Disease relevance of Dbh

• Tyrosine hydroxylase, but not dopamine beta-hydroxylase, is increased in rat frontal cortex after traumatic brain injury [1].
• No age differences were observed in DBH activity of any tissues examined or in the activities of any enzymes in the coeliac-mesenteric ganglion complex [2].
• A number of cDNA clones for rat dopamine beta-hydroxylase (DBH) were isolated from a rat pheochromocytoma tumor cDNA library [3].
• We report here that maternal hypoxia (11-13% O2) leads to 2-3-fold increases (p < 0.01) in fetal adrenal TH, DBH, and NPY mRNA levels on the day before birth [4].
• This study was designed to determine the effect of neonatally-produced hypothyroidism on reserpine-elicited tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (D beta H) induction in the superior cervical ganglion (SCG) in rats [5].

Psychiatry related information on Dbh

• Effects of various inhibitors of tyrosine hydroxylase and dopamine beta-hydroxylase on rat self-stimulation after reserpine treatment [6].
• Furthermore, administration of either the benzodiazepine receptor agonist diazepam or the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine prevented the increase in urinary isatin excretion induced by acute food deprivation, whereas the dopamine-beta-hydroxylase inhibitor diethyldithiocarbamate proved ineffective [7].
• The effects of the inhibitor of the tyrosine-hydroxylase H 44/68 and the inhibitor of the dopamine-beta-hydroxylase FLA 63 on the diurnal variations of the motor activity was studied in male Wistar rats, which were kept under standardized conditions of light and darkness (L:D = 12:12 h) [8].
• When dopamine-beta-hydroxylase is inhibited with FLA-63 (10 mg/kg) free feeding behavior is disrupted in satiated rats [9].
• The hypothesis was based on results from our previous studies which showed that administration to rats of diethyldithiocarbamate (DDC), a dopamine beta hydroxylase inhibitor, decreased the concentration of brain norepinephrine and reduced REM sleep permanently without the subsequent appearance of REM sleep rebound [10].

High impact information on Dbh

• Microinjection of monoclonal and polyclonal antibodies raised against synaptotagmin (p65), but not the other vesicle proteins, decreases K+/Ca(2+)-mediated dopamine beta-hydroxylase surface staining, a measure of regulated secretion in PC12 cells [11].
• We have used here antisera against tyrosine hydroxylase (TH; EC 1.14.16.2) and dopamine-beta-hydroxylase (DBH; EC 1.14.17.1), two enzymes specific to catecholaminergic cells, to show that a subpopulation of rat DRG neurones is catecholaminergic and that the neurotransmitter they make is probably dopamine [12].
• Recent studies with antiserum to dopamine-beta-hydroxylase (DBH), the enzyme that converts dopamine to noradrenaline, provided evidence for the existence of noradrenergic cells [13].
• Immune lesions of noradrenergic neurones in rat central nervous system produced by antibodies to dopamine-beta-hydroxylase [14].
• Dopamine-beta-hydroxylase activity and homovanillic acid in spinal fluid of schizophrenics with brain atrophy [15].

Chemical compound and disease context of Dbh

• At the same time, the adrenaline content and the PNMT activity of the ganglion greatly increased, while no significant changes were observed in the dopamine or noradrenaline content or TH or DBH activity [16].
• These SIF cells are different from the normal SIF cells of the same ganglion, most of which appear at a later stage of postnatal development when response to hydrocortisone is lost, which contain TH but neither DBH nor PNMT, and which permanently remain in the ganglion [16].
• These results indicate that SIF cells may release dopamine or noradrenaline to adequate stimuli while the intra-pancreatic ganglion cells with only DBH may not synthesize catecholamines in a normal biosynthetic pathway [17].
• Sixteen of 17 pheochromocytomas and all hyperplastic nodules stained positively for tyrosine hydroxylase and dopamine beta-hydroxylase, consistent with an ability to produce NE [18].
• We used in situ hybridization histochemistry to determine the effect of prenatal and early postnatal nicotine exposure on tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DbetaH), preproenkephalin (PPE), and D2-dopamine receptor mRNA levels in the rat carotid body and petrosal ganglion during postnatal development [19].

Biological context of Dbh

• These findings are the first to reveal that estrogen can stimulate DBH gene expression [20].
• Retrograde axonal transport of dopamine beta hydroxylase antibodies by neurons in the trigeminal ganglion [21].
• These findings suggest that DBH positive neurons in the TG depend upon target-derived NGF and NT3 for their noradrenergic phenotype [21].
• Amino acid residues likely to be involved in the active site of DBH and in copper ligand binding were identified [3].
• Data files were scanned in a number of ways to obtain total cell counts of TH-, DBH-, and PNMT-immunoreactive cells within a designated area or cell counts of only one type of immunoreactive cell [22].

Anatomical context of Dbh

• To examine the mechanism, PC12 cells were cotransfected with luciferase reporter constructs under control of DBH or TH promoters [pDBH/Luc(-2,236/+21) or pTH/Luc(-272/+27 or -773/+27)] with an expression vector for estradiol receptor alpha [20].
• In both the superior cervical ganglion (SCG) and the TG all neurons that transported anti-DBH transported NGF [21].
• Dendrites, perikarya and spinous structures of paraventricular neurons were observed to be the postsynaptic targets of DBH axon terminals [23].
• Electron microscopic analysis of tyrosine hydroxylase, dopamine-beta-hydroxylase and phenylethanolamine-N-methyltransferase immunoreactive innervation of the hypothalamic paraventricular nucleus in the rat [23].
• Age-related changes in the gene expression of the transcription factors, Phox2a and 2b, and two marker proteins, norepinephrine transporter (NET) and dopamine beta-hydroxylase (DBH), of noradrenergic neurons were characterized in the locus coeruleus (LC) and adrenal glands using in situ hybridization [24].

Associations of Dbh with chemical compounds

• The results show that there was no difference in TH mRNA content; however, DBH mRNA levels in areas A1, A2, and C1 of the middle-aged animals did not rise during the surge as was observed in the young animals [25].
• Ethanol potentiated the normal immobilization-induced increase in adrenomedullary TH, DBH, and PNMT messenger RNA (mRNA) [26].
• Age-associated changes in mRNA levels of Phox2, norepinephrine transporter and dopamine beta-hydroxylase in the locus coeruleus and adrenal glands of rats [24].
• These agonists were more effective than nicotine alone in increasing TH and DBH gene expression and significantly elevated [Ca(2+)](i) for up to 6 h [27].
• Prolonged cortisol administration failed to alter the mRNA levels of TH, DBH, and NPY in control animals but attenuated the response to stress [28].

Physical interactions of Dbh

• Estrogen receptor binding in regions of the rat hypothalamus and preoptic area after inhibition of dopamine-beta-hydroxylase [29].
• However, SDCVs also contain membrane proteins characteristic of certain secretory granules like the vesicular monoamine transporter and the membrane-bound form of dopamine beta-hydroxylase [30].

Co-localisations of Dbh

• Rab3a was found to colocalize partially with dopamine beta-hydroxylase, a chromaffin granule marker [31].
• In control rats, fibres travelling in a stereotyped ladder-like pattern in the thoracic gray matter contained growth-associated protein-43 co-localized with dopamine beta-hydroxylase or substance P [32].

Regulatory relationships of Dbh

• The injection reduced the immunoreactivity for dopamine beta-hydroxylase in the supraoptic nucleus and significantly decreased the number of the supraoptic neurons expressing Fos-like protein after cholecystokinin but not after hypertonic saline [33].

Other interactions of Dbh

• Omission of estrogen receptor alpha or addition of the estrogen receptor antagonist ICI 182,780 prevented the DBH promoter-driven increase in luciferase [20].
• The study implicates hormonal involvement in the stress-induced changes in TH, DBH, NPY, and proenkephalin gene expression in sympathetic ganglia [28].
• Changes in tyrosine hydroxylase and dopamine-beta-hydroxylase activities but not in phenylethanolamine-N-methyltransferase activity within central adrenaline neurons after 6-hydroxydopamine administration [34].
• Many but not all of the tyrosine hydroxylase-immunoreactive neurons are also immunoreactive to the dopamine synthesizing enzyme, aromatic-L-amino-acid-decarboxylase, but lack the noradrenaline-synthesizing enzyme, dopamine-beta-hydroxylase, thus favoring synthesis of dopamine [35].
• Fos-DBH positive neurons were also increased by BV acupoint stimulation in the LC and A5 [36].

Analytical, diagnostic and therapeutic context of Dbh

• No alterations in DBH levels were observed by Western blot at any time point examined, but there was a significant increase in TH expression 28 days after TBI (optical density 334 +/- 68% or 3.3-fold, ipsilateral and 218 +/- 39% or 2.2-fold, contralateral) relative to the sham controls [1].
• The intensity of both the TH and DBH immunofluorescence decreased as the glands and their innervation developed [37].
• In contrast, TH and DBH mRNA levels in the SCG, but not in adrenal medulla, were elevated by ACTH administration, similar to the levels attained after immobilization [28].
• Rat dopamine beta-hydroxylase: molecular cloning and characterization of the cDNA and regulation of the mRNA by reserpine [3].
• Increase of dopamine beta-hydroxylase immunoreactivity in non-noradrenergic nerves of rat cerebral arteries following long-term sympathectomy [38].

References