Regulation of D1 receptor-induced Na+ current response through SNARE-dependent exocytosis in Aplysia neurons

1. The effect of serotonin (5-HT) and forskolin on an inwardly rectifying K+ conductance (IKR) was studied using voltage-clamp techniques in several identified Aplysia neurons isolated and maintained in primary cell culture. 2. Inward rectification was observed in the current-voltage relationship of the identified neurons R15, R2, B1, and B2 and was predominately due to IKR, as demonstrated by the dependence of inward rectification on the extracellular K+ concentration, instantaneous kinetics of the membrane current response to hyperpolarizing voltage clamp pulses, and voltage-dependent Ba2+ block of the inwardly rectifying current. 3. 5-HT increased IKR conductance between 100 and 400% in the identified neuron R15 in culture and increased IKR conductance approximately 50% in the identified neurons B1, B2, and R2 in culture. The adenylate cyclase activator, forskolin, plus a phosphodiesterase inhibitor, Ro 20-1724, also increased IKR conductance in these neurons. 4. 5-HT and forskolin modulated other ion conductances as well in all of these cultured neurons.

Download Full-text

Augmenting effect of monomeric G-protein RhoA on the serotonin-induced Na+-current response in the ganglion cells of Aplysia

Neuroscience Research ◽

10.1016/s0168-0102(00)81013-5 ◽

2000 ◽

Vol 38 ◽

pp. S27

Author(s):

S Kawasaki

Keyword(s):

G Protein ◽

Ganglion Cells ◽

Current Response ◽

Na Current

Download Full-text

Regulation of cAMP-stimulated ion current by intracellular pH, Ca2+, and calmodulin blockers

Journal of Neurophysiology ◽

10.1152/jn.1988.59.1.248 ◽

1988 ◽

Vol 59 (1) ◽

pp. 248-258 ◽

Cited By ~ 13

Author(s):

D. J. Green ◽

R. Gillette

Keyword(s):

Intracellular Ph ◽

Ion Current ◽

Current Response ◽

Intracellular Acidification ◽

Common Site ◽

Na Current ◽

Camp Phosphodiesterase ◽

Intracellular Injection ◽

Site Of Action ◽

Intracellular Alkalinization

1. Iontophoretic injection of adenosine 3',5'-cyclic monophosphate (cAMP) into identified neurons elicited a slow transient Na+ current whose amplitude and duration were sensitive to altered intracellular pH (pHi), calmodulin blocking drugs, depolarization, and manipulations of internal and external Ca2+. 2. Intracellular acidification between resting pHi to several tenths of a pH unit increased the amplitude of the cAMP-stimulated current and prolonged its duration. 3. Intracellular alkalinization of similar magnitude also increased the amplitude and duration of the current response. The effects of alkalinization were somewhat labile. In cells alkalinized by NH4+-containing salines, washout of NH4+ with normal saline caused acidification and further enhanced the cAMP current response. The immediacy of the increase and the dual acid/basic sensitivity of the response suggest an accommodative process whereby the responsiveness of the cell to cAMP adapts to a maintained pHi. 4. The calmodulin blockers trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide increased the amplitude and duration of the current response. Phorbol ester activators of Ca2+/phospholipid-dependent kinase had no effect on the current. 5. Periods of depolarization preceding tests significantly reduced current response amplitude. This effect was dependent on saline Ca2+ and was blocked by Co2+. 6. Intracellular injection of the Ca2+ chelator ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N',-tetraacetic acid also augmented the amplitude and duration of the current response. 7. The above effects are consistent with a possible common site of action on cAMP degradation. This interpretation is consistent with previous evidence for pH-sensitive and Ca2+/calmodulin-dependent cAMP phosphodiesterase activity in Pleurobranchaea nervous tissue.

Download Full-text