similar between species, the extent and distribution of intralobular innervation are highly variable as well as species-dependent and may be inversely related to the density of gap junctions between contiguous hepatic parenchymal cells.
Anat Rec A Discov Mol Cell Evol Biol 2004 Sep
PMID:Anatomy of efferent hepatic nerves. 1538 19

After receiving information from afferent nerves, the hypothalamus sends signals to peripheral organs, including the liver, to keep homeostasis. There are two ways for the hypothalamus to signal to the peripheral organs: by stimulating the autonomic nerves and by releasing hormones from the pituitary gland. In order to reveal the involvement of the autonomic nervous system in liver function, we focus in this study on autonomic nerves and neuroendocrine connections between the hypothalamus and the liver. The hypothalamus consists of three major areas: lateral, medial, and periventricular. Each area has some nuclei. There are two important nuclei and one area in the hypothalamus that send out the neural autonomic information to the peripheral organs: the ventromedial hypothalamic nucleus (VMH) in the medial area, the lateral hypothalamic area (LHA), and the periventricular hypothalamic nucleus (PVN) in the periventricular area. VMH sends sympathetic signals to the liver via the celiac ganglia, the LHA sends parasympathetic signals to the liver via the vagal nerve, and the PVN integrates information from other areas of the hypothalamus and sends both autonomic signals to the liver. As for the afferent nerves, there are two pathways: a vagal afferent and a dorsal afferent nerve pathway. Vagal afferent nerves are thought to play a role as sensors in the peripheral organs and to send signals to the brain, including the hypothalamus, via nodosa ganglia of the vagal nerve. On the other hand, dorsal afferent nerves are primary sensory nerves that send signals to the brain via lower thoracic dorsal root ganglia. In the liver, many nerves contain classical neurotransmitters (noradrenaline and acetylcholine) and neuropeptides (substance P, calcitonin gene-related peptide, neuropeptide Y, vasoactive intestinal polypeptide, somatostatin, glucagon, glucagon-like peptide, neurotensin, serotonin, and galanin). Their distribution in the liver is species-dependent. Some of these nerves are thought to be involved in the regulation of hepatic function as well as of hemodynamics. In addition to direct neural connections, the hypothalamus can affect metabolic functions by neuroendocrine connections: the hypothalamus-pancreas axis, the hypothalamus-adrenal axis, and the hypothalamus-pituitary axis. In the hypothalamus-pancreas axis, autonomic nerves release glucagon and insulin, which directly enter the liver and affect liver metabolism. In the hypothalamus-adrenal axis, autonomic nerves release catecholamines such as adrenaline and noradrenaline from the adrenal medulla, which also affects liver metabolism. In the hypothalamus-pituitary axis, release of glucocorticoids and thyroid hormones is stimulated by pituitary hormones. Both groups of hormones modulate hepatic metabolism. Taken together, the hypothalamus controls liver functions by neural and neuroendocrine connections.
Anat Rec A Discov Mol Cell Evol Biol 2004 Sep
PMID:Neural connections between the hypothalamus and the liver. 1538 20

There is a rapid reversal in maternal skeletal metabolism and bone remodeling from accelerated bone resorption during lactation to skeletal rebuilding after lactation. The purpose was to determine the changes that occur in maternal osteoclasts during the transition from lactation to postlactation. Skeletal samples were taken from female rats on days 10 and 19 of lactation and 1 and 7 days after lactation. The pups were weaned on day 20. There was a rapid change in the osteoclast population after weaning, resulting in less resorption surface. Osteoclasts detached from bone surfaces, lost their ruffled borders, and became fragmented with immunocytochemical evidence of apoptosis within 24 hr after lactation. Concomitant with the rapid regression in the osteoclast population was an over fivefold increase in maternal calcitonin (CT) levels at 24 hr after weaning. Serum calcium and estrogen (E2) increased, but prolactin (PRL) and PTH decreased after weaning. The hormone changes, particularly that of CT, are consistent with the rapid regression of the osteoclast population at the end of lactation. These changes are similar to a reversal phase of a bone remodeling cycle where bone formation commences when resorption ceases on bone surfaces and suggests that the fate of osteoclasts during bone remodeling is programmed cell death. These results also suggest that bone remodeling is well synchronized prior to, during, and after lactation to accommodate the mineral requirements of the offspring as well as the mother.
Anat Rec (Hoboken) 2007 Jan
PMID:Rapid inactivation and apoptosis of osteoclasts in the maternal skeleton during the bone remodeling reversal at the end of lactation. 1744 Nov 99

For years, calcitonin gene-related peptide (CGRP) has been used as a marker peptide for Dogiel type II neurons, putative intrinsic primary afferent neurons, in the pig enteric nervous system. Recently, some studies showed CGRP-positive neurons displaying distinctly different shapes. The aims of this study were to evaluate (1) the proportion of myenteric type II neurons that contain CGRP and (2) the proportion of myenteric CGRP-positive neurons that display type II vs. non-type II morphologies and to conclude if this peptide could be suited as a marker for type II neurons. For this purpose, nine myenteric whole-mounts (each one from duodenum, jejunum, and ileum, respectively, derived from three pigs) were triple-immunostained for CGRP, neurofilaments (NF), and choline acetyl transferase (ChAT). Each whole-mount was evaluated twice. First, 50 NF-stained type II neurons were selected randomly and their coreactivities for CGRP and ChAT were observed. Second, 50 CGRP-positive neurons were located randomly and their NF morphology and ChAT coreactivity were observed. Altogether, 92% of all type II neurons investigated displayed CGRP immunoreactivity, whereas 94.9% of all CGRP-reactive neurons recorded displayed type II morphology. We observed three further shapes of CGRP-positive neurons: 7 type V neurons (all were ChAT-positive; mainly in the ileal whole-mounts), 6 type I-like neurons (all were ChAT-positive), and 14 type III-like neurons (mostly ChAT-negative; mainly in duodenal and jejunal specimens). We conclude that CGRP-antibodies can be used as markers for type II neurons in the pig small intestinal myenteric plexus in quantitative studies but it should be kept in mind that up to one-tenth of CGRP-reactive neurons may be non-type II neurons. In case of single cell evaluation, CGRP-immunoreactivity alone is not suited as a marker. In such cases additional, morphological analysis is necessary.
Anat Rec (Hoboken) 2007 Oct
PMID:Calcitonin gene-related peptide: a marker for putative primary afferent neurons in the pig small intestinal myenteric plexus? 1776 67


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