Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Lu, Jinling; Xing, Jihong; Li, Jianhua

doi:10.1016/j.brainres.2007.06.004

Cited by 13 publications

(12 citation statements)

References 48 publications

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“…We have confirmed that all the cells included for data analysis in this report located in the dl-PAG (Lu et al, 2007;Xing and Li, 2007). Whole cell patch-clamp experiments were performed and experimental data were collected from 68 dl-PAG neurons.…”

Section: Location Of the Recording Pipettesupporting

confidence: 63%

“…All drugs were dissolved in the aCSF solution immediately before they were used. According to experimental protocol, the drugs were delivered into the recording chamber at final concentrations using syringe pumps during the experiment (Lu et al, 2007;Xing and Li, 2007). The responses of EPSCs and IPSCs of the dl-PAG to application of drugs were recorded after control data were collected.…”

Section: Drugs and Their Application-ttxmentioning

confidence: 99%

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Purinergic P2X receptors presynaptically increase glutamatergic synaptic transmission in dorsolateral periaqueductal gray

Xing¹,

Lu²,

Li³

2008

Brain Research

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Purinergic P2X receptors have been reported to present in regions of the midbrain periaqueductal gray (PAG). The purpose of this study was to determine the role of presynaptic P2X receptors in modulating excitatory and inhibitory synaptic inputs to the dorsolateral PAG (dl-PAG), which has abundant neuronal connections. First, whole cell voltage-clamp recording was performed to obtain excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) of the dl-PAG neurons. Our data show that α, β-methylene ATP (a P2X receptors agonist), in the concentration of 50 µM, significantly increased the frequency of miniature EPSCs without altering the amplitude of miniature EPSCs in eight tested neurons. The effects were attenuated by PPADS, an antagonist to P2X receptors. Furthermore, α, β-methylene ATP increased the amplitude of evoked EPSCs, and decreased the paired-pulse ratio of eEPSCs in ten neurons. In contrast, activation of P2X had no distinct effect on IPSCs. In addition, immunofluoresent methods demonstrate that P2X labeling was co-localized with a presynaptic marker, synaptophysin, in the dl-PAG. The results of the current study provide the first evidence indicating that P2X receptors facilitate glutamatergic synaptic transmission in the dl-PAG via presynaptic mechanisms. SectionNeurophysiology, Neuropharmacology and other forms of Intercellular Communication

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Section: Location Of the Recording Pipettesupporting

confidence: 63%

Section: Drugs and Their Application-ttxmentioning

confidence: 99%

Purinergic P2X receptors presynaptically increase glutamatergic synaptic transmission in dorsolateral periaqueductal gray

Xing¹,

Lu²,

Li³

2008

Brain Research

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“…Likewise, if a compound augments transmitter release an attenuation of the second pulse to paired stimuli is seen. Thus, facilitation and attenuation of the PPR are generally used to reflect effects of a certain compound on the presynaptic process [17,18,23]. …”

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confidence: 99%

Angiotensin II inhibits GABAergic synaptic transmission in dorsolateral periaqueductal gray neurons

Xing

2009

Neuroscience Letters

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The purpose of this study was to determine the role of angiotensin II (Ang II) in modulating inhibitory and excitatory synaptic inputs to the dorsolateral periaqueductal gray (dl-PAG). The whole cell voltage-clamp recording was performed to examine inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs) of the dl-PAG neurons. Ang II, at the concentration of 2 µM, decreased the frequency of miniature IPSCs from 0.83 ± 0.02 to 0.45 ± 0.03 Hz (P < 0.05) in 10 tested neurons. This did not significantly affect the amplitude and decay time constant. The effect of Ang II on miniature IPSCs was blocked by the prior application of Ang II AT1 receptor antagonist losartan, but not by AT2 receptor antagonist PD123319. Additionally, Ang II decreased the amplitude of evoked IPSCs from 148 ± 15 to 89 ± 7 pA (P < 0.05), and increased the paired-pulse ratio from 96 ± 5% to 125 ± 7% (P < 0.05) in eight tested neurons. In contrast, Ang II had no distinct effects on the EPSCs. Our data suggest that Ang II inhibits GABAergic synaptic inputs to the dl-PAG through activation of presynaptic AT1 receptors. KeywordsAngiotensin II; Synaptic transmission; GABA; Midbrain PAG Angiotensin II (Ang II) plays an important role in the control of balance of hydromineral and fluid volume, as well as sympathetic nerve activity [5,26]. Also, Ang II can regulate arterial blood pressure in the development and maintenance of hypertension [6,30]. Ang II receptor subtypes, called AT1 and AT2, are engaged in action of Ang II [12].The prior studies have revealed the presence of both AT1 and AT2 throughout the rat brain [13,16]. In particular, AT1 receptors are present within the midbrain periaqueductal gray (PAG) area [16]. Ang II injected into the PAG of rats increases arterial blood pressure [11]. Ang II was likely injected into the lateral or dorsolateral PAG according to the coordinates presented in this previous study. The blockade of AT1 receptors but not AT2 attenuates the increase in blood pressure induced by injection of Ang II [11]. Thus AT1 receptors are likely to play a role in modulating blood pressure in regions of the PAG. However, the underlying mechanisms by which Ang II affects synaptic signaling to the PAG neurons have not specifically been studied. In this study we used an in vitro whole cell recording technique in [18,35]. The solution was adjusted to pH 7.25 with 1 M of KOH and osmolarity of 280-300 mOsm. The slice was placed in a recording chamber (Warner Instruments, Hamden, CT) and fixed with a grid of parallel nylon threads supported by a U-shaped stainless steel weight. The aCSF saturated with 95% O 2 -5% CO 2 was perfused into the chamber at 3.0 ml/ min. The temperature of the perfusion solution was maintained at 34 °C by an in-line solution heater with a temperature controller (Model TC-324; Warner Instruments). Whole cell recordings from the dl-PAG neurons were performed visually using differential interference contrast (DIC) optics on an upright microscope (BX50WI, Olympus, Tokyo, Japan). The tissue image wa...

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“…It has been reported that the activation of EP 3 receptors by using sulprostone, an EP 3 receptor agonist, inhibits the synaptic glutamate release in the dorsolateral PAG [22]. As a descending pathway, the dorsolateral PAG plays an inhibitory role in regulating nociception via the medulla [9].…”

Section: Discussionmentioning

confidence: 99%

Deficiency of female sex hormones augments PGE2 and CGRP levels within midbrain periaqueductal gray

Wang

Zhao

Wang

et al. 2014

Journal of the Neurological Sciences

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Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Cited by 13 publications

References 48 publications

Purinergic P2X receptors presynaptically increase glutamatergic synaptic transmission in dorsolateral periaqueductal gray

Purinergic P2X receptors presynaptically increase glutamatergic synaptic transmission in dorsolateral periaqueductal gray

Angiotensin II inhibits GABAergic synaptic transmission in dorsolateral periaqueductal gray neurons

Deficiency of female sex hormones augments PGE2 and CGRP levels within midbrain periaqueductal gray

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