The physiologically induced release of ascorbate in rat brain is dependent on impulse traffic, calcium influx and glutamate uptake

Miele, Maddalena; Boutelle, Martyn G.; Fillenz, Marianne

doi:10.1016/0306-4522(94)90316-6

Cited by 96 publications

(65 citation statements)

References 22 publications

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“…Collectively, these data emphasize that depolarizing stimuli that induce the release of neurotransmitters and pituitary hormones also release AA from the pituitary. A similar conclusion regarding depolarization-induced AA release was drawn from earlier studies using synaptosomes from different regions of the brain (31,32). NO is formed from L-arginine by the enzyme NOS (33-37).…”

Section: Discussionsupporting

confidence: 72%

Ascorbic acid stimulates gonadotropin release by autocrine action by means of NO

Karanth

Walczewska

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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Because high concentrations of ascorbic acid (AA) are found in the adenohypophysis, we hypothesized that it might have an acute effect on the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the gland, particularly because we have reported that AA rapidly inhibits stimulated LH-releasing hormone (LHRH) release from medial basal hypothalamic explants. Incubation of anterior pituitary halves from adult male rats with graded concentrations of AA for 1 h induced highly significant release of both FSH and LH with a minimal effective concentration of 10 ؊5 M. Release remained on a plateau from 10 ؊5 to 10 ؊2 M. When both AA and an effective concentration of LHRH were incubated together, there was no additive response to LHRH and the response was the same as to either compound alone. The FSH and LH release in response to AA was blocked by incubation with N G -monomethyl-L-arginine (NMMA) (300 M), a competitive inhibitor of NO synthase. NMMA also inhibited LHRH-induced LH and FSH release and gonadotropin release in the presence of both LHRH and AA, whereas sodium nitroprusside, a releaser of NO, stimulated LH and FSH release. Membrane depolarization caused by incubation in high potassium (K ؉ ‫؍‬ 28 or 56 mM) medium stimulated release of FSH, LH, and AA that was blocked by NMMA. We hypothesize that AA is released with FSH and LH from secretory granules. AA is transported back into gonadotropes by the AA transporter and increases intracellular [Ca 2؉ ]-activating NO synthase that evokes exocytosis of gonadotropins and AA by cGMP .anterior pituitary gland ͉ follicle-stimulating hormone ͉ luteinizing hormone ͉ N G -monomethyl-L-arginine ͉ sodium nitroprusside A scorbic acid (AA) is a six-carbon ketolactone-synthesized from glucose (1, 2). It is an essential vitamin for humans, primates, guinea pigs, and bats, as they lack L-gulono-␥-lactone oxidase, the last enzyme involved in its synthesis from glucose (1, 3). AA is abundant in many endocrine tissues (4, 5) and plays a pivotal role in the control of adrenal and gonadal steroidogenesis (6). Several tissues in the body accumulate AA and its biologically active oxidized form, dehydroascorbic acid. The anterior pituitary gland, brain, adrenal gland, and gonads have high concentrations of AA (2, 7-10). The concentration of AA in the brain ranges between 1.1 and 1.7 mM and remains constant despite variation in AA ingestion (11,12). Intracellular AA concentration is much higher than extracellular AA concentration, and changes in neuronal activity were shown to have a profound influence on extracellular AA (13-18). AA is further concentrated in isolated nerve terminals, and synaptic vesicles concentrate AA by an active transport mechanism (19,20).Previously, we evaluated the effect of AA on basal and stimulated release of luteinizing hormone (LH)-releasing hormone (LHRH) from medial basal hypothalamic explants produced by high potassium medium and N-methyl-D-aspartic acid (NMDA). Sodium nitroprusside (NP), which spontaneously releases NO-stimulate...

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Section: Discussionsupporting

confidence: 72%

Ascorbic acid stimulates gonadotropin release by autocrine action by means of NO

Karanth

Walczewska

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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“…Certainly, ascorbate is present in high concentrations in some tissues (e.g. 6 yimol ge' in brain; Martensson & Meister, 1991); it is considered to be an important extracellular antioxidant and, in the brain, has extracellular concentrations similar to those used in the present study (200-400 gM; Miele et al, 1994). GSH is also found in high (millimolar) concentrations in tissues, although in this case the highest levels are found intracellularly, extracellular concentrations being in the range 0.3-15 pM (Frei, 1994); a-TOC is mainly localised to membranes and lipoproteins (Frei, 1994).…”

Section: Discussionmentioning

confidence: 53%

Antioxidant protection of NO‐induced relaxations of the mouse anococcygeus against inhibition by superoxide anions, hydroquinone and carboxy‐PTIO

Lilley¹,

Gibson²

1996

British J Pharmacology

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The potential protective effect of several antioxidants [Cu/Zn superoxide dismutase (Cu/Zn SOD), ascorbate, reduced glutathione (GSH), and cx-tocopherol (a-TOC)] on relaxations of the mouse anococcygeus muscle to nitric oxide (NO; 15 giM) and, where appropriate, nitrergic field stimulation (10 Hz; 10 s trains) was investigated.2 The superoxide anion generating drug duroquinone (100 gIM) reduced relaxations to exogenous NO by 54+6%; this inhibition was partially reversed by Cu/Zn SOD (250 u ml-'), and by ascorbate (500 gM). Following inhibition of endogenous Cu/Zn SOD activity with diethyldithiocarbamate (DETCA), duroquinone (50 gM) also reduced relaxations to nitrergic field stimulation (by 53 + 6%) and this effect was again reversed by Cu/Zn SOD and by ascorbate. Neither GSH (500 gM) nor (X-TOC (400 gM) afforded any protection against duroquinone.3 Xanthine (20 mu ml-1):xanthine oxidase (100 Mm) inhibited NO-induced relaxations by 73 + 14%, but had no effect on those to nitrergic field stimulation, even after DETCA treatment. The inhibition of exogenous NO was reduced by Cu/Zn SOD (250 u ml-1) and ascorbate (400 gM), but was unaffected by GSH or oc-TOC (both 400 gM). 4 Hydroquinone (100 gM) also inhibited relaxations to NO (by 52 + 10%), but not nitrergic stimulation. In this case, however, the inhibition was reversed by GSH (5-100 Mm) and ascorbate (100-400 gM), although Cu/Zn SOD and a-TOC were ineffective. 5 2-(4-Carboxyphenyl)-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO, 50 gM) inhibited NO-induced relaxations by 50+4%, but had no effect on nitrergic responses; the inhibition was reduced by ascorbate (2-200 gM) and a-TOC (10-200 gM), but not by Cu/Zn SOD or GSH. 6 Hydroxocobalamin (5 -1000 gM) inhibited, equally, relaxations to both NO (-logIC40 3.14 + 0.33) and nitrergic stimulation (-logIC40 3.17+0.22). 7 Thus, a number of physiological antioxidants protected NO from superoxide anions, and from direct NO-scavengers. The possibility that the presence of these antioxidants within nitrergically-innervated tissues might explain the lack of effect of the NO inhibitors on nerve-induced relaxation, without the need to invoke a transmitter other than free radical NO, is discussed.

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“…The most problematic species is AA because its basal extracellular concentration is higher than that of DA and because stress has been reported to elevate (striatal) levels of AA (Miele et al, 1994). Repeatedly coating the electrode surface with Nafion is one of several procedures that has been shown to substantially reduce contributions by AA and other anionic species, including the DA metabolite DOPAC (Gerhardt et al, 1984;Nagy et al, 1985;Brazell et al, 1987;Crespi and Mobius, 1992).…”

Section: Mpfc Da Response To Stressmentioning

confidence: 99%

Influence of Naturally Occurring Variations in Maternal Care on Prepulse Inhibition of Acoustic Startle and the Medial Prefrontal Cortical Dopamine Response to Stress in Adult Rats

Zhang¹,

Chretien²,

Meaney³

et al. 2005

J. Neurosci.

139

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In rats, naturally occurring variations in maternal care contribute to the development of individual differences in the behavioral and neuroendocrine responses to stress during adulthood. The dopamine (DA) projection to the medial prefrontal cortex (mPFC) plays an important role in mediating stress responsivity and is thought to be involved also in regulating sensorimotor gating. In the present study, we compared prepulse inhibition (PPI) of acoustic startle as well as the left and right mPFC DA stress responses in the adult offspring of high-and low-licking/grooming (LG) dams. Our data indicate that the offspring of low-LG animals are impaired on measures of PPI compared with high-LG animals. We also observed in low-LG animals a significant blunting of the mPFC DA stress responses that was lateralized to the right hemisphere, whereas in high-LG animals, the left and right mPFC DA stress responses were equally attenuated. Although mPFC levels of DA transporter did not differ between the two groups of animals, mPFC levels of catechol-O-methyl transferase immunoreactivity of low-LG animals were significantly lower than those of high-LG animals. These data provide evidence that variations in maternal care can lead to lasting changes in mPFC DA responsivity to stress and suggest the possibility that such changes in mesocorticolimbic DA function can also lead to deficits in sensorimotor gating.

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The physiologically induced release of ascorbate in rat brain is dependent on impulse traffic, calcium influx and glutamate uptake

Cited by 96 publications

References 22 publications

Ascorbic acid stimulates gonadotropin release by autocrine action by means of NO

Ascorbic acid stimulates gonadotropin release by autocrine action by means of NO

Antioxidant protection of NO‐induced relaxations of the mouse anococcygeus against inhibition by superoxide anions, hydroquinone and carboxy‐PTIO

Influence of Naturally Occurring Variations in Maternal Care on Prepulse Inhibition of Acoustic Startle and the Medial Prefrontal Cortical Dopamine Response to Stress in Adult Rats

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