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1 ng somatostatin, calretinin, parvalbumin, or tyrosine hydroxylase.
2 om chromaffin cells and in the expression of tyrosine hydroxylase.
3 )/calmodulin-dependent protein kinase II and tyrosine hydroxylase.
4 d with dopamine antibodies but not with anti-tyrosine hydroxylase.
5 ing and immunohistochemistry directed toward tyrosine hydroxylase.
6 urons (DaNs) using the intracellular marker, tyrosine hydroxylase.
7 axons were stained immunohistochemically for tyrosine hydroxylase.
8 A neurons, identified by their expression of tyrosine hydroxylase.
9 and establishes the first bacterial class of tyrosine hydroxylases.
10 in knockdown did not alter the expression of tyrosine hydroxylases 1 and 2, choline acetyltransferase
13 Surprisingly, these cells immunolabeled for tyrosine hydroxylase, a key component in dopamine synthe
15 from striatal neurons, and many also express tyrosine hydroxylase, a marker of dopaminergic neurons.
18 ir targeting miRNAs, 145 and 133b; increased tyrosine hydroxylase and alpha-synuclein expression with
19 staining using antibodies targeted for anti-tyrosine hydroxylase and anti-calcitonin gene-related pe
20 s, including reductions in the expression of tyrosine hydroxylase and catechol-O-methyltransferase (C
22 5 knock-out and control mice show comparable tyrosine hydroxylase and dopamine transporter expression
23 antia nigra pars compacta were processed for tyrosine hydroxylase and dopamine transporter immunohist
24 NA levels were decreased in the NAc, whereas tyrosine hydroxylase and dopamine transporter mRNA level
25 imbic dopaminergic system was assessed using tyrosine hydroxylase and dynorphin in situ hybridization
27 ivity toward regular R-substrates (including tyrosine hydroxylase and GluR1) was significantly furthe
28 Timothy syndrome show abnormal expression of tyrosine hydroxylase and increased production of norepin
30 the B2AR and catecholamine synthetic enzymes tyrosine hydroxylase and phenylethanolamine-N-methyltran
31 ne (CRH), vasoactive intestinal polypeptide, tyrosine hydroxylase, and aromatase, and labeling densit
32 tered mRNA expression of dopamine receptors, tyrosine hydroxylase, and dopamine transporter genes in
33 eptors (GalR1-R3), tryptophan hydroxylase 2, tyrosine hydroxylase, and nitric oxide synthase as well
37 s immunoreactive for the DA synthetic enzyme tyrosine hydroxylase; and 3) nearly all RMTg axons forme
39 DNA methylation of a specific set of genes, tyrosine hydroxylase, brain-derived neurotrophic factor
40 also led to a decrease in protein levels of tyrosine hydroxylase, but not of tryptophan hydroxylase.
41 compartment as identified by costaining with tyrosine hydroxylase, but not outside these clusters.
42 We find that transgenes under control of the tyrosine hydroxylase, but not the dopamine transporter,
43 one opsin, as well as other retinal markers (tyrosine hydroxylase, calbindin, PKCalpha and Brna3), in
46 urons that exhibited dual immunostaining for tyrosine hydroxylase (catecholaminergic neurons) and c-F
47 anges were associated with a greater loss of tyrosine hydroxylase cell content and intense neuroinfla
48 ucted for simultaneous detection of NOS with tyrosine hydroxylase, choline acetyltransferase, calbind
51 ons, implying cholinergic regulation; and by tyrosine hydroxylase-containing axons, implying adrenerg
53 g Kluver-Barrera (myelin and cell bodies) or tyrosine hydroxylase (dopaminergic neurons) immunohistoc
57 decreased DA re-uptake and resulted in more tyrosine hydroxylase expressing neurons in the SN than i
58 Whole-cell recordings were obtained from tyrosine hydroxylase-expressing (TH(+)) neurons in stria
59 loss of the E3-ubiquitin ligase, UBE3A, from tyrosine hydroxylase-expressing neurons impairs mesoaccu
60 ly thought to originate exclusively from the tyrosine-hydroxylase-expressing (TH(+)) neurons in the v
61 dopamine levels or dopamine transporter and tyrosine hydroxylase expression after lesioning with MPT
62 e, release, D2 autoreceptor sensitivity, and tyrosine hydroxylase expression and activity as mechanis
63 AT) undergo alternative activation to induce tyrosine hydroxylase expression and catecholamine produc
64 as: an increase in LC bursting activity; in tyrosine hydroxylase expression and that of the noradren
65 n, gene expression analysis revealed reduced tyrosine hydroxylase expression and the regulation of ge
66 tive turnover throughout life and regulating tyrosine hydroxylase expression in an activity-dependent
67 pancreas, GLUT2 expression in the liver, and tyrosine hydroxylase expression in dopaminergic neurons.
69 brain cortex neurotransmitter synthesis and tyrosine hydroxylase expression on intracellular ascorba
70 nts but not adults, there was an increase in tyrosine hydroxylase expression that was selective to th
71 macrine cells (brain nitric oxide synthetase/tyrosine hydroxylase expression) and ganglion cell axons
73 (CT-alpha-syn) in axons, rescued the loss of tyrosine hydroxylase fibers in striatum, and improved mo
76 Overall, the putative function of Orf13 as a tyrosine hydroxylase has been confirmed and establishes
77 essing neurons almost invariably stained for tyrosine hydroxylase, identifying them as dopaminergic.
78 ditory end organ, the saccule, combined with tyrosine hydroxylase immunofluorescence (TH-ir) revealed
80 f putative dopaminergic cells and fibers (by tyrosine hydroxylase immunohistochemistry) and dopamine
81 tracer injections, both in combination with tyrosine hydroxylase immunohistochemistry, to characteri
84 nt did not alter Fos-immunoreactivity within tyrosine hydroxylase-immunolabeled neurons of VTA, but d
86 easuring striatal dopamine levels, total and tyrosine hydroxylase immunoreactive neuron numbers and B
87 allopregnanolone promotes the restoration of tyrosine hydroxylase immunoreactive neurons and total ce
88 O-treated rats had increased preservation of tyrosine hydroxylase immunoreactive neurons in the subst
89 mid-forebrain bundle increased the number of tyrosine hydroxylase immunoreactive neurons in the subst
90 with melanin concentrating hormone (MCH) and tyrosine hydroxylase immunoreactive neurons of the hypot
91 mmunoreactive bipolar cells (one likely also tyrosine hydroxylase immunoreactive) that bore ciliated
92 mmunohistochemistry revealed that almost all tyrosine hydroxylase-immunoreactive (TH-ir) axons in the
93 eatment resulted in a significant sparing of tyrosine hydroxylase-immunoreactive (THir) neurons in th
94 is possibility, we quantified the density of tyrosine hydroxylase-immunoreactive axons as a measure o
97 ates of the number of melanin-containing and tyrosine hydroxylase-immunoreactive neurons in the subst
100 d the innervation patterns of both 5-HT- and tyrosine hydroxylase-immunoreactive processes relative t
101 ad1b and gad2 expression in combination with tyrosine hydroxylase immunoreactivity in 4-day-old larva
104 ity measurements of dopamine transporter and tyrosine hydroxylase immunoreactivity, which were all si
105 striatal dopamine, and stereologic counts of tyrosine hydroxylase-immunostained neurons in substantia
106 (Nacc) shell, accompanied by a reduction of tyrosine hydroxylase immunostaining and postsynaptic den
107 n using virally mediated RNA interference of tyrosine hydroxylase impaired temporal control, and seco
108 rons in the sympathetic ganglia, increase in tyrosine hydroxylase in both nerve terminals in the SAT
110 a and astrocytes and decreased expression of tyrosine hydroxylase in periglomerular cells, vesicular
111 -mouse IgG1(a) autoantibody colocalized with tyrosine hydroxylase in the basal ganglia within dopamin
113 erations in dopaminergic phenotypic markers (tyrosine hydroxylase) in the early stages of Parkinson's
114 nsity of sensory (CGRP) but not sympathetic (tyrosine hydroxylase) innervation for Old versus Young M
115 catenin in the midline progenitors using the tyrosine hydroxylase-internal ribosomal entry site-Cre (
117 rgic centres of Insm1 mutants, expression of tyrosine hydroxylase is delayed in the locus coeruleus a
118 rate-limiting enzyme for dopamine synthesis, tyrosine hydroxylase, is specifically disrupted in the r
119 comprising the first 50 amino acids of human tyrosine hydroxylase, isoform 1 (hTH1), that contain the
122 onal protein C/D, choline acetyltransferase, tyrosine hydroxylase, neuronal nitric oxide synthase, an
123 it for both at embryonic day [E]12.5-E13.5), tyrosine hydroxylase neurons (E15.5), nitric oxide synth
127 n C/D, as well as choline acetyltransferase, tyrosine hydroxylase, nitric oxide synthetase, and vasoa
129 aSWNTs attenuated METH-induced increases in tyrosine hydroxylase or synaptic protein expression.
130 f D2S but not D2L prevents the inhibition of tyrosine hydroxylase phosphorylation and, thereby, of do
131 m neurons expressing Per2 and Per3 and their tyrosine hydroxylase phosphorylation is regulated in a c
134 ve study to determine the plastic changes of tyrosine hydroxylase-positive (TH1(+); mainly dopaminerg
135 with allopregnanolone restored the number of tyrosine hydroxylase-positive and total cell numbers in
137 esicular ACh transporter immunoreactivity in tyrosine hydroxylase-positive cardiac sympathetic fibers
138 with motor impairment, as well as postmortem tyrosine hydroxylase-positive cell counts and striatal d
139 dures demonstrated that these cells were not tyrosine hydroxylase-positive cells in the Kolliker-Fuse
141 ositive neurons in the nigra and decrease in tyrosine hydroxylase-positive fibers and neurotransmitte
142 ned how dopamine is stored and released from tyrosine hydroxylase-positive GFP (TH(+)-GFP) mouse peri
145 h striatal dysfunctions preceding SN loss of tyrosine hydroxylase-positive neurons and that other neu
146 ra pars compacta, there was a 50-90% loss of tyrosine hydroxylase-positive neurons from the earliest
147 rdingly, castration also induced the loss of tyrosine hydroxylase-positive neurons in the nigra and d
148 it of motor function, diminished the loss of tyrosine hydroxylase-positive neurons in the substantia
149 symptoms are associated with massive loss of tyrosine hydroxylase-positive neurons in the substantia
150 showed neuroprotective effects by preserving tyrosine hydroxylase-positive neurons in the substantia
151 striatal denervation and loss of melanin and tyrosine hydroxylase-positive neurons, is poorly underst
152 at microRNA-7 (miR-7), which is expressed in tyrosine hydroxylase-positive nigral neurons in mice and
153 /vehicle-treated animals, almost 40% loss of tyrosine hydroxylase-positive norepinephrine neurons was
155 hysiotropic tuberoinfundibular dopaminergic (tyrosine hydroxylase-positive) neurons; however, <10% of
158 red fluorescent protein under control of the tyrosine hydroxylase promoter and loaded with the calciu
159 ats with loxP-flanked (floxed) alleles and a tyrosine hydroxylase promoter-driven cre allele and demo
160 tional activity, as measured by induction of tyrosine hydroxylase promoter-luciferase activity, compa
161 s elicits a non-cell-autonomous reduction of tyrosine hydroxylase protein level in the axonal project
162 n measured immunolabeling for phosphorylated tyrosine hydroxylase (pTH-ir), the rate-limiting enzyme
163 deletion led to decreases in phosphorylated tyrosine hydroxylase (pTH-Ser40) levels in the VTA and d
164 GABA neurons were not numerous, and most non-tyrosine hydroxylase/retrogradely labeled cells lacked G
165 stochemistry of the sympathetic nerve marker tyrosine hydroxylase revealed a progressive loss of adre
166 n sections in this same plane is stained for tyrosine hydroxylase, revealing the distribution of cate
168 t with 6-OHDA and brains were stained with a tyrosine hydroxylase-silver nucleolar (TH-AgNOR) stain.
169 ff and was accompanied by a higher number of tyrosine hydroxylase(+) SN neurons (increase of approxim
174 ortem study, a semi-quantitative analysis of tyrosine hydroxylase staining was conducted in nigral do
176 me of these additional fibers also expressed tyrosine hydroxylase, suggesting a sympathetic origin.
177 well as with the dopamine synthesis enzymes tyrosine hydroxylase (TH) and aromatic amino acid decarb
180 nstrate that Hand1 is dispensable for normal tyrosine hydroxylase (TH) and dopamine beta-hydroxylase
182 europathy was studied by staining femurs for tyrosine hydroxylase (TH) and neurofilament 200 (NF-200)
183 tiation into dopaminergic neurons expressing tyrosine hydroxylase (TH) and nuclear receptor related-1
184 ly it also greatly reduced the expression of tyrosine hydroxylase (Th) and other markers of the dopam
186 substantia nigra that expressed both FG and tyrosine hydroxylase (TH) and striatal terminals express
187 opamine beta-hydroxylase; these neurons lack tyrosine hydroxylase (TH) and thus are not catecholamine
188 thetic enzymes of DA and 5-HT, respectively, tyrosine hydroxylase (TH) and tryptophan hydroxylase (TP
189 ted to express the neuronal markers Tuj1 and tyrosine hydroxylase (TH) at E10.5, they exited the cell
193 et of this diverse cell population expresses tyrosine hydroxylase (TH) during postnatal rat developme
194 lacing test, and a 272% increase in striatal tyrosine hydroxylase (TH) enzyme activity at 3 weeks aft
196 ation of the flight circuit in pupae reduces Tyrosine Hydroxylase (TH) expression in the PAM neurons
197 PAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in the striatum.
199 d dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitoc
200 O1 directly targets and negatively regulates tyrosine hydroxylase (TH) expression, the rate-limiting
202 ergic interneurons that express the gene for tyrosine hydroxylase (TH) have been identified previousl
203 grity by measuring fiber length density with tyrosine hydroxylase (TH) immunohistology and dopamine t
204 In this study we used Nissl staining and tyrosine hydroxylase (TH) immunoreactivity to compare th
206 study, we analyzed the activity of striatal tyrosine hydroxylase (TH) in rats at 1 day, 1 week, and
207 are fewer dopaminergic neurons labeled with tyrosine hydroxylase (TH) in the male AVPV than the fema
208 tegmental area (VTA) dopaminergic activity, tyrosine hydroxylase (TH) levels and dopamine synthesis.
209 luciferase reporter gene into the endogenous tyrosine hydroxylase (TH) locus enables rapid and easy q
211 ns were significantly reduced by 29% and the tyrosine hydroxylase (TH) negative neurons unaffected af
212 Here we introduce an unexpected neuron, the tyrosine hydroxylase (TH) neuron of the arcuate nucleus
213 whether hypothalamic arcuate (ARC) dopamine/tyrosine hydroxylase (TH) neurons interact with other AR
217 techolaminergic fibers with somatostatin and tyrosine hydroxylase (TH) or dopamine beta-hydroxylase (
219 urons after 25 days of differentiation ( 40% tyrosine hydroxylase (TH) positive, maturing into 25% ce
220 te that VTA GABAergic neurons that coexpress tyrosine hydroxylase (TH) projecting to lateral habenula
221 nced green fluorescent protein driven by the tyrosine hydroxylase (TH) promoter (TH-EGFP) to identify
222 ng 6.3 kb of upstream sequences from the rat tyrosine hydroxylase (TH) promoter to a NFH promoter, an
223 ollowed by an upstream enhancer from the rat tyrosine hydroxylase (TH) promoter, to a neurofilament h
224 ine that expresses eGFP under control of the tyrosine hydroxylase (TH) promoter, we found that mu opi
226 (3-NT), an indirect index of NO production, tyrosine hydroxylase (TH) protein levels (dopamine termi
227 irment of mitochondrial function and loss of tyrosine hydroxylase (TH) protein, indicative of dopamin
228 rograde tracing and immunohistochemistry for tyrosine hydroxylase (TH) to identify bulbospinal catech
229 is a bona fide coactivator and stimulator of tyrosine hydroxylase (TH) transcription in neuronal cell
231 leucoagglutinin (PHA-L) injections, whereas tyrosine hydroxylase (TH) was used as a marker for DA ax
232 opeptide Y (NPY)(+), parvalbumin (PV)(+) and tyrosine hydroxylase (TH)(+), we further elucidate this
233 e Y (NPY)(+), proopiomelanocortin (POMC)(+), tyrosine hydroxylase (TH)(+)] and glia (tanycytes).
235 (IL)-4 stimulation induces the expression of tyrosine hydroxylase (TH), a key enzyme in the catechola
236 luorescent protein (GFP) and the promoter of tyrosine hydroxylase (TH), a key synthetic enzyme for ca
237 tochemistry to detect the phosphorylation of tyrosine hydroxylase (TH), a rate-limiting enzyme in the
238 RTqPCR for paired-like homeobox 2b (PHOX2B), tyrosine hydroxylase (TH), and doublecortin (DCX) mRNA i
240 th that of choline acetyltransferase (ChAT), tyrosine hydroxylase (TH), and serotonin (5HT) by double
241 esicular acetylcholine transporter [VAChT]), tyrosine hydroxylase (TH), and serotonin (5HT) to identi
242 d from tyrosine by the rate-limiting enzyme, tyrosine hydroxylase (TH), and tyrosine is catabolized b
243 besides neuroprotection, BRF110 up-regulates tyrosine hydroxylase (TH), aromatic l-amino acid decarbo
244 n interact with tyrosinase (TYR) and inhibit tyrosine hydroxylase (TH), both of which are enzymes inv
245 inal whole mounts stained with antibodies to tyrosine hydroxylase (TH), DA cells gave rise to varicos
246 her vector decreased expression of rat SNCA, tyrosine hydroxylase (TH), dopamine transporter (DAT) or
247 n blot analysis to compare protein levels of tyrosine hydroxylase (TH), glutamate decarboxylase (GAD6
248 projections labeled with antibodies against tyrosine hydroxylase (TH), melanin-concentrating hormone
250 pha), specific to pain-sensing C-fibers, and tyrosine hydroxylase (Th), specific to low-threshold mec
251 immunohistochemical techniques for detecting tyrosine hydroxylase (TH), the initial rate-limiting enz
253 In contrast, myeloid-specific deletion of tyrosine hydroxylase (TH), the rate-limiting enzyme in c
254 elanization and reduced immunoreactivity for tyrosine hydroxylase (TH), the rate-limiting enzyme in d
255 protein 1 (MTA1) is an upstream modulator of tyrosine hydroxylase (TH), the rate-limiting enzyme in d
256 used immunohistochemical methods to localize tyrosine hydroxylase (TH), the rate-limiting enzyme in t
257 dopaminergic, as judged by the expression of tyrosine hydroxylase (TH), the rate-limiting enzyme of d
258 eased expression of DA neuron-enriched genes tyrosine hydroxylase (TH), vesicular monoamine transport
259 tivate expression of neuronal genes, such as tyrosine hydroxylase (TH), which is the rate-limiting en
261 ypic lamina-specific neurite arborization of tyrosine hydroxylase (TH)-expressing dopaminergic amacri
262 n slices from neonatal (postnatal days 6-10) tyrosine hydroxylase (TH)-GFP transgenic mice, was about
263 -immunoreactive(ir) axonal varicosities were tyrosine hydroxylase (TH)-ir and the same proportion wer
265 t are further divided into two subtypes: (1) tyrosine hydroxylase (TH)-positive C-LTMRs that form the
266 a3 and -beta5i subunits are colocalized with tyrosine hydroxylase (TH)-positive cells in the SN of co
267 he diagnosis of PD and demonstrated >300,000 tyrosine hydroxylase (TH)-positive grafted cells per sid
269 d significant protection against the loss of tyrosine hydroxylase (TH)-positive neurons of substantia
277 ing [striatal dopamine transporter (DAT) and tyrosine hydroxylase (TH)] and alterations in the mean n
278 expression of a set of five genes [including tyrosine hydroxylase (Th)] that are necessary for differ
279 s assessed using antibodies directed against tyrosine hydroxylase (TH, DAergic marker), Iba-1 (pan-mi
280 by simultaneous detection of VGluT2 mRNA and tyrosine hydroxylase (TH; for identification of dopamine
281 protein 43 (GAP-43; sprouted nerve fibers), tyrosine hydroxylase (TH; sympathetic nerve fibers), CD3
282 esicular acetylcholine transporter [VAChT]), tyrosine hydroxylase (TH; the rate-limiting enzyme in ca
283 ubpopulation that expresses VGluT2 but lacks tyrosine hydroxylase (TH; VGluT2-only neurons), present
284 ted neurons in the NST was approximately 29% tyrosine hydroxylase [TH]-positive [i.e., presumably nor
286 translation of the two non-allelic forms of tyrosine hydroxylase (th1 and th2) in zebrafish larvae.
287 urons nor alter protein expression levels of tyrosine hydroxylase, the DA transporter or vesicular mo
288 t attributable to lack of phosphorylation of tyrosine hydroxylase, the key enzyme involved in DA synt
289 sociated with reduced striatal expression of tyrosine hydroxylase, the rate-limited enzyme in DA synt
290 ion of Foxa1/2 results in down-regulation of tyrosine hydroxylase, the rate-limiting enzyme of dopami
291 oactive intestinal peptide, substance P, and tyrosine hydroxylase to quantify nerves, S100beta for gl
292 ectively inhibits phosphorylated (activated) tyrosine hydroxylase to reduce dopamine production via n
295 levels, sympathetic axons (immunostained for tyrosine hydroxylase) undergo robust collateral sproutin
296 ons, leading to downregulation of the enzyme tyrosine hydroxylase, which is essential for dopamine sy
297 sion also caused ectopic zonal expression of tyrosine hydroxylase, which is only expressed in adult P
298 de, vesicular acetylcholine transporter, and tyrosine hydroxylase, which selectively label spinal aff
300 te-limiting catalyzing catecholamine enzyme (tyrosine hydroxylase) within the LC and their neocortica
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