Release of dopamine β-hydroxylase and chromogranin A upon stimulation of the splenic nerve

Smith, A D; Potter, W.P. De; Moerman, E; Schaepdryver, A.F. De

doi:10.1016/s0040-8166(70)80030-1

Cited by 175 publications

(49 citation statements)

References 55 publications

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“…In vascular tissues, electrical stimulation of perivascular adrenergic nerves releases many substances, together with NA. They involve adenosine triphosphate (ATP), dopamine /3-hydroxylase, or metabolites of NA (SMITH et a!.,1970;Su,1975;KLEIN et a!.,1982;MISHIMA et al, 1984). Among these substances, ATP depolarizes vascular smooth muscle cells and decreases the membrane resistance (SuzuKi, 1985).…”

Section: Discussionmentioning

confidence: 99%

Increase in membrane resistance during noradrenaline-induced depolarization in arterial smooth muscle.

Suzuki

1986

Jpn.J.Physiol

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The effects of noradrenaline on membrane resistance of smooth muscle cells of the guinea-pig main pulmonary artery were assessed from the change in amplitude of electrotonic potentials produced by extracellulary applied current pulses. Noradrenaline was applied exogenously by bath application or endogenously by stimulating perivascular nerves. Exogenous noradrenaline depolarized the smooth muscle membrane with an associated increase in amplitude of electrotonic potentials and produced spike responses. Perivascular nerve stimulation evoked an excitatory junction potential with slow time course. The amplitude of electrotonic potential was slightly decreased during generation of the excitatory junction potential, but the reduction was less than that observed during current-induced depolarization. These observations suggest that the depolarizations produced by either endogenous or exogenous noradrenaline are accompanied by an increase in membrane resistance of arterial smooth muscle.

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Section: Discussionmentioning

confidence: 99%

Increase in membrane resistance during noradrenaline-induced depolarization in arterial smooth muscle.

Suzuki

1986

Jpn.J.Physiol

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“…The enzyme dopamine -hydroxylase is found in noradrenergic neurons, and is released into synapses at the same time as the catecholamines (Smith, de Potter, Moerman & de Scaepdryver, 1970) where it catalyses the conversion of dopamine to noradrenaline (Kaufman & Friedman, 1965). DH therefore plays a critical role in controlling the balance of dopamine and noradrenaline available in the cortex.…”

Section: Introductionmentioning

confidence: 99%

Noradrenergic genotype predicts lapses in sustained attention

et al. 2009

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Publication informationNeuropsychologia, 47 (2): 591-594Publisher Elsevier Item record/more information http://hdl.handle.net/10197/6316 Publisher's statementThis is the author's version of a work that was accepted for publication in Neuropsychologia. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neuropsychologia (VOL 47, ISSUE 2, (2009) AbstractSustained attention is modulated by the neurotransmitter noradrenaline. The balance of dopamine and noradrenaline in the cortex is controlled by the DBH gene. The principal variant in this gene is a C/T change at position -1021, and the T allele at this locus is hypothesised to result in a slower rate of dopamine to noradrenaline conversion than the C allele.200 participants who were genotyped for the DBH C-1021T marker performed the Sustained Attention to Response Task (SART). DBH genotype was found to significantly predict performance; participants with more copies of the T allele made more errors of commission, indicative of lapses in sustained attention. A significant negative correlation was also observed for all participants between errors of commission and mean reaction time.The decrease in noradrenaline occasioned by the T allele may impair sustained attention by reducing participants' ability to remain alert throughout the task and by increasing their susceptibility to distractors.

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“…Yet, although it is clear that different CGA storage granules may exhibit different cleavage patterns [4,5], very few data are available on CGA breakdown in sympathetic nerve axons [2,14] and almost none in nerve terminals, presumably because of difficulties in obtaining the appropriate vesicle preparations [16]. Moreover, while the release of CGA from sympathetic neurons has already been demonstrated [17,19], no evidence has yet been provided for the release of CGA 9roducts from adrenergic nerve terminals. Since the functional significance of CGA-derived peptide~ is a growing field of interest we have studied CGA breakdown in sympathetic neurons by comparing CGA immunoreactivity (CGA-IR) in preparations of LDYs from ox and dog sympathetic ganglia, splenic nerve and spleen, representing adrenergic cell bodies, axons and nerve terminals, respectively.…”

Section: Introductionmentioning

confidence: 99%

Chromogranin A processing in sympathetic neurons and release of chromogranin A fragments from sheep spleen

Miserez¹,

Annaert²,

Dillen³

et al. 1992

FEBS Letters

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Chromograam A (CGA) has been localized to the large dense cored vesicles (LDV) of sympathetic neurons SDS-PAGE and lmmunoblotlmg of soluble LDV proteins hem ox and dog adrenergic neuronal cell bodies, unonb and nerve terminals, revealed an increasing number of CGAimmunoreactive forms, consistent with proteolyt~e processing dunng axonal transport. Spleme nerve electrical stimulauon (10 Hz, 2 rain) revealed that, apart from CGA these CGA-proeessmg products are released from the sheep spleen. The secretion of CGA-defived fragments from sympathetic neurons might suggest a role in the regulation of synaptic transmission.

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Release of dopamine β-hydroxylase and chromogranin A upon stimulation of the splenic nerve

Cited by 175 publications

References 55 publications

Increase in membrane resistance during noradrenaline-induced depolarization in arterial smooth muscle.

Increase in membrane resistance during noradrenaline-induced depolarization in arterial smooth muscle.

Noradrenergic genotype predicts lapses in sustained attention

Chromogranin A processing in sympathetic neurons and release of chromogranin A fragments from sheep spleen

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