Formation of deaminated metabolites of dopamine in noradrenaline neurons

Andén, Nils‐Erik; Grabowska-Andén, Maria

doi:10.1007/bf00647830

Cited by 49 publications

(14 citation statements)

References 15 publications

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“…We demonstrated pre viously that, under basal conditions, this peak mainly cor responded in PVN to the Dopac which is synthesized by noradrenergic terminals [21 ]. This assumption was based on electrochemical, anatomical, and pharmacological argu ments and is in agreement with other studies showing that noradrenergic neurons synthesize an appreciable amount of Dopac [2] and that this metabolite is the main free cat echol present in the extracellular space in the vicinity of noradrenergic neurons [5,12,28]. The extracellular Dopac concentration in PVN was found to be 2.0 pA/ [21], Voltammograms recorded from the PVN of freely mov ing rats showed a catechol peak which appeared at + 50 mV and which was mainly due to Dopac of noradrenergic ori gin.…”

Section: Effect O F Ether Stress On Ne Release Recorded From Freely Msupporting

confidence: 77%

Ether Stress Stimulates Noradrenaline Release in the Hypothalamic Paraventricular Nucleus

Mermet¹,

Gorton²

1988

Neuroendocrinology

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Differential normal-pulse voltammetry was combined with treated carbon fibre electrodes for monitoring in vivo extracellular catechols synthesized by noradrenergic terminals innervating the paraventricular hypothalamic nucleus. From urethane-anaesthetized rats, pretreated with a monoamine oxidase inhibitor, pargyline, we were able to monitor a catechol signal which unequivocally corresponded to extracellular noradrenaline, and we observed that ether inhalation for 2 min induced an immediate increase in this signal. Electrical stimulation of the ventral noradrenergic pathway (10 Hz for 40 s) induced a similar effect. On the other hand, from freely moving rats which were not treated with pargyline, we recorded a catechol peak which mainly corresponded to 3,4-dihydroxyphenylacetic acid which was synthesized by noradrenergic terminals. However, electrochemical and biochemical evidence strongly suggested that the increase in this signal induced by a 2-min ether stress does not correspond to 3,4-dihydroxyphenylacetic acid, but to an increase in the extracellular noradrenaline concentration. In both experimental situations the time course of the effects was identical: ether stress induced an immediate and pronounced increase in norepinephrine release, and this effect lasted as long as the stimulus duration. This effect appeared specific for noradrenergic terminals, since no effect on dopamine release was observed when recorded from the striatum or behind the paraventricular hypothalamic nucleus from the A₁₃ dopaminergic group. In conclusion, our data are consistent with those which suggest a facilitatory action of norepinephrine on neurose-cretory neurons whose cell bodies are located in the paraventricular hypothalamic nucleus and which play a major role in the hormonal response to stress.

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Section: Effect O F Ether Stress On Ne Release Recorded From Freely Msupporting

confidence: 77%

Ether Stress Stimulates Noradrenaline Release in the Hypothalamic Paraventricular Nucleus

Mermet¹,

Gorton²

1988

Neuroendocrinology

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“…It is likely that the prolonged elevation of DA and DOPAC in the Par reflects the activation of tyrosine hydroxylase in NA neurones so that an excess of newly synthesized DA might not be converted to NA due to a partial saturation of DA‐β‐hydroxylase. Consistent with this hypothesis is the long‐lasting increase of DOPAC in the Par, where DOPAC is considered to reflect DA deaminated inside noradrenergic nerve terminals (Andén and Grabowska‐Andén 1983; Scatton et al . 1984).…”

Section: Discussionmentioning

confidence: 89%

Stimulation of the locus coeruleus elicits noradrenaline and dopamine release in the medial prefrontal and parietal cortex

Devoto

Flore²,

Saba

et al. 2004

Journal of Neurochemistry

135

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Our previous studies have suggested that dopamine and noradrenaline may be coreleased from noradrenergic nerve terminals in the cerebral cortex. To further clarify this issue, the effect of electrical stimulation of the locus coeruleus on extracellular noradrenaline, dopamine and DOPAC in the medial prefrontal cortex, parietal cortex and caudate nucleus was analysed by microdialysis in freely moving rats. Stimulation of the locus coeruleus for 20 min with evenly spaced pulses at 1 Hz failed to modify cortical catecholamines and DOPAC levels. Stimulation with bursts of pulses at 12 and 24 Hz increased, in a frequency-related manner, not only noradrenaline but also dopamine and DOPAC in the two cortices. In both cortices noradrenaline returned to baseline within 20 min of stimulation, irrespective of the stimulation frequency, whereas dopamine returned to normal within 20 and 60 min in the medial prefrontal cortex and within 60 and 80 min in the parietal cortex after 12 and 24 Hz stimulation, respectively. DOPAC remained elevated throughout the experimental period. Phasic stimulation of the locus coeruleus at 12 Hz increased noradrenaline in the caudate nucleus as in the cerebral cortices but was totally ineffective on dopamine and DOPAC. Tetrodotoxin perfusion into the medial prefrontal cortex dramatically reduced noradrenaline and dopamine levels and suppressed the effect of electrical stimulation. These results indicate that electrical stimulation-induced increase of dopamine is a nerve impulse exocytotic process and suggest that cortical dopamine and noradrenaline may be coreleased from noradrenergic terminals.

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“…There is evidence that much of the HV A in plasma and urine is from metabolism of DA in noradrenergic neurons (Anden and Grabowska-Anden 1983;Anden et al 1985;Scheinin et al 1984;Scheinin 1986;Schei nin and Virtanen 1986;Kopin et al 1988a,b,c). In our haloperidol-treated patients, urinary HV A and MHPG changed in opposite directions over the fIrst several weeks.…”

Section: Discussionmentioning

confidence: 99%

Studies of Catecholamine Metabolism in Schizophrenia/Psychosis-II

Maas

Contreras

Miller

et al. 1993

Neuropsychopharmacol

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Acutely psychotic schizophrenic patients were maintained on debrisoquin (DBQ) throughout 5 weeks of treatment with haloperidol. Treatment with haloperidol caused initial increases in urinary homovanillic acid (HVA) output that returned toward baseline by the 5th week. During haloperidol treatment, plasma levels of HVA tended to decrease, concurrent with increased renal cltll rance of HV A. Plasma 3-methoxy-4-hydroxyphenyl-

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Formation of deaminated metabolites of dopamine in noradrenaline neurons

Cited by 49 publications

References 15 publications

Ether Stress Stimulates Noradrenaline Release in the Hypothalamic Paraventricular Nucleus

Ether Stress Stimulates Noradrenaline Release in the Hypothalamic Paraventricular Nucleus

Stimulation of the locus coeruleus elicits noradrenaline and dopamine release in the medial prefrontal and parietal cortex

Studies of Catecholamine Metabolism in Schizophrenia/Psychosis-II

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