Roles of brain phosphatidylinositol-specific phospholipase C and diacylglycerol lipase in centrally administered histamine-induced adrenomedullary outflow in rats

Shimizu, Takahiro; Yamaguchi, Naoko; Okada, Shoshiro; Lu, Lianyi; Sasaki, Tsuyoshi; Yokotani, Kunihiko

doi:10.1016/j.ejphar.2007.05.061

Cited by 9 publications

(7 citation statements)

References 42 publications

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“…5a, right panel). In addition, cells were incubated with the phosphatidylcholine-specific PLC (PC-PLC) blocker D609 [48,50]. Following preincubation with 100 and 500 μM D609, the effect of muscarine was −39.1± 2.2% (n=7; Fig.…”

Section: Expression Of Components Of the Muscarinic Signaling Pathwaymentioning

confidence: 99%

“…5a, right panel). Next, U73122 and ET-18-OCH 3 , which have been shown to block the PI-PLC [2,19,45,50,51], were used during MAChR stimulation. For this type of experiments, slices were preincubated in a solution containing 10 μM of the blocker dissolved in 2‰ DMSO for 2 h. In comparison to control cells from non-preincubated slices (as above) and slices that were incubated for 2 h with DMSO alone (−41.5± 1.3%; n=4), the reduction of I SO by muscarine was significantly (p<0.01) smaller following preincubation with U73122 (−25.3±3.1%; n=8; Fig.…”

Section: Expression Of Components Of the Muscarinic Signaling Pathwaymentioning

confidence: 99%

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Identification of the muscarinic pathway underlying cessation of sleep-related burst activity in rat thalamocortical relay neurons

Bista

Meuth

Kanyshkova

et al. 2011

Pflugers Arch - Eur J Physiol

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Modulation of the standing outward current (I (SO)) by muscarinic acetylcholine (ACh) receptor (MAChR) stimulation is fundamental for the state-dependent change in activity mode of thalamocortical relay (TC) neurons. Here, we probe the contribution of MAChR subtypes, G proteins, phospholipase C (PLC), and two pore domain K(+) (K(2P)) channels to this signaling cascade. By the use of spadin and A293 as specific blockers, we identify TWIK-related K(+) (TREK)-1 channel as new targets and confirm TWIK-related acid-sensitve K(+) (TASK)-1 channels as known effectors of muscarinic signaling in TC neurons. These findings were confirmed using a high affinity blocker of TASK-3 and TREK-1, namely, tetrahexylammonium chloride. It was found that the effect of muscarinic stimulation was inhibited by M(1)AChR-(pirenzepine, MT-7) and M(3)AChR-specific (4-DAMP) antagonists, phosphoinositide-specific PLCβ (PI-PLC) inhibitors (U73122, ET-18-OCH(3)), but not the phosphatidylcholine-specific PLC (PC-PLC) blocker D609. By comparison, depleting guanosine-5'-triphosphate (GTP) in the intracellular milieu nearly completely abolished the effect of MAChR stimulation. The block of TASK and TREK channels was accompanied by a reduction of the muscarinic effect on I (SO). Current-clamp recordings revealed a membrane depolarization following MAChR stimulation, which was sufficient to switch TC neurons from burst to tonic firing under control conditions but not during block of M(1)AChR/M(3)AChR and in the absence of intracellular GTP. These findings point to a critical role of G proteins and PLC as well as TASK and TREK channels in the muscarinic modulation of thalamic activity modes.

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Section: Expression Of Components Of the Muscarinic Signaling Pathwaymentioning

confidence: 99%

Section: Expression Of Components Of the Muscarinic Signaling Pathwaymentioning

confidence: 99%

Identification of the muscarinic pathway underlying cessation of sleep-related burst activity in rat thalamocortical relay neurons

Bista

Meuth

Kanyshkova

et al. 2011

Pflugers Arch - Eur J Physiol

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“…Next we used edelfosine, which is another PLC inhibitor and is widely used to reveal the participation of PLC in signalling pathways, to confirm the previous result. [23][24][25] Given that PLC acts mechanistically upstream of the SOC channels, edelfosine was not predicted to inhibit the MTx-induced AR. Edelfosine had no effect on human spermatozoa (Figure 5a), Figure 3 U73343 and U73122 block the MTx-induced AR in human (a) and mouse (b) spermatozoa.…”

Section: Resultsmentioning

confidence: 99%

The opening of maitotoxin-sensitive calcium channels induces the acrosome reaction in human spermatozoa: differences from the zona pellucida

Chávez¹,

Blas²,

Vega-Beltrán³

et al. 2010

Asian J Androl

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The acrosome reaction (AR), an absolute requirement for spermatozoa and egg fusion, requires the influx of Ca²(+) into the spermatozoa through voltage-dependent Ca²(+) channels and store-operated channels. Maitotoxin (MTx), a Ca²(+)-mobilizing agent, has been shown to be a potent inducer of the mouse sperm AR, with a pharmacology similar to that of the zona pellucida (ZP), possibly suggesting a common pathway for both inducers. Using recombinant human ZP3 (rhZP3), mouse ZP and two MTx channel blockers (U73122 and U73343), we investigated and compared the MTx- and ZP-induced ARs in human and mouse spermatozoa. Herein, we report that MTx induced AR and elevated intracellular Ca²(+) ([Ca²(+)](i)) in human spermatozoa, both of which were blocked by U73122 and U73343. These two compounds also inhibited the MTx-induced AR in mouse spermatozoa. In disagreement with our previous proposal, the AR triggered by rhZP3 or mouse ZP was not blocked by U73343, indicating that in human and mouse spermatozoa, the AR induction by the physiological ligands or by MTx occurred through distinct pathways. U73122, but not U73343 (inactive analogue), can block phospholipase C (PLC). Another PLC inhibitor, edelfosine, also blocked the rhZP3- and ZP-induced ARs. These findings confirmed the participation of a PLC-dependent signalling pathway in human and mouse zona protein-induced AR. Notably, edelfosine also inhibited the MTx-induced mouse sperm AR but not that of the human, suggesting that toxin-induced AR is PLC-dependent in mice and PLC-independent in humans.

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“…Interestingly, these supplements have been shown to drastically reduce the levels of arachidonic acid in the hippocampus (Puskás et al, 2003). Recently, we reported the possibility that brain phosphatidylinositol-derived arachidonic acid is involved in the centrally administered histamine-induced elevation of plasma catecholamines (Shimizu et al, 2007). Dietary -3 PUFA has been shown to increase the incorporation of -3 PUFA (docosahexaenoic acid) in the brain structural phosphatidylinositol and to reduce blood pressure in hypertensive rats (de Wilde et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Effects of centrally administered prostaglandin E3 and thromboxane A3 on plasma noradrenaline and adrenaline in rats: Comparison with prostaglandin E2 and thromboxane A2

Shimizu

Yokotani

2009

European Journal of Pharmacology

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Previously, we reported the involvement of brain -6 prostanoids, especially prostaglandin E 2 and thromboxane A 2 , in the activation of central sympathoadrenomedullary outflow in rats. -3 Prostanoids, including prostaglandin E 3 and thromboxane A 3 , are believed to be less bioactive than -6 prostanoids, although studies on the functions of -3 prostanoids in the central nervous system have not been reported. In the present study, therefore, we compared the effects of centrally administered -3 prostanoids, prostaglandin E 3 and thromboxane A 3 , with those of -6 prostanoids, prostaglandin E 2 and thromboxane A 2 , on the plasma catecholamines in anesthetized rats. Intracerebroventricularly (i.c.v.) administered prostaglandin E 2 (0.15, 0.3 and 1.5 nmol/animal) and prostaglandin E 3 (0.3 and 3 nmol/animal) predominantly elevated plasma noradrenaline but not adrenaline, but the latter was less efficient than the former. On the other hand, U-46619 (an analog of thromboxane A 2 ) (30, 100 and 300 nmol/animal, i.c.v.) and ∆ 17 -U-46619 (an analog of thromboxane A 3 ) (100 and 300 nmol/animal, i.c.v.) both elevated plasma catecholamines (adrenaline >> noradrenaline) to the same degree. These results suggest that centrally administered prostaglandin E 3 is less effective than prostaglandin E 2 to elevate plasma noradrenaline, and that thromboxane A 3 is almost as equipotent as thromboxane A 2 to elevate plasma catecholamines in rats.3

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Roles of brain phosphatidylinositol-specific phospholipase C and diacylglycerol lipase in centrally administered histamine-induced adrenomedullary outflow in rats

Cited by 9 publications

References 42 publications

Identification of the muscarinic pathway underlying cessation of sleep-related burst activity in rat thalamocortical relay neurons

Identification of the muscarinic pathway underlying cessation of sleep-related burst activity in rat thalamocortical relay neurons

The opening of maitotoxin-sensitive calcium channels induces the acrosome reaction in human spermatozoa: differences from the zona pellucida

Effects of centrally administered prostaglandin E3 and thromboxane A3 on plasma noradrenaline and adrenaline in rats: Comparison with prostaglandin E2 and thromboxane A2

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