Disease relevance of deoxyepinephrine

• Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease. Pathophysiologic and clinical implications [1].
• Bilateral implantation of fetal mesencephalic tissue can induce substantial long-term functional improvement in patients with parkinsonism and severe dopamine depletion and is accompanied by increased uptake of fluorodopa by the striatum [2].
• We conclude that dopamine agonists are usually effective treatments for macroprolactinoma and that after a response has been obtained, it can be maintained in many patients with a greatly reduced dose [3].
• The selective destruction by MPTP of nigrostriatal dopamine neurons that is responsible for the movement disorder also appears to result in an increase in central noradrenergic activity, which is not possible in Parkinson's disease [4].
• Although bromocriptine, a dopamine receptor agonist, is now widely used in the treatment of acromegaly, there have been no controlled trials of its biochemical or clinical effects on this disorder [5].
• This suggests that dopamine dysfunction is involved with symptoms of inattention but may also contribute to substance abuse comorbidity in ADHD [6].
• Endothelial and ovarian cancer cells expressed all dopamine receptors except for the lack of DR3 expression in ovarian cancer cells [7].

Psychiatry related information on deoxyepinephrine

• One behavioural paradigm that supports this hypothesis is intracranial self-stimulation (ICS), during which animals repeatedly press a lever to stimulate their own dopamine-releasing neurons electrically [8].
• Converging pharmacological, human post-mortem and genetic studies implicate the dopamine D3 receptor in drug addiction [9].
• When rats are given a series of electroconvulsive shocks (ECSs) over several days, they display enhanced behavioural responses to both serotonin- and dopamine-receptor agonists [10].
• Dopamine receptors are primary targets for drugs used in the treatment of psychomotor disorders such as Parkinson's disease and schizophrenia [11].
• Somatostatin receptors and dopamine receptors are colocalized in neuronal subgroups, and somatostatin is involved in modulating dopamine-mediated control of motor activity [12].
• Midbrain dopamine neurons have long been implicated in mediating reward behavior and the motivational aspects of feeding behavior [13].
• Mice injected with peptides that disrupt D2-DAT interaction exhibit decreased synaptosomal dopamine uptake and significantly increased locomotor activity, reminiscent of DAT knockout mice [14].

High impact information on deoxyepinephrine

• Drug therapy may play an increasing role, especially dopamine agonists, which control either hGH or prolactin secretion and can cause shrinkage of tumor tissue [15].
• Dopamine beta-hydroxylase of adrenal chromaffin granules: structure and function [16].
• In the central nervous system, dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion, and affect as well as neuroendocrine secretion [17].
• In the periphery, dopamine receptors are present more prominently in kidney, vasculature, and pituitary, where they affect mainly sodium homeostasis, vascular tone, and hormone secretion [17].
• The diverse physiological actions of dopamine are mediated by at least five distinct G protein-coupled receptor subtypes [17].

Chemical compound and disease context of deoxyepinephrine

• BACKGROUND: There is debate about whether the initial treatment for patients with Parkinson's disease should be levodopa or a dopamine agonist [18].
• The clinical syndrome of striatal dopamine deficiency: parkinsonism induced by MPTP [19].
• Haloperidol-induced catalepsy is mediated by postsynaptic dopamine receptors [20].
• Here we confirm the blocking effects of IAP and GTP gamma S (a nonhydrolysable analogue of GTP) on the ACh-induced K+-current recorded from the ganglion cells of the sea slug Aplysia and compare their effects on histamine (HA)-induced and dopamine (DA)-induced K+-currents [21].
• Thus, the cocaine receptor related to substance abuse is proposed to be the one associated with dopamine uptake inhibition [22].

Biological context of deoxyepinephrine

• Blood-pressure changes after six months correlated best with differences in plasma activity of dopamine-beta-hydroxylase with patients supine (r = 0.54; P less than 0.05) and upright (r = 0.62; P less than 0.05) [23].
• Letter: Effects of dopamine on heart rate [24].
• Alterations of peripheral sympathetic-nervous-system activity, as reflected by changes of dopamine-beta-hydroxylase in plasma, were evaluated, and plasma volume and plasma renin activity were measured [23].
• Thus, the antagonistic effects of dopamine and glutamate on the excitability of striatal neurons are reflected in antagonistic effects of these neurotransmitters on the state of phosphorylation of DARPP-32 [25].
• Dopamine-like renal and mesenteric vasodilation caused by apomorphine 6-propylnorapomorphine and 2-amino-6, 7-dihydroxy-1,2,3,4-tetrahydronaphthalene [26].

Anatomical context of deoxyepinephrine

• The three regions with the highest levels, caudate, putamen and substantia nigra, are characterized by a high dopamine metabolism [27].
• Parkinson's disease is characterized by the loss of midbrain dopamine neurons that innervate the caudate and the putamen [28].
• In the caudate nucleus, the only subdivision with severe dopamine reduction was the most dorsal rostral part (4 percent of the dopamine remaining); the other subdivisions still had substantial levels of dopamine (up to approximately 40 percent of control levels) [1].
• In an effort to modify the motor disability of advanced Parkinson's disease, we implanted embryonic mesencephalic tissue containing dopamine cells into the caudate and putamen of seven patients [29].
• Although the case patients continued to be disabled by their disease, unilateral intracaudate grafts of fetal tissue containing dopamine diminished the symptoms and signs of parkinsonism during 18 months of evaluation [28].

Associations of deoxyepinephrine with other chemical compounds

• While reclining, dysautonomic patients had normal norepinephrine concentrations and blood pressure, but after standing they did not have a normal increase in their levels of norepinephrine (P less than 0.005), dopamine-beta-hydroxylase (P less than 0.05) or plasma protein concentration (P less than 0.01); they became hypotensive [30].
• Here we show that targetted inactivation of MAOB in mice increases levels of PEA but not those of 5-HT, NE and DA, demonstrating a primary role for MAOB in the metabolism of PEA [31].
• In contrast, there is no pronounced loss of serotonin in the neostriatum or of dopamine and its metabolites in other brain areas in MPTP-treated animals [32].
• Midbrain dopamine neurons normally help to shape behaviour by reinforcing biologically rewarding events, but addictive drugs such as cocaine can inappropriately exert a reinforcing influence by acting upon the mesolimbic dopamine system [33].
• In vivo electrochemical detection of catechols in the neostriatum of anaesthetized rats: dopamine or DOPAC [34]?
• We then examined rats in which the PFC dopamine innervation was lesioned and 3 weeks later were started on chronic treatment with an atypical (olanzapine) or typical (haloperidol) antipsychotic drug [35].
• Our results are indicative of competition between the DAT ligand (123)I-FP-CIT and synaptic dopamine elevated by haloperidol, suggesting that the assessment of (123)I-FP-CIT binding may be suitable to study variations in synaptic dopamine in vivo [36].
• The fluorescence resonance energy transfer (FRET) between CdSe-ZnS QDs and fluorophore-labeled galactose or fluorophore-labeled dopamine linked to phenyl boronic acid-functionalized QDs is used to develop competitive assays for the optical detection of galactose, glucose, or dopamine [37].

Gene context of deoxyepinephrine

• We identified the LIM homeodomain transcription factor Lmx1b in the mesencephalic dopamine (mesDA) systems of embryos and adults [38].
• Similarly, dopamine suppressed GH and PRL release by nonadenomatous pituitary cells in a dose-dependent manner, which was again blocked by D2 receptor blockade [39].
• Coincubation of TRH and dopamine resulted in variable effects on GH and PRL secretion [39].
• We used the human dopamine-beta-hydroxylase (DbetaH) promoter to direct transgenic expression of EDNRB to colonizing ENS precursors in the sl/sl rat [40].
• In a recent issue of Nature, two independent reports by and show that loss of Drosophila PINK1 leads to defects in mitochondrial function resulting in male sterility, apoptotic muscle degeneration, and minor loss of dopamine neurons that is rescued by overexpression of the ubiquitin E3 ligase, parkin [41].
• Amantadine, an organic cation transporter-1 (OCT-1) and organic cation transporter-2 (OCT-2) mixed inhibitor, decreased dopamine flux to a greater extent than guanidine, a more specific organic cation transporter-2 inhibitor [42].
• Studies of working memory and inhibitory control differences in typically developing children due to differences in catechol-O-methyltransferase (COMT) genotype, which selectively affect prefrontal dopamine levels [43].
• Biotinylation experiments followed by immunostaining by phospho-TrkB-specific antibodies indicated that the mechanism involved increased TrkB surface expression by dopamine D1 receptor activation [44].

Analytical, diagnostic and therapeutic context of deoxyepinephrine

• Positron-emission tomography with [18F]fluorodopa before and after surgery in one patient revealed a bilateral restoration of caudate dopamine synthesis to the range of normal controls, but continued bilateral deficits in the putamen [28].
• Survival of implanted fetal dopamine cells and neurologic improvement 12 to 46 months after transplantation for Parkinson's disease [29].
• We conclude that the putamen--particularly its caudal portions--may be the most appropriate site for intrastriatal application of dopamine-producing autografts in patients with idiopathic Parkinson's disease [1].
• We use microdialysis to measure the dopamine response in the caudate nucleus after the infusion of amphetamine into the dorsolateral prefrontal cortex [45].
• Here we study dopamine release from dopamine terminals in the nucleus accumbens core and shell in the brain by using rapid-responding voltammetric microsensors during electrical stimulation of dopamine cell bodies in the ventral tegmental area/substantia nigra brain regions [8].

References