Parasympathetic inhibition of pineal indole metabolism by prejunctional modulation of noradrenaline release

Drijfhout, W. J.; Grol, Cor J.; Westerink, Ben H.C.

doi:10.1016/0014-2999(96)00283-x

Cited by 35 publications

(19 citation statements)

References 29 publications

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“…Such data suggest the presence of muscarinic receptors in a presynaptic location, i.e. on the sympathetic nerve endings (Drijfhout, Grol & Westerink, 1996). The existence of nicotinic ACh receptors (nAChRs) in the pineal organ was inferred from immunocytochemical investigations (Reuss, Schroder, Schr6der & Maelicke, 1992) and binding studies with radiolabelled specific ligands (Stankov, Cimino, Marini, Lucini, Fraschini & Clementi, 1993) and it has been suggested that nicotine has an inhibitory effect on pineal melatonin synthesis.…”

mentioning

confidence: 99%

Stimulation of a nicotinic ACh receptor causes depolarization and activation of L‐type Ca2+ channels in rat pinealocytes.

Letz

Schomerus

Maronde

et al. 1997

The Journal of Physiology

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1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel to the electrophysiological experiments, intracellular Ca2P measurements were performed using fura-2. The mammalian pineal organ transduces information about the ambient photoperiod into a neuroendocrine message by rhythmic synthesis and secretion of melatonin (for review see Arendt, 1995). In mammals the sympathetic innervation of the pineal organ is mandatory to maintain the lightsynchronized circadian rhythm of melatonin production that is highest during the second half of the night. In rats, noradrenaline acts upon melatonin biosynthesis by stimulating both al-and /,3-adrenergic receptors. Stimulation of /,3-receptors increases intracellular cAMP, which mediates the activation of serotonin-N-acetyl-transferase, the rate-limiting enzyme of melatonin biosynthesis.Activation of az1-receptors potentiates the /,3-adrenergic effect via an increase in intracellular calcium concentration ([Ca2+]1) (for review see Klein, 1985). Thus, the essential role of noradrenaline for stimulation of melatonin biosynthesis has been firmly established. In contrast, it is still unclear whether and how neuronal pathways other than the noradrenergic sympathetic innervation (for review see Korf, 1996) are involved in the regulation of melatonin biosynthesis and pineal functions in mammals. Several morphological investigations point toward the existence of a parasympathetic innervation of the mammalian pineal gland, which may originate from the pterygopalatine ganglion and employ acetylcholine as primary neurotransmitter (for review see M0ller, 1992). Further evidence for a cholinergic innervation of the pineal organ has been obtained by recent immunocytochemical studies (E. Weihe, M. K.-H.

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mentioning

confidence: 99%

Stimulation of a nicotinic ACh receptor causes depolarization and activation of L‐type Ca2+ channels in rat pinealocytes.

Letz

Schomerus

Maronde

et al. 1997

The Journal of Physiology

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“…Beside α 2 -autoreceptors, the release of NE from the nerve endings in the rat pineal gland is modulated by NPY, substance P, acetylcholine, γ-aminobutyric acid and melatonin (Rosenstein et al 1990, Chuluyan et al 1991, Simonneaux et al 1994b, Drijfhout et al 1996b, Mukda et al 2009). The above presented list of substances is probably much longer, because at least 30 different metabotropic and ionotropic receptors have been found to control the amount of transmitter being released from the sympathetic nerve terminals, located in various body structures (Boehm and Kubista 2002).…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland

Ziółkowska¹,

Lewczuk²,

Przybylska‐Gornowicz³

2015

Polish Journal of Veterinary Sciences

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Norepinephrine (NE) released from the sympathetic nerve endings is the main neurotransmitter controlling melatonin synthesis in the mammalian pineal gland. Although neuropeptide Y (NPY) co-exists with NE in the pineal sympathetic nerve fibers it also occurs in a population of non-adrenergic nerve fibers located in this gland. The role of NPY in pineal physiology is still enigmatic. The present study characterizes the effect of NPY on the depolarization-evoked 3 H-NE release from the pig pineal explants.The explants of the pig pineal gland were loaded with 3 H-NE in the presence of pargyline and superfused with Tyrode medium. They were exposed twice to the modified Tyrode medium containing 60 mM of K + to evoke the 3 H-NE release via depolarization. NPY, specific agonists of Y 1 -and Y 2 -receptors and pharmacologically active ligands of α 2 -adrenoceptors were added to the medium before and during the second depolarization. The radioactivity was measured in medium fractions collected every 2 minutes during the superfusion. NPY (0.1 -10 μM) significantly decreased the depolarization-induced 3 H-NE release. Similar effect was observed after the treatment with Y 2 -agonist: NPY 13-36 , but not with Y 1 -agonist: [Leu 31 ,Pro 34 ]-NPY. The tritium overflow was lower in the explants exposed to the 5 μM NPY and 1 μM rauwolscine than to rauwolscine only. The effects of 5 μM NPY and 0.05 μM UK 14,304 on the depolarization-evoked 3 H-NE release were additive.The results show that NPY is involved in the regulation of NE release from the sympathetic terminals in the pig pineal gland, inhibiting this process via Y 2 -receptors.

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“…In adult rats, mAChRs are absent from the pinealocyte membrane, but are present on sympathetic nerve fibres. Activation of these receptors blocks NE release from sympathetic nerve terminals, thus leading to a decreased melatonin output [7]. Thus, ACh …”

Section: Cholinergic Signal Transduction In Pinealocytes Of Adult Ratsmentioning

confidence: 99%

“…All [37]. [7]. Such data suggest the presence of muscarinic acetylcholine receptors (mAChRs) in a presynaptic location, i.e.…”

mentioning

confidence: 99%

Cholinergic signal transduction cascades in rat pinealocytes: functional and ontogenetic aspects

Schomerus¹,

Korf²

1999

Reprod. Nutr. Dev.

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Parasympathetic inhibition of pineal indole metabolism by prejunctional modulation of noradrenaline release

Cited by 35 publications

References 29 publications

Stimulation of a nicotinic ACh receptor causes depolarization and activation of L‐type Ca2+ channels in rat pinealocytes.

Stimulation of a nicotinic ACh receptor causes depolarization and activation of L‐type Ca2+ channels in rat pinealocytes.

Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland

Cholinergic signal transduction cascades in rat pinealocytes: functional and ontogenetic aspects

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