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

We examined changes in the tyrosine hydroxylase (TH)-immunoreactive fibers following 5 min of cerebral ischemia in gerbils using an immunohistochemical method 1, 3 and 30 days after ischemia. Almost all CA-1 pyramidal neurons were lost 3 days after ischemia, whereas noradrenergic fibers were maintained 30 days after ischemia. The present study demonstrated that TH-immunoreactive fibers and cells were resistant to transient ischemia, and that there was no sprouting or hyperactivity in noradrenergic systems after ischemia.
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PMID:Resistance of hippocampal CA-1 noradrenergic fibers to five minutes of transient cerebral ischemia in the gerbil. 136 Oct 91

We have previously reported that a developmental axon-sparing striatal injury induced by hypoxia-ischemia results in a diminished adult number of substantia nigra (SN) tyrosine hydroxylase (TH)-positive neurons, in the absence of direct nigral injury. To examine the specific role of striatal injury, we made selective striatal lesions in the 7-day-old rat with quinolinic acid (QA), 40, 80, 120 and 480 nmol. Striatal lesions resulted in a decrease in the adult number of TH-positive neurons in the ipsilateral SN. The decrease was correlated with the reduction in striatal area (r = 0.76, p < 0.01); a 25-30% reduction in SN neurons was observed at 50-60% striatal area loss. The area of SN pars compacta (SNpc) in animals with 120- and 480-nmol QA lesions was reduced by 12 and 15%, respectively (p < 0.01) and this reduction also correlated with the loss of striatal area (r = 0.63, p < 0.01). Individual TH-positive neuron size and neuron-packing density were unaltered in SNpc on the experimental side. We conclude that the adult number of SN dopaminergic neurons depends on developmental support by the striatum. We hypothesize that less support by the smaller striatum may result in accentuated developmental cell death in the SNpc.
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PMID:Effect of striatal lesion with quinolinate on the development of substantia nigra dopaminergic neurons: a quantitative morphological analysis. 136 70

Recent studies in the rat have suggested that hippocampal norepinephrine can regulate the amount of damage seen after transient forebrain ischemia. We used the gerbil to study the role of norepinephrine in ischemic damage. Using tyrosine hydroxylase immunocytochemistry and chemical measurements of norepinephrine, we determined that the gerbil hippocampus has a similar but topographically different norepinephrine innervation than the rat. Brains from gerbils treated with 100 mg/kg of N-(2-chloroethyl)-N-methyl-2-bromobenzylamine (DSP4) had 60% less norepinephrine than saline-treated controls, similar to the effect of the drug in rats. We administered DSP4 to gerbils two weeks before exposing them to 5 min of bilateral carotid artery occlusion. Animals treated with DSP4 and subjected to ischemia had worse pyramidal cell loss in the CA3 and CA4 regions than saline-treated ischemic controls. CA1 pyramidal cell loss (about 90%) was severe in both the saline- and DSP4-treated animals. These data provide further evidence that norepinephrine can regulate the neuronal death in the hippocampal formation after transient forebrain ischemia. Furthermore, this is the first demonstration of that regulation in the gerbil and suggests that noradrenergic input to the hippocampus may be important in ischemia in other species besides the rat.
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PMID:DSP4 treatment worsens hippocampal pyramidal cell damage after transient ischemia. 165 18

To evaluate the development of striatal ischemic cell damage in relation to alterations in dopamine (DA) transmission, one year old male Wistar rats underwent a 15 min incomplete cerebral ischemia (ICI) induced by occlusion of the common carotid arteries and by hypovolemic hypotension. The animals were divided into the following experimental groups: sham operated rats, rats with ICI without reperfusion, and rats with ICI followed by 60 min, 24 h, 72 h and 144 h of recirculation. The ischemia induced striatal lesions were investigated in serial coronal brain sections, stained with cresylviolet or immunostained for dopamine and cAMP regulated phosphoprotein (DARPP-32), for tyrosine hydroxylase (TH) and for glial fibrillary acidic protein (GFAP) immunoreactivities (IR). Measurements of striatal dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels were made on analogous experimental groups using HPLC methods. Signs of degeneration in small to medium sized neurons were already seen after 60 min of postischemic reperfusion together with slight decreases of DARPP-32 IR and increases of GFAP IR. The damage continued to increase up to 144 h, and after 24 h of recirculation there were clearly defined areas of reduced DARPP-32 IR, overlapping with increased TH IR and increased GFAP IR. The levels of DA, DOPAC and HVA increased sharply after 60 min (151%, 462% and 201%, respectively) remained high after 24 h and normalized after 72 h of recirculation. The DA metabolism was high after 60 min and had already normalized after 24 h of recirculation. The increased DA metabolism in striatal nerve terminals in response to ischemic injury may reflect an early degenerative change in the DA terminals. The long-lasting increase in TH IR may to some extent represent an adaptive change in response to the disappearance of DA receptor-containing nerve cells. Based on the present findings it is possible that an increased D1 transmission in neostriatum immediately following the ischemic injury may contribute to striatal nerve cell degeneration in which an enhancement of NMDA receptor transduction may be implicated.
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PMID:Changes in striatal dopamine neurohistochemistry and biochemistry after incomplete transient cerebral ischemia in the rat. 166 38

Previous in vitro studies have shown that biochemical indices of striatal dopaminergic systems are preserved following neonatal hypoxia-ischemia. There has been no previous assessment of these systems in vivo. Using the accumulation of striatal dopa following administration of a dopa decarboxylase inhibitor as an in vivo measure of tyrosine hydroxylase (TH) activity, we have found that baseline TH activity, and its regulation by both neuronal activity and presynaptic autoreceptors are also preserved following hypoxia-ischemia.
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PMID:Preserved striatal tyrosine hydroxylase activity, assessed in vivo, following neonatal hypoxia-ischemia. 168 13

The selective loss of hippocampal CA-1 pyramidal neurons has been reported not to be accompanied by damage to presynaptic terminals in the stratum radiatum as shown by electron microscopic observations. However, we examined changes in the tyrosine hydroxylase (TH) immunoreactive fibers following transient ischemia in rats using an immunohistochemical method 1, 3, 7 and 30 days after ischemia. The present study indicates that ischemic neuronal injury spreads to pre-synaptic fibers after the disappearance of the post-synaptic CA-1 pyramidal neurons.
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PMID:Decrease of pre-synaptic noradrenergic fiber density in rat hippocampus after transient ischemia. 168 11

Little is known of the alterations in the neurochemical anatomy of the striatum following neonatal hypoxic-ischemic injury. In an experimental model in rodent, it has been shown that striatal biochemical markers of dopaminergic systems appear to be relatively spared. We sought to define the morphologic correlates of this finding by staining striatal tyrosine hydroxylase (TH)-positive fibers with the immunoperoxidase technique. Since this model is unilateral, it is possible to examine relative changes in the density of TH-positive staining of the striatum at the population level within the same section. We find that in immature animals (3-4 weeks) there is an increase in the relative density of striatal TH-positive staining on the injured side. There is also an increase in the relative density of staining in the nucleus accumbens, in the absence of shrinkage of that nucleus. There is no relationship between the degree of density increase in the striatum, and its degree of shrinkage. This increase in relative density is a persistent change, as it is also observed in adult rats (9-12 weeks). While the functional significance of these findings are unknown, they are compatible with a relative increase in the dopaminergic innervation of the hypoxia-ischemia injured striatum.
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PMID:Unilateral hypoxic-ischemic injury in neonatal rat results in a persistent increase in the density of striatal tyrosine hydroxylase immunoperoxidase staining. 170 95

The effects of a continuous 16-day gestational exposure to nicotine on development of central and peripheral catecholaminergic pathways were examined in the offspring of dams who received a minipump implant on the 4th day of gestation. Prenatal nicotine exposure resulted in a selective suppression of maturational increases in norepinephrine and dopamine levels and utilization rates in the cerebral cortex and also reduced transmitter levels in sympathetic pathways to the lung and kidney. The regional selectivity of the effect, combined with measurements of synaptosomal uptake of [3H]norepinephrine and of tyrosine hydroxylase activity, all suggested that the alterations in transmitter disposition reflected reduced neural activity as opposed to actions on general cellular development or synaptogenesis. Although the lag in development was largely made up by weaning, deficits in norepinephrine utilization reappeared in young adulthood in the cerebral cortex and midbrain + brainstem, suggesting that lasting functional alterations may occur as a consequence of prenatal nicotine exposure. Comparisons with the results obtained with maternal nicotine injections (which produce largely stimulatory effects on norepinephrine levels and turnover) suggest that the hypoxia/ischemia associated with injected nicotine causes a reactive hyperinnervation; the adverse actions of nicotine on neurotransmitter development are thus highly dependent upon the route of drug administration.
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PMID:Prenatal exposure to nicotine via maternal infusions: effects on development of catecholamine systems. 325 40

Involvement of the IEGs in brain injury and ischemia is under intensive investigation (Gubits et al., 1993). There are several families of the IEGs. They include the fos, jun, and zinc finger genes that encode transcription factors. Products of the fos family (c-fos, fra-1, fra-2, and fos B) bind to members of the jun family (c-jun, jun B, jun D) via leucine zippers, and this dimer then binds to the AP-1 site (consensus sequence -TGACTCA-) in the promoter of target genes, which in turn regulate the expression of late response genes that produce long-term changes in cells. For example, c-fos may regulate the long-term expression of preproenkephalin, nerve growth factor, dynorphin, vasoactive intestinal polypeptide, tyrosine hydroxylase and other genes with AP-1 sites in their promoters (Curran and Morgan, 1987; Sheng and Greenberg, 1990). It is likely that the c-fos gene up-regulation observed in ischemic astrocytes leads to the changes observed in the expressions of hsp and cytoskeleton protein genes in this experimental model. This is supported by the findings of Sarid (1991) and Pennypacker et al. (1994) who have shown that AP-1 DNA binding activity in hippocampus recognized an AP-1 sequence from the promoter region of the GFAP which is a potential target gene. van de Klundert et al. (1992) also suggested the involvement of AP-1 in transcriptional regulation of vimentin. IEGs can be induced within minutes by extracellular stimuli including transmitters, peptides, and growth factors. In this study, we have shown that c-fos induction by ischemia was rapid and transient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gene expression in astrocytes during and after ischemia. 756 84

We report our findings in the guinea pig involving dopamine in postsynaptic regulation of the activity of glutamatergic inner hair cells (IHCs) and in protection of primary auditory neurons during transient ischemia. Seven days after intracochlear perfusion of 6-hydroxydopamine, no immunoreactivity to tyrosine hydroxylase (TH) was demonstrable within the organ of Corti. TH and aromatic amino acid decarboxylase were immunolocalized at an ultrastructural level within lateral olivocochlear varicosities synapsing with radial auditory dendrites postsynaptic to the IHCs. The D2 agonist piribedil induced a dose-dependent decrease in the amplitude of the compound action potential of the auditory nerve. Piribedil also prevented appearance of ischemia-induced swelling of the radial dendrites.
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PMID:Synaptic connections and putative functions of the dopaminergic innervation of the guinea pig cochlea. 757 83


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