Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of complex carbohydrate antigens was analysed in developing sympathoadrenal cells of the rat using monoclonal antibodies that react with unique carbohydrate structures. CC1 and CC4 are monoclonal antibodies that react specifically with beta-N-acetylgalactosamine and alpha-galactose/alpha-fucose moieties, respectively. CC1-reactive glycoconjugates are expressed in embryonic superior cervical ganglion (SCG) cells as early as embryonic day 15 (E15). CC4 is expressed in the SCG only for a brief period starting at E18 and then disappearing at P5. During their transient period of expression, CC1 antigens are expressed uniformly throughout the SCG at E15-17, but are then restricted to the rostral portion of the SCG from E18 to P4. CC4 is also concentrated in the rostral portion of the SCG between E21 and P4. In the adrenal medulla, CC1 and CC4 antigens display a post-natal onset of expression commencing approximately at P14 and continue to be expressed on a subset of cells which contain tyrosine hydroxylase (TH). The expression of CC1, however, is restricted to phenylethanolamine-N-methyltransferase-(PNMT)-negative chromaffin cells, whereas CC4 is not. CC1 and CC4-expressing cells appear to be scattered throughout the adrenal medulla without any particular topographic orientation. These findings suggest that the CC1 monoclonal antibody defines a stage-specific differentiation antigen in the sympathoadrenal lineage. Additionally, the CC1 antigen may confer important positional information in the embryonic SCG by distinguishing rostral from caudal neuronal cell bodies.
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PMID:A monoclonal anti-glycoconjugate antibody defines a stage and position-dependent gradient in the developing sympathoadrenal system. 147 90

Using specific antiserum against tyrosine hydroxylase, the key enzyme in catecholamine synthesis, we found tyrosine hydroxylase immunoreactive neurons (TH-IN) in the cerebral cortex of Swiss Webster mice. They were found in the deeper layers of the cerebral isocortex in all the mice examined up to 60 days postnatal (P60). However, they appeared to be more numerous in early postnatal days. On P3 and P5, a few neurons with faintly stained perikarya were detected in the layer V and VI. The number and intensity of TH-IN increased gradually after P7, reaching to the maximum between P10 and P14 and then gradually decreased. Many of these neurons were multipolar but some were bipolar. Significance of TH-IN in the cortex and their apparent increase in immunoreactivity during the second postnatal week is not certain. Such an increase may be a transient increase in activity or phenotypic expression of tyrosine hydroxylase (TH) by young neurons in response to as yet unknown intrinsic environmental changes during this particular period of the brain development.
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PMID:Tyrosine hydroxylase-immunoreactive neurons in the mouse cerebral cortex during the postnatal period. 197 39

A precise topographical analysis of the distribution of tyrosine hydroxylase-like immunoreactive processes was performed in the frontal, cingular and parietal cortex of the rat during late embryonic and early postnatal life. Until birth, labeled processes were only observed in the restricted cortical areas known to receive a dopaminergic innervation in the adult brain. Their distribution differed markedly from that of noradrenergic fibers as identified by their dopamine-beta-hydroxylase-like immunoreactivity. Thus we considered TH-like immunoreactivity to be a selective marker of the cortical dopaminergic innervation during late fetal life, at least with the antibody we used. With this marker, dopaminergic fibers were first detected in the anterior frontal cortex at day 16 of embryonic life (E16). They developed as two bundles passing medially and laterally to the ventricular layer without penetrating it. From E20 on, the terminal fields extended to the cingular and rhinal cortex, still being restricted to the intermediate zone. No fibers were visible in the lateral and dorsal frontal cortex at this time, nor in the cortical plate and molecular layer in any cortical area. At E21, rare labeled fibers were seen in the molecular layer of the medial frontal and cingular cortex. After birth, the terminal fields of the TH-containing fibers extended further caudally in the cingular cortex and also superficially in the cortical plate. Moreover, labeled axons now also appeared in the lateral frontal and parietal cortex where their density gradually increased. At P14, two different patterns of distribution were observed: a high density of TH-positive fibers in the cortical areas known to receive a dopaminergic innervation; a low density of fibers in the other cortical areas which represented noradrenergic fibers. Indeed these TH-containing presumed noradrenergic fibers were absent at P14 following a bilateral destruction of the locus coeruleus in 4-day-old pups.
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PMID:Development of the dopaminergic innervation of the rat cerebral cortex. A light microscopic immunocytochemical study using anti-tyrosine hydroxylase antibodies. 618 53

Skin innervation during wound healing was investigated using immunocytochemical staining with the panneuronal marker antiprotein gene product (PGP) 9.5, which labels the entire innervation of the skin throughout development and in the adult. Full-thickness skin wounds in the hairy skin of the foot in neonatal rats result in pronounced hyperinnervation of the tissue that persists long after the wound has healed (at least 12 weeks). Quantification of this hyperinnervation by image analysis indicates that skin innervation density in the wounded area can increase up to 300%. The effect is greatest when wounds are performed at postnatal day (P) 0 or 7, declining when performed at P14 and P21 to resemble the weaker and transient effect in the adult. Staining with selective markers for different neuronal populations innervating skin (monoclonal anti-RT97 staining the myelinated axons of large light sensory ganglion cells; anticalcitonin gene-related peptide staining unmyelinated C axons, thinly myelinated A delta axons, and a subpopulation of large A fibres) reveal that both A- and C-fibre sensory axons contribute to this response. Destruction of the majority of the C-fibre population with neonatal capsaicin pretreatment, which leaves large A fibres intact, significantly reduces the hyperinnervation response at 14 days, confirming a major contribution from both A and C fibres. Sympathetic axons, stained with anti-tyrosine hydroxylase, do not sprout into the wounded area. Furthermore, pretreatment of neonates with 6-hydroxydopamine, which destroys the sympathetic innervation, does not significantly reduce the overall sprouting response, as identified by anti-PGP9.5 staining. Behavioural sensory testing revealed a 50% drop in the mechanical threshold in the wounded area after 3 weeks. These remarkably long-term and specific effects on sensory terminal axons following neonatal skin wounding indicate the plasticity of cutaneous innervation density following alterations in the target tissue at a critical stage of development.
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PMID:Long-term sensory hyperinnervation following neonatal skin wounds. 759 44

We have previously reported that few striatal axons from adult host brain innervate intrastriatal grafts of fetal ventral mesencephalic tissue. To see whether the immature rat brain would favor striatal innervation of the graft, unilateral implantation of fetal ventral mesencephalic tissue was carried out at 7 (P7), 14 (P14), or 60 (adults) days of age in neonatally dopamine-(DA)-lesioned and nonlesioned rats. Immunocytochemistry for tyrosine hydroxylase (TH), and/or dopamine- and adenosine 3',5'-monophosphate-regulated phosphoprotein-32 (DARPP-32) was performed 2-6 months later. In the great majority of immature and in all adult recipients, the resulting graft consisted of a distinct intrastriatal mass of tissue surrounded by the host parenchyma. Most TH-immunopositive neurons were found within the confines of such grafts, although some were lying at short distances into the host striatal tissue, particularly in immature recipients. In a few immature recipients, there was, however, extensive intermingling of TH-positive neurons with the adjacent host brain tissue. In all recipients grafted at P7, P14, or as adults, the distinct, intraparenchymal grafts contained moderate numbers of DARPP-32-positive processes, mainly at their periphery. These results indicate that the limited capacity of host striatal neurons to grow axons into transplanted fetal ventral mesencephalic tissue is not markedly different in young versus adult rats. A better integration of the ventral mesencephalic graft into the striatal circuitry of immature--as opposed to adult--recipients should therefore rely more on the higher tendency of DA neurons to become located into the host tissue following transplantation in young rats.
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PMID:Host striatal projections into fetal ventral mesencephalic tissue grafted to the striatum of immature or adult rat. 810 77

In adult weaver (wv) mutant mice up to 70% of the mesostriatal dopaminergic neurons are lost and major alterations of the dopaminergic dendrites of the substantia nigra have been described. We sought to determine the time of onset of these alterations. Cell counts of the main dopaminergic (DA) mesencephalic cell groups (A8, A9, A10), as labeled with tyrosine hydroxylase immunocytochemistry were done in wild-type and homozygous wv/wv pups. No loss of the DA neurons, was detectable at postnatal day 7 (P7), while reductions in substantia nigra (and retrorubral area) amounted to 35% at P14 and 47% by P21. On the other hand, the severe reduction of dopaminergic dendrites, particularly of their distal compartments was already visible from P3 on. During the first postnatal week, this was associated to abnormal clustering of the dopaminergic neurons. These early neuritic alterations were present, though to a milder degree, in heterozygous (wv/+) mice.
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PMID:Early postnatal changes of the dopaminergic mesencephalic neurons in the weaver mutant mouse. 857 83

Quantitative information about dopaminergic neuron numbers in the mesencephalon is needed to assess the significance of physiological cell death in the regulation of the development of this neural system. Therefore, stereological techniques were applied to determine absolute numbers of mesencephalic neurons immunoreactive to tyrosine hydroxylase during the ontogenetic period between embryonic day (E) 13 and postnatal day (P) 90. Male and female CBA/J mice were examined separately. The most rapid development with a 2.5-fold increase of total counts of immunostained cells per midbrain took place in the prenatal period. Beginning at E21, immunostained cells were counted separately in their three main locations, substantia nigra (SN), ventral tegmental area (VTA), and retrorubral field (RRF). Neuron numbers in RRF and VTA reached adult levels perinatally. In contrast, counts of immunostained cells in SN continued to increase postnatally. The only sign of cell loss was a transient decrease in VTA cell numbers (but not in total numbers of immunostained midbrain neurons) between E21 and P14. There were no statistically significant sex differences in cell numbers at any time point investigated. It is concluded that physiological cell death is not a major factor in the developmental regulation of dopaminergic cell numbers in the mouse midbrain.
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PMID:Pre- and postnatal development of dopaminergic neuron numbers in the male and female mouse midbrain. 881 75

The transient appearance of GTP cyclohydrolase I (GCH)-immunoreactive (ir) cells in the ventral lateral geniculate nuclear region of mice was detected by use of an avidin-biotin peroxidase complex method with an antibody specific for an oligopeptide of rat GCH (residues from 12 to 23, GFPERELPRPGA). In this brain region, we found for the first time novel GCH-ir cells already at postnatal day 1 (P1). The numbers reached maximum at P14 and decreased until P29, and they had mostly disappeared by P56. These cells were tyrosine hydroxylase negative and aromatic L-amino acid decarboxylase negative, indicating a lack of dopamine or serotonin production, and thus do not belong to the monoaminergic neuron system.
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PMID:Transient appearance of GTP cyclohydrolase I--positive non-monoaminergic neurons in the ventral lateral geniculate nucleus of postnatal mice. 888

We have previously shown that apoptotic natural cell death occurs within the substantia nigra (SN) pars compacta of the rat postnatally. However, the occurrence of natural cell death in phenotypically defined dopaminergic neurons has not previously been identified, nor has its time course been defined in pre- or postnatal development. We therefore examined the SN at intervals from E19 to P28 using immunostaining for tyrosine hydroxylase with a Nissl counterstain to identify intranuclear apoptotic chromatin clumps. We have found that natural cell death in dopaminergic neurons is biphasic. An initial, broad peak begins at E20, reaches maximum at P2, and abates by P8. A second peak occurs at P14. We conclude that most of the natural cell death in this neuronal population occurs in the early postnatal period.
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PMID:The time course of developmental cell death in phenotypically defined dopaminergic neurons of the substantia nigra. 905 Dec 60

During development, the sympathetic neurons innervating sweat glands undergo a neurotransmitter switch from noradrenergic to cholinergic between postnatal day (P) 4, when the sympathetic neurons first contact the sweat glands, and P21. Several in vitro experiments suggest that norepinephrine (NE), produced by sympathetic neurons, stimulates sweat glands to produce a factor that then induces the phenotypic switch. We tested this hypothesis in vivo using dopamine beta-hydroxylase-deficient mice (DBH -/-), which are unable to synthesize NE and epinephrine, and tyrosine hydroxylase-deficient mice (TH -/-), which are unable to synthesize any catecholamines. The cholinergic agonist pilocarpine and electrostimulation of the sciatic nerve both elicited a sweat response in adult DBH -/- mice that was indistinguishable from the response of controls, and the cholinergic antagonist atropine effectively blocked these responses. We did note, however, a 1- to 2-week delay in the acquisition of the sweat response in DBH -/- mice. Although diminished in magnitude, a sweat response to pilocarpine was also noted in TH -/- mice at P21. Immunohistochemistry demonstrated that TH and vasoactive intestinal peptide were detectable at P14 and increased to adult levels by P21 in DBH +/- and DBH -/- mice. These observations indicate that NE is not essential for the acquisition of the cholinergic phenotype, but it may facilitate its postnatal development.
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PMID:Norepinephrine facilitates the development of the murine sweat response but is not essential. 915 44


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