Adenosine inhibition via A1 receptor of N-type Ca2+ current and peptide release from isolated neurohypophysial terminals of the rat

Wang, G.

doi:10.1113/jphysiol.2001.016394

Cited by 4 publications

(4 citation statements)

References 6 publications

(13 reference statements)

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“…2B) each had a mean stimulated AVP release of 195.04 pg ± 1.22 pg. Such close similarities in total peptide release between individual collection lines, following high potassium depolarization, has consistently been observed in our lab (see, e.g., Wang et al, 1997, 1999, 2002). In this way, if there was no effect on the second filter from secretion from the first filter, then the total peptide secreted (both filters) should be twice the peptide secreted from just one filter alone.…”

Section: Resultssupporting

confidence: 86%

“…Since the biophysical properties of ion channels alone cannot explain the HNS interburst characteristics (Lemos and Wang, 2000), we hypothesize that the release of ATP is a mechanism underlying release efficacy in the NHT. Its presence would enhance the release of AVP from the neurohypophysis early during the bursting pattern followed by a subsequent build up of adenosine, metabolized from ATP, which would inhibit release by inhibiting the N‐type (Wang et al, 2002) calcium current via the A 1 receptor (Knott et al, 2007). Furthermore, since ATP is stored at high concentrations in most secretory vesicles and has been shown to be released from chromaffin cells and many neurons (Zimmermann, 1994), we postulate that the release of ATP is important in modulating release from other, if not all, bursting nervous system terminals.…”

Section: Discussionmentioning

confidence: 99%

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Endogenous ATP potentiates only vasopressin secretion from neurohypophysial terminals

Knott

Marrero

Custer

et al. 2008

Journal Cellular Physiology

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Exogenous ATP induces inward currents and causes the release of arginine-vasopressin (AVP) from isolated neurohypophysial terminals (NHT); both effects are inhibited by the P2X2 and P2X3 antagonists, suramin and PPADS. Here we examined the role of endogenous ATP in the neurohypophysis. Stimulation of NHT caused the release of both AVP and ATP. ATP induced a potentiation in the stimulated release of AVP, but not of oxytocin (OT), which was blocked by the presence of suramin. In loose-patch clamp recordings, from intact neurohypophyses, suramin or PPADS produces an inhibition of action potential currents in a static bath, that can be mimicked by a hyperpolarization of the resting membrane potential (RMP). Correspondingly, in a static versus perfused bath there is a depolarization of the RMP of NHT, which was reduced by either suramin or PPADS. We measured an accumulation of ATP (3.7 +/- 0.7 microM) released from NHT in a static bath. Applications of either suramin or PPADS to a static bath decreased burst-stimulated capacitance increases in NHT. Finally, only vasopressin release from electrically stimulated intact neurohypophyses was reduced in the presence of Suramin or PPADS. These data suggest that there was sufficient accumulation of ATP released from the neurohypophysis during stimulations to depolarize its nerve terminals. This would occur via the opening of P2X2 and P2X3 receptors, inducing an influx of Ca2+. The subsequent elevation in [Ca2+](i) would further increase the stimulated release of only vasopressin from NHT terminals. Such purinergic feedback mechanisms could be physiologically important at most CNS synapses.

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Section: Resultssupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Endogenous ATP potentiates only vasopressin secretion from neurohypophysial terminals

Knott

Marrero

Custer

et al. 2008

Journal Cellular Physiology

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“…The imperative motor factor of sleep (i.e., adenosine) strongly inhibits oxytocin release (Wang et al, 2002) and can be classified as an attachment termination factor (Table 1) 23 . The interaction between ghrelin (i.e., the imperative motor factor of hunger) and oxytocin is at present a topic of (neuro)endocrinological research.…”

Section: The Interaction Between Oxytocin and Imperative Motor Factorsmentioning

confidence: 99%

On the Nature of the Mother-Infant Tie and Its Interaction With Freudian Drives

Kirsch

Buchholz

2020

Front. Psychol.

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“…We have previously shown that ATP, acting via P2X receptors, potentiates only AVP release from HNS terminals (4), whereas its metabolite adenosine, via A1 receptors acting on transient Ca 2+ currents, inhibits both AVP and OT secretion (5). We have shown that exogenous ATP induces inward currents (6) and causes the release of only vasopressin (AVP) from neurohypophysial terminals (4); both effects are inhibited by suramin and pyridoxal‐phosphate‐6‐azophenyl‐2′,4′‐disulfonic acid (PPADS), selective but not specific, P2X2 and P2X3 receptor antagonists.…”

mentioning

confidence: 99%

P2X Purinergic Receptor Knockout Mice Reveal Endogenous ATP Modulation of Both Vasopressin and Oxytocin Release from the Intact Neurohypophysis

Custer

Knott

Cuadra

et al. 2012

J Neuroendocrinology

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Bursts of action potentials are crucial for neuropeptide release from the Hypothalamic Neurohypophysial System (HNS). The biophysical properties of the ion channels involved in release of these neuropeptides cannot explain the efficacy of such bursting patterns on secretion. We have previously shown that ATP, acting via P2X receptors, potentiates only AVP release from HNS terminals, whereas, its metabolite adenosine, via A1 receptors acting on transient Ca2+ currents, inhibits both AVP and OT secretion. Thus, purinergic feedback-mechanisms have been proposed to explain bursting efficacy at HNS terminals. Therefore, in the present study we have used specific P2X receptor knockout (rKO) mice and purportedly selective P2X receptor antagonists to determine the P2X receptor subtype responsible for endogenous ATP induced potentiation of electrically stimulated neuropeptide release. Intact neurohypophyses (NH) from wild type (WT), P2X3 rKO, P2X2&3 rKO and P2X7 rKO mice were electrically stimulated with four 25 second bursts (3V at 39Hz) separated by 21 second interburst intervals with or without the P2X2 and P2X3 receptor antagonists, suramin or PPADS. These frequencies, number of bursts, and voltages were determined to maximize both AVP and OT release by electrical stimulations. Treatment of WT mouse NH with suramin/PPADS significantly reduced electrically stimulated AVP release. A similar inhibition by suramin was observed in electrically stimulated NH from P2X3 and P2X7 rKO mice but not P2X2&3 rKO mice, indicating that endogenous ATP facilitation of electrically stimulated AVP release is mediated primarily by the activation of the P2X2 receptor. Surprisingly, electrically stimulated OT release from WT, P2X3, P2X2&3 and P2X7 rKO mice was potentiated by suramin, indicating non-purinergic effects by this “selective” antagonist. Nevertheless, these results show that sufficient endogenous ATP is released by bursts of action potentials to act at P2X2 receptors in a positive-feedback mechanism to differentially modulate neuropeptide release from CNS terminals.

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Adenosine inhibition via A1 receptor of N-type Ca2+ current and peptide release from isolated neurohypophysial terminals of the rat

Cited by 4 publications

References 6 publications

Endogenous ATP potentiates only vasopressin secretion from neurohypophysial terminals

Endogenous ATP potentiates only vasopressin secretion from neurohypophysial terminals

On the Nature of the Mother-Infant Tie and Its Interaction With Freudian Drives

P2X Purinergic Receptor Knockout Mice Reveal Endogenous ATP Modulation of Both Vasopressin and Oxytocin Release from the Intact Neurohypophysis

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