Prostaglandin D2-sensitive, sleep-promoting zone defined in the ventral surface of the rostral basal forebrain.

Matsumura, Hitoshi; Nakajima, T.; Osaka, Toshimasa; Satoh, Shinsuke; Kawase, Kumiko; Kubo, Etsuko; Kantha, Sachi Sri; Kasahara, Keiko; Hayaishi, Osamu

doi:10.1073/pnas.91.25.11998

Cited by 126 publications

(98 citation statements)

References 27 publications

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“…In the late 1970s, Hayaishi et al (14) found large amounts of PGDS in the brains of rat and other mammals, including humans. PGD 2 circulates in the ventricular system, subarachnoid space, and extracellular spaces of the brain and interacts with receptors on the ventromedial surface of the rostral basal forebrain to initiate the signal to let the brain sleep (15). PGDS is a member of the lipocalin superfamily composed of various secretory lipophilic ligandcarrier proteins (6,7).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin D Synthase (β-Trace) in Meningeal Hemangiopericytoma

et al. 2001

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The level of prostaglandin D synthase (PGDS), a major protein constituent of cerebrospinal fluid (CSF), is altered in various brain diseases, including meningitis. However, its role in the brain remains unclear. PGDS is mainly synthesized in the arachnoid cells, the choroid plexus and oligodendrocytes in the central nervous system. Among brain tumors, meningiomas showed intense immunoreactivity to PGDS in the perinuclear region. Thus, PGDS has been considered a specific cell marker of meningioma. In this study, we examined 25 meningeal hemangiopericytomas (HPCs) and found that 16 of the tumors (64%) showed immunoreactivity for PGDS in the perinuclear region. For comparison, 15 meningiomas, 14 soft-tissue HPCs, 1 mesenchymal chondrosarcoma, 3 choroid plexus papillomas, and 7 oligodendrogliomas were also examined. Meningiomas showed positive immunoreactivity for PGDS in 13 cases (80%). Except for one case located at the sacrum, none of the other soft-tissue HPCs showed immunostaining for PGDS. Mesenchymal chondrosarcoma arises in the bones of the skull, and its histological pattern resembles that of HPC; however, it showed no immunoreactivity for PGDS. Neither choroid plexus papillomas nor oligodendrogliomas were immunopositive for PGDS. These findings suggest that meningeal HPCs may have a unique molecular phenotype that is distinct from that of the soft-tissue HPCs. The origin of meningeal HPCs may be more closely related to the arachnoid cells.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin D Synthase (β-Trace) in Meningeal Hemangiopericytoma

et al. 2001

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“…1). In brief, PGD 2 infused into the subarachnoid space underlying the rostral basal forebrain was effective in inducing sleep but not when infused into most parts of the brain parenchyma of rats (2). The amount of PGD 2 -induced sleep was reduced by pretreatment with KF17837, the specific adenosine A 2A receptor antagonist, in a dose-dependent manner (3).…”

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confidence: 94%

Dominant localization of prostaglandin D receptors on arachnoid trabecular cells in mouse basal forebrain and their involvement in the regulation of non-rapid eye movement sleep

Mizoguchi

Eguchi

Kimura

et al. 2001

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

173

124

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Infusion of prostaglandin (PG) D2 into the lateral ventricle of the brain induced an increase in the amount of non-rapid eye movement sleep in wild-type (WT) mice but not in mice deficient in the PGD receptor (DP). Immunofluorescence staining of WT mouse brain revealed that DP immunoreactivity was dominantly localized in the leptomeninges (LM) of the basal forebrain but that PGD synthase immunoreactivity was widely distributed in the LM of the entire brain. Electron microscopic observation indicated that DPimmunoreactive particles were predominantly located on the plasma membranes of arachnoid trabecular cells of the LM. The region with the highest DP immunoreactivity was clearly defined as bilateral wings in the LM of the basal forebrain located lateral to the optic chiasm in the proximity of the ventrolateral preoptic area, one of the putative sleep centers, and the tuberomammillary nucleus, one of the putative wake centers. The LM of this region contained DP mRNA 70-fold higher than that in the cortex as judged from the results of quantitative reverse transcription-PCR. PGD2 infusion into the subarachnoid space of this region increased the extracellular adenosine level more than 2-fold in WT mice but not in the DP-deficient mice. These results indicate that DPs in the arachnoid trabecular cells of the basal forebrain mediate an increase in the extracellular adenosine level and sleep induction by PGD2. P rostaglandin (PG) D 2 is a potent endogenous sleeppromoting substance in monkeys and rats, and its somnogenic mechanism is the best characterized among those of various sleep-inducing substances (reviewed in ref. 1). In brief, PGD 2 infused into the subarachnoid space underlying the rostral basal forebrain was effective in inducing sleep but not when infused into most parts of the brain parenchyma of rats (2). The amount of PGD 2 -induced sleep was reduced by pretreatment with KF17837, the specific adenosine A 2A receptor antagonist, in a dose-dependent manner (3). Administration of CGS21680, a selective A 2A receptor agonist, into the subarachnoid space induced sleep (4), suggesting that PGD 2 -induced sleep is mediated by adenosine through the adenosine A 2A receptor system. Furthermore, PGD 2 infusion significantly increased Fos expression in the leptomeninges (LM) and neurons within the ventrolateral preoptic area, one of the putative sleep centers, and simultaneously decreased Fos expression in the tuberomammillary nucleus, one of the putative wake centers (5).PGD synthase (PGDS) is mainly produced in the LM and choroid plexus of the brain (6) and secreted into the cerebrospinal fluid (CSF) to become ␤-trace, a major CSF protein (reviewed in ref. 7). We recently reported that human PGDSoverexpressing transgenic mice exhibited excessive amounts of non-rapid eye movement (NREM) sleep, but not rapid eye movement (REM) sleep, in response to the noxious stimulus by tail clipping, coupled with a significant increase in the PGD 2 content in the brain (8). Therefore, PGD 2 , PGDS, and the PGDS gene are considered...

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“…It was previously observed that somatosensory stimulation could elicit bursting activity in the septum [30][31][32][33]. Further the septal neurons are sensitive to pain stimulation as noted by Dutar et al, that majority of septohippocamal neurons in rats are activated by noxious stimuli [18].…”

Section: Discussionmentioning

confidence: 91%

Modulation of Pain by Naloxone and a Possible Role of Neurotransmitters with Selective Lesion of Septal Nuclei

Somade¹,

Brid²

2015

J Spine

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Septum occupies a strategic position in limbic system and has been implicated in variety of behaviors. Present study was designed to evaluate the role of medial septum in modulation of pain and explore the role of neurotransmitters.The present study was divided in two parts in first part the tail flick latencies were observed in rats with septal lesions and compared with sham operated ones. While in the second part, the effect of intraseptal injections of neurotransmitters and naloxone on tail flick latencies ofcannulated rats was recorded after intraseptal lesions.It was observed that the septal lesions decrease pain threshold. The interaseptal injection of Acetylcholine (5 µg to 20 µg) and Naloxone (5 µg to 20 µg) increases pain threshold. While the Interaseptal injection of Noradrenaline and Scopolamine decreases pain threshold.The findings of the present study suggest that septum may be involved in modulation of pain. The neurotransmitters like Acetylcholine, Noradrenaline and opioid peptides may have an individual or collective role to play in the observed pain modulation.

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Prostaglandin D2-sensitive, sleep-promoting zone defined in the ventral surface of the rostral basal forebrain.

Cited by 126 publications

References 27 publications

Prostaglandin D Synthase (β-Trace) in Meningeal Hemangiopericytoma

Prostaglandin D Synthase (β-Trace) in Meningeal Hemangiopericytoma

Dominant localization of prostaglandin D receptors on arachnoid trabecular cells in mouse basal forebrain and their involvement in the regulation of non-rapid eye movement sleep

Modulation of Pain by Naloxone and a Possible Role of Neurotransmitters with Selective Lesion of Septal Nuclei

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