Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 7-bromo-1,4-dihydro-2-phenyl-4,4-bis(4-pyridinylmethyl)2H-isoquinolin-3-one dihydrochloride (BDPBI) on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of the giant African snail (Achatina fulica Ferussac). The effects of m-3M3FBS, a phospholipase activator and HTMT, a histamine (H1) receptor agonist, on the neuron were also tested. The RP4 neuron showed spontaneous firing of action potential. Extracellular application of BDPBI (150 micromol/l) reversibly elicited bursts of potential (BoP) on the neuron. m-3M3FBS and HTMT also elicited BoP on the RP4 neuron. The BoP elicited by BDPBI were blocked by U73122 (6 micromol/l), a compound commonly used as a phospholipase C (PLC) inhibitor. Neomycin (3.5 mmol/l), a high-magnesium solution (30 mmol/l), replacing the physiological sodium ion with lithium ion or adding diphenhydramine, chloropheniramine decreased the BoP elicited by BDPBI. The BoP elicited by BDPBI were not inhibited after administration with (1) prazosin, propranolol, atropine, d-tubocurarine, hexamethonium, haloperidol, cimetidine, (2) calcium-free solution, (3) high-potassium (12 mmol/l) solution, and (4) pretreatment with KT-5720. The BoP elicited by HTMT was not inhibited after administration of diphenhydramine or chloropheniramine. Voltage-clamped studies revealed that BDPBI decreased the amplitudes of calcium and steady-state outward currents while it did not alter the amplitude of the fast inward current. No negative slope relationship of the steady-state current voltage relationship was found in BDPBI-treated neurons. It is concluded that BDPBI reversibly elicited BoP in the central snail neuron. The effect was not due to (1) the extracellular calcium ion fluxes, or (2) the activation of cholinergic, adrenergic or histamine receptors. The BDPBI-elicited BoP were dependent on the phospholipase activity in the neuron.
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PMID:Effects of a new isoquinolinone derivative on induction of action potential bursts in central snail neuron. 1610 41

The effects of (+/-)3,4-methylenedioxyamphetamine (MDA) were studied in an identifiable RP4 neuron of the African snail, Achatina fulica Ferussac, using the two-electrode voltage-clamp method. The RP4 neuron generated spontaneous action potentials. Extracellular or intracellular application of MDA elicited action potential bursts of the central RP4 neuron. The action potential bursts elicited by MDA were not blocked when neurons were immersed in high-Mg2+ solution, Ca2+-free solution, nor after continuous perfusion with atropine, d-tubocurarine, propranolol, prazosin, haloperidol, sulpiride or methiothepin. Notably, the induction of action potential bursts was blocked by pretreatment with protein kinase C (PKC) inhibitors, chelerythrine and Ro 31-8220, but not by protein kinase A (PKA) inhibitors, KT-5720 and H89, nor by the phospholipase C (PLC) inhibitor, U73122. PKC activators, i.e., phorbol 12,13-dibutyrate (PDBu) and 1-oleoyl-2-acety-sn-glycerol (OAG; a membrane-permeant DAG analog), facilitate the induction of action potential bursts elicited by MDA. Voltage-clamp studies revealed that MDA decreased the delayed rectifying K+ current (I(KD)) of the RP4 neuron. Further, although Ro 31-8220 did not affect the I(KD), Ro 31-8220 decreased the inhibitory effect of MDA on the I(KD). These results suggest that the generation of action potential bursts elicited by MDA was not due to (1) the synaptic effects of neurotransmitters, (2) the cholinergic, adrenergic, dopaminergic or serotoninergic receptors of the excitable membrane. Instead, the MDA-elicited action potential bursts are closely related to PKC activity and the inhibitory effects on the I(KD).
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PMID:(+/-)3,4-Methylenedioxyamphetamine elicits action potential bursts in a central snail neuron. 1715 97