Arginine‐Vasopressin Stimulates Inositol Phospholipid Metabolism in Rat Hippocampus

Stephens, Len R.; Logan, S.D.

doi:10.1111/j.1471-4159.1986.tb13016.x

Cited by 70 publications

(22 citation statements)

References 21 publications

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“…This is in agreement with our previous findings that an antagonist of V1a-receptors, SR 49059, specifically inhibited the vasopressin-induced [Ca¥]é rise (Dayanithi et al 1996). In addition, studies on IP× accumulation measurements have shown that in many brain areas, vasopressin stimulation of the production of phosphatidyl-inositols is inhibited by a V1-type antagonist (Stephens & Logan, 1986;Moratalla et al 1988;Shewey & Dorsa, 1988;Hatton et al 1992). In the supraoptic nucleus, the vasopressin-induced [Ca¥]é increase is totally dependent upon extracellular Ca¥ but nevertheless is also significantly depressed by emptying the Ca¥ from intracellular stores by thapsigargin (Dayanithi et al 1996).…”

Section: Discussionsupporting

confidence: 81%

“…Little is known about vasopressin-induced intracellular transduction pathways in the brain. It has been reported that vasopressin increases the production of inositol phosphates in the hippocampus (Diaz-Brinton et al 1994;Stephens & Logan, 1986), in septum (Shewey & Dorsa, 1988;Lebrun et al 1990;Poulin & Pittman, 1993) and in dorsomedial medulla oblongata (Moratalla et al 1988). In other studies, the vasopressin failed to activate adenylate cyclase (AC) in hippocampus and septum (Barberis, 1983;Dorsa et al 1983;Audigier & Barberis, 1985;Brinton & McEwen, 1989).…”

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confidence: 97%

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Activation of multiple intracellular transduction signals by vasopressin in vasopressin‐sensitive neurones of the rat supraoptic nucleus

Sabatier

Richard

Dayanithi

1998

The Journal of Physiology

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The intracellular mechanisms activated by the binding of vasopressin to its receptor(s) and which result in the increase of [Ca2+]i were investigated in freshly dissociated supraoptic nucleus neurones. Various pharmacological agents were used to investigate the possible involvement of phospholipase C (PLC) and adenylate cyclase (AC) intracellular pathways in the transduction of the vasopressin action. Both the PLC inhibitor U‐73122 and the protein kinase C (PKC) inhibitor calphostin C, reduced the [Ca2+]i rise elicited by vasopressin. The cAMP analogue, 8‐Br‐cAMP produced an increase in [Ca2+]i and IBMX, a phosphodiesterase inhibitor, potentiated the response to vasopressin. After pre‐incubation with the AC inhibitor SQ‐22536, 7 out of 18 vasopressin‐sensitive neurones showed no inhibition of the vasopressin response, while the response to vasopressin was reduced by greater than 35 % in each of the other 11 neurones. The activation of protein kinase A (PKA) with Sp‐cAMPS caused an increase in [Ca2+]i which was additive to the vasopressin‐elicited [Ca2+]i increase. After incubation with the PKA inhibitors Rp‐cAMPS or H‐89, the [Ca2+]i responses triggered by Sp‐cAMPS and vasopressin were, respectively, abolished and greatly reduced. A combined administration of SQ‐22536 (AC inhibitor) followed by U‐73122 (PLC inhibitor), or U‐73122 followed by H‐89 (PKA inhibitor), virtually abolished the response to vasopressin. In vasopressin‐responsive neurones, the pituitary adenylate cyclase‐activating polypeptide (PACAP) induced a [Ca2+]i increase similar to the response to vasopressin and in both cases the increase was inhibited to the same extent by a combination of U‐73122 and Rp‐cAMPS. In conclusion, we suggest that the autoregulation exerted specifically by vasopressin on vasopressin‐sensitive neurones involves the activation of both PLC‐ and AC‐linked pathways.

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Section: Discussionsupporting

confidence: 81%

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confidence: 97%

Activation of multiple intracellular transduction signals by vasopressin in vasopressin‐sensitive neurones of the rat supraoptic nucleus

Sabatier

Richard

Dayanithi

1998

The Journal of Physiology

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“…Brinton and McEwen (17) demonstrated that AVP enhanced the cAMP accumulation induced by norepinephrine in cultured hippocampal neurons, whereas OT did not. Similarly, it has been reported that 10 Ϫ7 M AVP leads to IP 3 production in rat hippocampal slices via V 1 receptors, whereas OT has no affect (15). Both AVP and OT at the concentration of 2.5 ϫ 10 Ϫ7 M induced IP 3 production in cultured hippocampal neurons, but these affects were exerted through the V 1 receptor (16).…”

Section: Or V 2 Receptor-mediated Inhibitory Actions On I Gly -mentioning

confidence: 58%

“…In both electrophysiological (9,11) and behavioral (13,14) studies, the effect of AVP was blocked by a selective V 1 receptor antagonist. It has also been reported that AVP induced the production of IP 3 through the V 1 receptor in rat cultured hippocampal neurons (15,16). Brinton and McEwen (17) demonstrated that AVP potentiates the norepinephrine-induced cAMP accumulation in a calcium-dependent manner in the rat hippocampal slice preparation through the V 1 receptor.…”

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confidence: 91%

Intracellular Pathways of V1 and V2Receptors Activated by Arginine Vasopressin in Rat Hippocampal Neurons

Omura¹,

Nabekura²,

Akaike³

1999

Journal of Biological Chemistry

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To explore the intracellular pathways activated by vasopressin receptors, the effects of arginine vasopressin (AVP) and its analogues mediating glycine (Gly)-induced Cl ؊ currents (I Gly ) were examined in acutely dissociated rat hippocampal CA1 neurons using the whole-cell patch recording technique. AVP and its analogues inhibited I Gly in a concentration-dependent manner. The inhibitory actions of AVP(4 -9) (AVP metabolite) and NC-1900 (AVP(4 -9) analogue) were reversed by a V 1 receptor antagonist, or pretreatment with 1,2-bis The hypothalamic vasopressin-containing neurons project to the hippocampal regions (4, 5). Autoradiographic ligand-binding studies found vasopressin receptors in the pyramidal cell layer of the hippocampus (6, 7). The vasopressin receptor in the hippocampus has been shown to be the V 1 subtype in histological studies using a 3 H-labeled V 1 antagonist (8, 9). Moreover, the possible existence of V 2 receptor in the rat hippocampus has also been suggested at the mRNA level (10). Extracellular recording revealed an increase of firing rate of hippocampal neurons stimulated by AVP (11). In addition, AVP has been shown to induce an increase of spike discharge in the hippocampal CA1 pyramidal neurons in studies using microelectrode techniques (12). In both electrophysiological (9, 11) and behavioral (13, 14) studies, the effect of AVP was blocked by a selective V 1 receptor antagonist. It has also been reported that AVP induced the production of IP 3 through the V 1 receptor in rat cultured hippocampal neurons (15, 16). Brinton and McEwen (17) demonstrated that AVP potentiates the norepinephrine-induced cAMP accumulation in a calcium-dependent manner in the rat hippocampal slice preparation through the V 1 receptor. It has been demonstrated that the activation of V 1a receptor potentiated the V 2 receptor-mediated cAMP accumulation in Chinese hamster ovary (CHO) cells transfected with both receptor cDNAs (18). However, the specific mechanism by which cAMP accumulates as a consequence of V 1 receptor activation has yet been elucidated for hippocampal neurons.The intracellular cAMP levels may be modified by calcium through regulation of the activity of some adenylate cyclase isoforms. Nine subtypes of adenylate cyclase have been identified by cloning and expression studies, and they have been divided into six subfamilies based on their functional properties and sequence similarities: type 1, type 2-like group (types 2, 4 and 7), type 3, type 5-like group (types 5 and 6), type 8, and type 9 (19 -23). The presence of types 1, 2, 4, and 8 messenger RNAs was revealed by the polymerase chain reaction in pyramidal neurons in the CA1 region (21,(23)(24)(25). The types 1 and 8

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“…Muscarinic agonists have been demonstrated to stimulate hydrolysis of PtdInsP2 in this tissue (Stephens & Logan, 1989a) leading to rapid formation of several inositol phosphates including Insl,4,5P3 and Insl,3,4,5P4 (Stephens & Logan, 1989b (Stephens & Logan, 1986 Incubations were terminated by addition of 250p1 of ice-cold pefchloric acid (10%w/v) and put on ice for 1Omin.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of agonist‐stimulated inositol lipid metabolism by the anticonvulsant carbamazepine in rat hippocampus

McDermott

Logan

1989

British J Pharmacology

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Responses to carbachol, histamine and the sodium-channel agent veratrin were reduced by carbamazepine whilst the responses to 5-hydroxytryptamine, noradrenaline and substance P were unaffected. 5 Inhibition of carbachol, histamine and veratrin-induced stimulation by carbamazepine share a similar dependence on length of pre-incubation time with the drug. However, the effect of carbamazepine (100pM) on the respective dose-response curves suggests that the mechanism of inhibition of the carbachol response differs from the inhibition of the histamine and veratrin responses. These effects may be significant in the mechanism of action of carbamazepine as an anticonvulsant and in its effectiveness against manic depression.

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Arginine‐Vasopressin Stimulates Inositol Phospholipid Metabolism in Rat Hippocampus

Cited by 70 publications

References 21 publications

Activation of multiple intracellular transduction signals by vasopressin in vasopressin‐sensitive neurones of the rat supraoptic nucleus

Activation of multiple intracellular transduction signals by vasopressin in vasopressin‐sensitive neurones of the rat supraoptic nucleus

Intracellular Pathways of V1 and V2Receptors Activated by Arginine Vasopressin in Rat Hippocampal Neurons

Inhibition of agonist‐stimulated inositol lipid metabolism by the anticonvulsant carbamazepine in rat hippocampus

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