Arachidonic acid amide inhibitors of gap junction cell-cell communication

Boger, Dale L.; Sato, Haruhiko; Lerner, Aaron E.; Guan, Xiaojun; Gilula, Norton B.

doi:10.1016/s0960-894x(99)00148-1

Cited by 31 publications

(22 citation statements)

References 20 publications

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“…Given the recently proposed involvement of AA in oocyte maturation of some teleosts [32] and the inhibitory effect of AA on GJ coupling in a number of tissues [41][42][43], the present study examined the hypothesis that AA is part of the signaling pathway for MIH-dependent uncoupling of heterologous GJ. However, the present results showed that neither AA nor its COX metabolites, PGE 2 and PGF 2␣ , are able to uncouple heterologous GJ in maturationally competent croaker follicles within the time frame necessary for MIH-dependent uncoupling and maturation [38].…”

Section: Maturationmentioning

confidence: 99%

“…In addition, as noted already, AA and its metabolites as well as PKC are generally believed to be part of the transduction pathway of hormonally induced ovulation across vertebrate species. Although AA and its metabolites also are effective uncouplers of GJ channels in a variety of tissues [41][42][43], to our knowledge the role of AA in the periovulatory uncoupling of heterologous GJ has never been examined.…”

Section: Introductionmentioning

confidence: 99%

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Role of Arachidonic Acid and Protein Kinase C During Maturation-Inducing Hormone-Dependent Meiotic Resumption and Ovulation in Ovarian Follicles of Atlantic Croaker1

Patiño

Yoshizaki

Bolamba

et al. 2003

Biology of Reproduction

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The roles of arachidonic acid (AA) and protein kinase C (PKC) during in vitro maturation-inducing hormone (MIH)-dependent meiotic resumption (maturation) and ovulation were studied in ovarian follicles of Atlantic croaker (Micropogonias undulatus). The requirement for cyclooxygenase (COX) metabolites of AA was examined using a nonspecific COX inhibitor, indomethacin (IM), as well as two COX products, prostaglandin (PG) F(2alpha) and PGE(2), whereas the role of lipoxygenase (LOX) was investigated using a specific LOX inhibitor, nordihydroguaiaretic acid (NDGA). The involvement of PKC was examined using phorbol 12-myristate 13-acetate (PMA), a PKC activator, as well as GF109203X (GF), a specific inhibitor of PKC and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7), nonspecific inhibitor of protein kinases. Genomic mechanisms were examined with the transcription-inhibitor actinomycin D (ActD) and the functionality of heterologous (oocyte-granulosa) gap junctions (GJ) with a dye transfer assay. The AA (100 microM) and PGF(2alpha) (5 microM) did not induce maturation, and NDGA (10 microM) did not affect MIH-dependent maturation. However, IM (100 microM) partially inhibited MIH-dependent maturation. Conversely, AA and both PGs induced, and IM and NDGA inhibited, MIH-dependent ovulation in matured follicles. The PMA (1 microg/ml) did not induce maturation but caused ovulation in matured follicles, whereas PKC inhibitors (GF, 5 microM; H7, 50 microM) did not affect MIH-dependent maturation but inhibited MIH- and PMA-dependent ovulation. The PMA-dependent ovulation was inhibited by IM but not by NDGA. In addition, ActD (5 microM) blocked MIH-dependent, but not PMA-dependent, ovulation, and PGF(2alpha) restored MIH-dependent ovulation in ActD-blocked follicles. The AA and PGs did not induce, and GF did not inhibit, MIH-dependent heterologous GJ uncoupling. In conclusion, AA and PKC mediate MIH-dependent ovulation but not meiotic resumption or heterologous GJ uncoupling in croaker follicles, but a permissive role of COX products of AA during maturation is possible. A novel model of MIH-dependent ovulation is proposed in which 1). LOX and COX metabolites of AA are both required for ovulation, but at upstream and downstream sites of the pathway, respectively, relative to PKC, and 2). PKC is downstream of genomic activation.

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Section: Maturationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of Arachidonic Acid and Protein Kinase C During Maturation-Inducing Hormone-Dependent Meiotic Resumption and Ovulation in Ovarian Follicles of Atlantic Croaker1

Patiño

Yoshizaki

Bolamba

et al. 2003

Biology of Reproduction

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“…It blocks glial gap junction communication (11,12,21,22), differentially modulates the serotonergic system (7,23,24), modulates sleep and memory in rats analogous to oleamide (25), and exhibits a range of biological properties (17,26,27). Most exciting of these properties is the demonstration that endogenous anandamide levels increase on pain stimulation, implicating its role in suppressing pain neurotransmission and in behavioral analgesia (28).…”

mentioning

confidence: 99%

Exceptionally potent inhibitors of fatty acid amide hydrolase: The enzyme responsible for degradation of endogenous oleamide and anandamide

Boger

Sato

Lerner

et al. 2000

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

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263

264

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The development of exceptionally potent inhibitors of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of oleamide (an endogenous sleep-inducing lipid), and anandamide (an endogenous ligand for cannabinoid receptors) is detailed. The inhibitors may serve as useful tools to clarify the role of endogenous oleamide and anandamide and may prove to be useful therapeutic agents for the treatment of sleep disorders or pain. The combination of several features-an optimal C12-C8 chain length, -unsaturation introduction at the corresponding arachidonoyl ⌬ 8,9 ͞⌬ 11,12 and oleoyl ⌬ 9,10 location, and an ␣-keto N4 oxazolopyridine with incorporation of a second weakly basic nitrogen provided FAAH inhibitors with Kis that drop below 200 pM and are 10 2 -10 3 times more potent than the corresponding trifluoromethyl ketones.

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“…It inhibits gastric pepsins (Roberts and Taylor 1980) and has a number of mineralocorticoid actions (Armanini et al 1982), including inhibition of 11-␤ -dehyrogenase and 11-oxoreductase (Stewart et al 1990). Anandamide, on the other hand, is a highly lipophilic arachidonic acid-derived ethanolamide that has been shown to block gap junction transmission (Boger et al 1999), more specifically, in striatum (Venance et al 1995). At doses at or above 10 mg/kg it acts as an agonist at central cannabinoid CB1 receptors, producing catalepsy and hypothermia (Costa et al 1999;Crawley et al 1993;Fride and Mechoulam 1993).…”

mentioning

confidence: 99%

A Role for Electrotonic Coupling in the Striatum in the Expression of Dopamine Receptor-mediated Stereotypies,

Moore

Grace

2002

Neuropsychopharmacology

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Stimulation of dopamine (DA) receptors in the striatum evokes a number of alterations in motor behavior in rats, as well as causing several alterations in cellular physiology, including changes in membrane potential, cell excitability, afferent drive, and electrotonic coupling. One cellular property that is potently modulated by DA stimulation is electrotonic coupling, a process shown to subserve motor pattern generation. To examine whether electrotonic coupling plays a role in mediating a specific set of DA receptor-mediated motor behaviors, we tested the effects of two inhibitors of gap junction conductance, carbenoxolone (CARB) and anandamide (AEA), on apomorphine (APO)-induced motor responses. We then used intra-striatal infusions of CARB to determine the role of electrotonic coupling specifically in the ventral striatum in the expression of i.p.) significantly increased motor activity (a composite score) and the frequencies of oral and sniffing stereotypies. APO also disrupted grooming initiation and completion. APO-induced oral stereotypies were selectively blocked by systemic administration of CARB (7.0, 35.0 mg/kg Adaptive behaviors, both learned and spontaneous, consist of sequences of "micro" movements executed by closely-related muscle groups. There is evidence that the initiation and execution of individual movements, such as oral movements involved in feeding, as well as the linking of these movements into a behavioral sequence, depend upon neuronal networks within the Beninger et al. 1991;Braun and Chase 1986;Byrnes et al. 1994;Delfs and Kelley 1990). Thus, in the context of behavioral sequencing, the simple 'repetitive' stereotypy (Berridge and Aldridge 2000a) produced by D2 receptor over-stimulation in the striatum (Delfs and Kelley 1990) can be seen as the inability to release one 'simple' behavior in order to allow initiation of the next simple behavior in a normal, adaptive sequence (Pedro et al. 1994;Szechtman et al. 1999). One means by which neuronal networks may interact within the striatum is via communication among clusters of functionally related striatal neurons. Such a network interaction may be mediated via gap junctions. It is well-established that electrotonic transmission between developing neurons is important in the formation and stabilization of functional networks (Bannerman et al. 2000;Peinado et al. 1993;Roerig and Feller 2000). However, there is also evidence that in the adult brain, electrotonic coupling directly mediates forms of neuronal network activity (Bou-Flores and Berger 2001;Jefferys 1995;Perez Velazquez and Carlen 2000) which, in turn, contribute to rhythmic behavioral patterning (Bou-Flores and Berger 2001;Rothwell 1998). Thus, it is likely that motor patterning may involve activity within neuronal networks coordinated via gap junctions. In the striatum, cells express connexins, the protein building blocks of gap junctions (Belluardo et al. 2000;Bennett et al. 1999). Striatal neurons also exhibit dye coupling, the transfer of dye molecules between neurons thro...

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Arachidonic acid amide inhibitors of gap junction cell-cell communication

Cited by 31 publications

References 20 publications

Role of Arachidonic Acid and Protein Kinase C During Maturation-Inducing Hormone-Dependent Meiotic Resumption and Ovulation in Ovarian Follicles of Atlantic Croaker1

Role of Arachidonic Acid and Protein Kinase C During Maturation-Inducing Hormone-Dependent Meiotic Resumption and Ovulation in Ovarian Follicles of Atlantic Croaker1

Exceptionally potent inhibitors of fatty acid amide hydrolase: The enzyme responsible for degradation of endogenous oleamide and anandamide

A Role for Electrotonic Coupling in the Striatum in the Expression of Dopamine Receptor-mediated Stereotypies,

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