Stimulation of a sodium influx by cAMP in Helix neurons

Aldenhoff, Josef B.; Hofmeier, G.; Lux, H. D.; Swandulla, Dieter

doi:10.1016/0006-8993(83)90736-9

Cited by 57 publications

(50 citation statements)

References 20 publications

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“…An inward current can have a number of mechanisms: 1) a decrease in potassium conductance, 2) a decrease in calcium-activated potassium conductance, 3) a decrease in chloride conductance, 4) an increase in calcium conductance, 5) an increase in TTX-resistant slow sodium current. Many of the ionic mechanisms that have been proposed previously to account for cAMP-induced inward currents in neurons of various gastropod species involve either increases in Nat-current (ALDENHOFF et al, 1983;KONONENKO et al, 1983;CONNOR and HOCKBERGER, 1984) or increases in Cat-current (PELLMAR, 1981). Our conclusion that intracellularly injected CAMP can induce a TTX-resistant, slow sodium inward current in an identified neuron L5 of Aplysia kurodai is based on the following observations: 1) the CAMP-induced inward current decreased with an decreasing [Na+]o, 2) replacement of sodium with Tris almost completely eliminated the cAMP-induced current recorded at a holding potential of -60 mV, 3) exposure of L5 to 50 / M TTX for 28 min did not affect the CAMP-induced current, and 4) the calcium channel blocker, Ni2+ caused a slight reduction (70 % of control) in the cAMPinduced current.…”

Section: Discussionmentioning

confidence: 99%

“…3C). The CAMP-induced inward current in Helix and Archidoris neurons is also insensitive to ouabain and amiloride (ALDENHOFF et al, 1983;KONONENKO et al, 1983;CONNOR and HOCKBERGER, 1984). Figure 3D illustrates typical records of the CAMP-induced inward current when L5 was exposed to Aplysia Ringer at 20 and 7°C.…”

Section: Camp Induced Inward Currentmentioning

confidence: 99%

“…An increased K+-current has been observed in response to bath and intracellularly applied cAMP or its analogs to molluscan neurons (TREISTMAN, 1981;EWALD and ECKERT, 1983). On the other hand, several investigators have reported that intracellular injections of cAMP cause either an increase in inward current (PELLMAR, 1981;ALDENHOFF et al, 1983;GREEN and GILLETTE, 1983;KONO-NENKO et al, 1983;CONNOR and HOCKBERGER, 1984), or a decrease in outward current (KLEIN and KANDEL, 1980;DETERRE et al, 1982;KACZMAREK and STRUMWASSER, 1984) across the molluscan neuronal membranes.…”

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confidence: 99%

“…Recent investigations of the effects of intracellularly elevated cAMP levels on molluscan neuronal membrane potentials have proposed several mechanisms of action (PELLMAR, 1981;DETERRE et al, 1982;ALDENHOFF et al, 1983;KONONENKO et al, 1983;SWANDULLA and LUx, 1984;CONNOR and HOCKBERGER, 1984). An increased K+-current has been observed in response to bath and intracellularly applied cAMP or its analogs to molluscan neurons (TREISTMAN, 1981;EWALD and ECKERT, 1983).…”

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confidence: 99%

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Influences of pressure-injected cyclic AMP on the membrane current and characteristics of an identified neuron of Aplysia kurodai.

1985

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The ionic mechanism of the effect of intracellularly injected adenosine 3',5'-cyclic monophosphate (CAMP) on the membrane of identified neuron L5 of Apl ysia kurodai was investigated with conventional voltage-clamp and ion-substitution techniques. The intracellular elevation of CAMP caused an inward current ('CAMP), which was not accompanied by a significant change in membrane conductance at potentials more hyperpolarized than -60 mV. The current increased over the voltage range (-50 to -30 mV) associated with a conductance decrease and decreased at potentials more hyperpolarized than -60 mV. Elevated intracellular CAMP was found to enhance a region of negative slope resistance in steady-state I -V relations. Duration of the 'CAMP was greatly prolonged by bath-applied isobutylmethylxanthine (50 ,uM), but imidazole (10 mM) had an opposite effect on the 'CAMP. Tolbutamide (5 mM), a protein kinase inhibitor, reduced the DAMP. The current was not affected by the presence of bath-applied TTX (50 µM), ouabain (50 /LM), or triaminopyrimidine (5 mM). Reduction of [Na+]o reversibly decreased the DAMP. Li+ could largely substitute for Nat Alterations of [K+]o, and bath application of 4-AP (5 mM) and TEA (30 mM) did not affect the DAMP, In the presence of Nat, Cl-, and divalent cations such as Ca2+ and Ba2+ inhibited the DAMP. These results suggest that fast elevation of intracellular cAMP induces a TTX-resistant slow Na+ inward current, and the current might be due to activation of CAMP-dependent protein kinase.

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Section: Discussionmentioning

confidence: 99%

Section: Camp Induced Inward Currentmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Influences of pressure-injected cyclic AMP on the membrane current and characteristics of an identified neuron of Aplysia kurodai.

1985

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“…14-2 elicits an inward current (see also Kononenko, Kostyuk & Scherbatko, 1983;Aldenhoff, Hofmeier, Lux & Swandulla, 1983b;Green & Gillette, 1983;Swandulla & Lux, 1984;Connor & Hockburger, 1984a). This inward current can be almost completely eliminated by increasing the Ca content of the sea water from 10 to 60 mM or by replacing the Na in the sea water by mannitol (see Fig.…”

Section: Effects Of Cholinergic Antagonists On the K Conductance And mentioning

confidence: 99%

Synaptic block of a transmitter‐induced potassium conductance in Aplysia neurones.

Kehoe¹

1985

The Journal of Physiology

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A voltage‐clamp study was made of a slow excitatory post‐synaptic potential (slow e.p.s.p.) that can be elicited in the medial cells of the left pleural ganglion of Aplysia californica by the firing of at least three different presynaptic neurones (labelled I, II and III). Each of these three neurones elicits other permeability changes in addition to the slow e.p.s.p., and all elements of these synaptic responses were shown to be mediated monosynaptically. The slow e.p.s.p., associated with an increase in membrane resistance, was shown to be due to a decrease in K permeability. When the slow e.p.s.p. was present spontaneously, it could be blocked by three compounds (tetraethylammonium (TEA), phenyltrimethylammonium (PTMA), or methylxylocholine (beta‐TM 10], all previously shown to block the cholinergic receptor that mediates an increase in K conductance in the medial cells (see Kehoe, 1972b). Furthermore, in ganglia in which no slow e.p.s.p. was seen in response to firing of the neurones I, II, and III, such a response became manifest when agonists capable of activating the cholinergic receptor were applied (e.g. acetylcholine (ACh), carbachol, arecoline, or F2268). The slow e.p.s.p. thus appears to result from the reduction, induced by any one of three 'blocking neurones', of a cholinergically controlled K conductance. Finally, when presynaptic neurone I (the only neurone tested) was fired shortly before or during the activation of presynaptic neurone IV, previously shown to be cholinergic (Kehoe, 1972b), the K component of the cholinergic post‐synaptic inhibitory potential was markedly reduced. The concentration at which a given agonist caused the manifestation of the synaptic diminution in K conductance (i.e. the slow e.p.s.p.) was found to be the same as that at which it caused a reduction in the synaptically activated, cholinergic, K‐dependent conductance elicited by presynaptic neurone IV. Intracellularly injected adenosine 3',5'‐cyclic monophosphate (cyclic AMP) imitated the effect of the 'blocking neurones' on the K conductance activated by bath‐applied cholinomimetics. This effect was superimposed on a cyclic‐AMP‐induced, voltage‐dependent inward current that disappeared when the cell was bathed in Na‐free sea water, or when the extracellular Ca concentration was increased to 60 mM. The effect of cyclic AMP on the cholinergic K conductance remained even after this cyclic‐AMP‐activated inward current was eliminated.(ABSTRACT TRUNCATED AT 400 WORDS)

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Excitation of locus coeruleus neurons by an adenoine 3′,5′‐cyclic monophosphate‐activated inward current: Extracellular and intracellular studies in rat brain slices

Wang

Aghajanian

1987

Synapse

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The firing rate of locus coeruleus (LC) neurons in rat brain slices was increased reversibly by agents that either elevate intracellular levels of adenosine 3',5'-cyclic monophosphate (cAMP) or mimic its actions (e.g., forskolin, and activator of adenylate cyclase, 8-Br-cAMP, a membrane permeable analog of cAMP, and Ro20-1724, a preferential inhibitor of cAMP-phosphodiesterase). Intracellular recordings showed that 8-Br-cAMP and forskolin induce a depolarization of LC neurons, accompanied by a decrease in input resistance. The 8-Br-cAMP- and forskolin-elicited depolarization persisted in the presence of cobalt, a calcium channel blocker. Steady-state current-voltage curves revealed that in the voltage range of -50 to -120 mV, 8-Br-cAMP and forskolin induced an inward current, which did not reverse at the potassium equilibrium potential and could not be blocked by tetrodotoxin. Partial replacement of sodium with Tris or choline markedly reduced the depolarization elicited by 8-Br-cAMP. We conclude that 8-Br-cAMP and forskolin act through a common mechanism to increase the firing rate of locus coeruleus neurons by inducing a cAMP-activated inward current, carried out at least in part by sodium ions.

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Stimulation of a sodium influx by cAMP in Helix neurons

Cited by 57 publications

References 20 publications

Influences of pressure-injected cyclic AMP on the membrane current and characteristics of an identified neuron of Aplysia kurodai.

Influences of pressure-injected cyclic AMP on the membrane current and characteristics of an identified neuron of Aplysia kurodai.

Synaptic block of a transmitter‐induced potassium conductance in Aplysia neurones.

Excitation of locus coeruleus neurons by an adenoine 3′,5′‐cyclic monophosphate‐activated inward current: Extracellular and intracellular studies in rat brain slices

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