Cholinergic-induced [3H] noradrenaline release in rat brain cortical slices is mediated via a pertussis toxin sensitive GTP binding protein and involves activation of protein kinase C

Ari, Itzhak Lev; Schwarz, Lydia; Atlas, Daphine

doi:10.1016/0898-6568(89)90031-4

Cited by 7 publications

(4 citation statements)

References 35 publications

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“…However, phenylephrine is known to act on the NE transporter to enhance NE release (Ari et al, 1989). Thus, phenylephrine effects might be mediated through NE acting at non-␣ 1adrenoceptors.…”

Section: Ne and Phenylephrine Stimulate Cgmp Accumulation Only In Eb mentioning

confidence: 99%

Ovarian Hormone Dependence of α₁-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Chu¹,

Etgen

1999

J. Neurosci.

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The ovarian hormones estradiol (E(2)) and progesterone (P) facilitate rat lordosis behavior in part by regulating the expression of and signal transduction by adrenoceptors in the hypothalamus (HYP) and preoptic area (POA). The major adrenoceptor subtype mediating E(2) and P facilitation of lordosis is the alpha(1)-adrenoceptor. In the present studies, we tested the hypotheses that (1) alpha(1)-adrenoceptors in the HYP enhance lordosis responses by activating the nitric oxide (NO)-cGMP signaling pathway, and (2) coupling of alpha(1)-adrenoceptors to this signal transduction pathway is hormone-dependent. Basal levels of cGMP were significantly higher in HYP and POA slices from animals treated with E(2) and P when compared with slices from ovariectomized controls or females treated with only E(2) or P. When slices of HYP and POA from ovariectomized female rats were incubated with norepinephrine or the selective alpha(1)-adrenoceptor agonist phenylephrine, cGMP accumulation was observed only if slices had been derived from females treated with both E(2) and P before experimentation. Moreover, alpha(1)-adrenoceptor stimulation of cGMP synthesis was blocked by an inhibitor of NO synthase, confirming that these receptors act by NO-mediated stimulation of soluble guanylyl cyclase. Behavioral studies demonstrated further that the cell-permeable cGMP analog 8-bromoadenosine-cGMP reverses the inhibitory effects of the alpha(1)-adrenoceptor antagonist prazosin on lordosis behavior in E(2)- and P-treated female rats. Thus, the NO-cGMP pathway mediates the facilitatory effects of alpha(1)-adrenoceptors on lordosis behavior in female rats, and previous exposure of the HYP and POA to both E(2) and P are required to link alpha(1)-adrenoceptors to this pathway.

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Section: Ne and Phenylephrine Stimulate Cgmp Accumulation Only In Eb mentioning

confidence: 99%

Ovarian Hormone Dependence of α₁-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Chu¹,

Etgen

1999

J. Neurosci.

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“…The protein kinase C (PKC) subspecies a, 811, y, and c are present in presynaptic nerve terminals 1303 (Shearman et al, 1991a;Saito et al, 1993) and have been implicated for some time in the facilitation of transmitter release from synaptosomes (Chandler and Leslie, 1989 ;Davis and Patrick, 1990;Dekker et al, 1990Dekker et al, , 1991Barrie et al, 1991 ;Coffey et al, 1993), neuronal cultures (Finch and Jackson, 1990), and brain slices (Ari et al, 1989;Bartmann et al, 1989;Huang et al, 1989) . Some insight into the mechanism of PKCmediated potentiation has been gained by the observation that glutamate exocytosis from synaptosomes that have been stimulated by 4-aminopyridine (4-AP) is extensively activated by high concentrations of phorbol esters and inhibited by PKC inhibitors, whereas KCl-evoked glutamate exocytosis from the same preparation is totally insensitive to these agents (Barrie et al ., 1991) .…”

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confidence: 99%

Glutamate Exocytosis and MARCKS Phosphorylation Are Enhanced by a Metabotropic Glutamate Receptor Coupled to a Protein Kinase C Synergistically Activated by Diacylglycerol and Arachidonic Acid

Coffey

Herrero

Sihra

et al. 1994

Journal of Neurochemistry

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4-Aminopyridine evokes repetitive firing of synaptosomes and exocytosis of glutamate by inhibiting a dendrotoxin-sensitive K+ channel responsible for stabilizing the membrane potential . We have shown previously that activation of protein kinase C (PKC) by high concentrations of phorbol ester (4,ß-phorbol dibutyrate) can increase release by inhibiting a dendrotoxin-insensitive ion channel, whereas the metabotropic glutamate receptor (mGIuR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate [(1S,3R)-ACPD] mimics the action of 48phorbol dibutyrate, but only in the presence of 2 btM arachidonic acid (AA) . In this article, we investigate the role of AA . AA plus (1S,3R)-ACPD is without effect on KCIinduced glutamate exocytosis, indicating that the regulatory pathway acts upstream of the release-coupled Ca 2+ channel or Ca 2 '-secretion coupling . Diacylglycerol concentrations are greatly enhanced by (1 S,3R)-ACPD alone, independently of AA, indicating that AA acts downstream of phospholipase C . Myristoylated alanine-rich C kinase substrate (MARCKS) is the major presynaptic substrate for PKC . mGIuR activation by (1S,3R)-ACPD enhances phosphorylation of MARCKS, but only in the presence of AA. These results strongly suggest that AA acts on presynaptic PKC synergistically with diacylglycerol generated by the phospholipase-coupled mGIuR, consistent with the known behaviour of certain purified PKC isoforms . The magnitude of the effects observed in a population of rat cerebrocortical synaptosomes suggests that this is a major mechanism regulating the release of the brain's dominant excitatory neurotransmitter and supports the concept that AA, or a related compound with a similar locus of action, may in certain circumstances play a role in synaptic plasticity . Key Words: Glutamate exocytosis-MARCKS phosphorylation-Protein kinase C-Metabotropic glutamate receptor-Diacylglycerol-Arachidonic acid .

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“…As shown in Figure 5(a), blockade of Gi proteins by pretreatment with PTX did not modify LPI effects on release (Figure 5(a); [ 3 H]‐GABA release median LPI 142% rank 141–149% vs. median LPI‐PTX 145% rank 135–146%, mean rank difference 0, p = .99, ns, n = 4 experiments, KS = 9.955, p = .0027, Kruskal–Wallis test followed by Dunn's). In the same way, ChTx treatment by 3 h after the previous activation of Gs proteins (Ari et al., 1989) did not modify GPR55 effects on release (Figure 5(b); [ 3 H]‐GABA release median LPI 150% rank 131–167% vs. median LPI‐ChTx 141% rank 127–153%, mean rank difference 1, p = .7336, ns, n = 3 experiments, KS = 8.568, p = .0076, Kruskal–Wallis test followed by Dunn's).…”

Section: Resultsmentioning

confidence: 99%

“…*p < 0.05, p < 0.01, ns, with no significant differences among groups p = .99, ns, n = 4 experiments, KS = 9.955, p = .0027, Kruskal-Wallis test followed by Dunn's). In the same way, ChTx treatment by 3 h after the previous activation of Gs proteins(Ari et al, 1989) did not modify GPR55 effects on release (Figure5(b); [ 3 H]-GABA release median LPI 150% rank 131-167% vs. median LPI-ChTx 141% rank 127-153%, mean rank difference 1, p = .7336, ns, n = 3 experiments, KS = 8.568, p = .0076, Kruskal-Wallis test followed by Dunn's).The roles of PLC and PKC (effectors of GPR55;Lauckner et al, 2008) on LPI effects were studied by blockade with selective inhibitors. As shown in Figures5(c) and 5(d), blockade of PLC with U-73122(Jin et al, 1994, 10 μM) and PKC with Gö6983(Young et al, 2005, 10 μM) did not modify the stimulation of release induced by LPI (Figure 5(c); [ 3 H]-GABA release median LPI 156% rank 148-169% vs. median LPI + U 73122 157% rank 155-163%, mean rank difference −0.333, p = .9082, ns, KS = 8.622, p = .0099; Figure 5(d); [ 3 H]-GABA release median LPI 164% rank 145-174% vs. median LPI + Gö 6983 162% rank 143-178%, mean rank difference 0, p > .99, ns, n = 4 experiments, KS = 11.73, p = .0007, Kruskal-Wallis test followed by Dunn's).…”

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confidence: 97%

Presynaptic nigral GPR55 receptors stimulate [³H]‐GABA release through [³H]‐cAMP production and PKA activation and promote motor behavior

Sánchez‐Zavaleta

Ávalos-Fuentes

González-Hernández

et al. 2022

Synapse

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Striatal medium-sized spiny neurons express mRNA and protein of GPR55 receptors that stimulate neurotransmitter release; thus, GPR55 could be sent to nigral striatal projections, where it might modulate GABA release and motor behavior. Here, we study the presence of GPR55 receptors at striato-nigral terminals, their modulation of GABA release, their signaling pathway, and their effect on motor activity. By double immunohistochemistry, we found the colocation of GPR55 protein and substance P in the dorsal striatum. In slices of the rat substantia nigra, the GPR55 agonists LPI and O-1602 stimulated [ 3 H]-GABA release induced by high K + depolarization in a dose-dependent manner. The antagonists CID16020046 and cannabidiol prevented agonist stimulation in a dose-dependent way. The effect of GPR55 on nigral [ 3 H]-GABA release was prevented by lesion of the striatum with kainic acid, which was accompanied by a decrement of GPR55 protein in nigral synaptosomes, indicating the presynaptic location of receptors. The depletion of internal Ca 2+ stores with thapsigargin did not prevent the effect of LPI on [ 3 H]-GABA release, but the remotion or chelation of external calcium did. Blockade of Gi, Gs, PLC, PKC, or dopamine D1 receptor signaling proteins did not prevent the effect of GPR55 on release. However, the activation of GPR55 stimulated [ 3 H]-cAMP accumulation and PKA activity. Intranigral unilateral injection of LPI induces contralateral turning. This turning was prevented by CID16020046, cannabidiol, and bicuculline but not by SCH 23390. Our data indicate that presynaptic GPR55 receptors stimulate [ 3 H]-GABA release at striato-nigral terminals through [ 3 H]-cAMP production and stimulate motor behavior.

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Cholinergic-induced [3H] noradrenaline release in rat brain cortical slices is mediated via a pertussis toxin sensitive GTP binding protein and involves activation of protein kinase C

Cited by 7 publications

References 35 publications

Ovarian Hormone Dependence of α₁-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Ovarian Hormone Dependence of α₁-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Glutamate Exocytosis and MARCKS Phosphorylation Are Enhanced by a Metabotropic Glutamate Receptor Coupled to a Protein Kinase C Synergistically Activated by Diacylglycerol and Arachidonic Acid

Presynaptic nigral GPR55 receptors stimulate [³H]‐GABA release through [³H]‐cAMP production and PKA activation and promote motor behavior

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Cholinergic-induced [3H] noradrenaline release in rat brain cortical slices is mediated via a pertussis toxin sensitive GTP binding protein and involves activation of protein kinase C

Cited by 7 publications

References 35 publications

Ovarian Hormone Dependence of α1-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Ovarian Hormone Dependence of α1-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Glutamate Exocytosis and MARCKS Phosphorylation Are Enhanced by a Metabotropic Glutamate Receptor Coupled to a Protein Kinase C Synergistically Activated by Diacylglycerol and Arachidonic Acid

Presynaptic nigral GPR55 receptors stimulate [3H]‐GABA release through [3H]‐cAMP production and PKA activation and promote motor behavior

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Ovarian Hormone Dependence of α₁-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Ovarian Hormone Dependence of α₁-Adrenoceptor Activation of the Nitric Oxide–cGMP Pathway: Relevance for Hormonal Facilitation of Lordosis Behavior

Presynaptic nigral GPR55 receptors stimulate [³H]‐GABA release through [³H]‐cAMP production and PKA activation and promote motor behavior