The significance of adrenaline-induced potentiation of electrogenic sodium pumping in bullfrog sympathetic ganglia

1985 ◽  
Vol 63 (9) ◽  
pp. 1182-1189 ◽  
Author(s):  
Peter A. Smith ◽  
Kochu-Rani Dombro
Keyword(s):  
Sympathetic Ganglia ◽  
Short Term ◽  
Experimental Conditions ◽  
Membrane Hyperpolarization ◽  
Gap Technique ◽  
Electrophysiological Responses ◽  
Sucrose Gap ◽  
Electrophysiological Effects ◽  
Lines Of Evidence ◽  
Stimulation Of

Two different electrophysiological responses in amphibian sympathetic ganglia were studied by means of the sucrose gap technique; (i) the potassium-activated hyperpolarization (KH) which serves as an index of electrogenic Na+ pumping, and (ii) the hyperpolarization induced by adrenaline (AdH). Under appropriate experimental conditions, 0.1 μM adrenaline potentiated the KH to 121.5 ± 7.5% of control (n = 7). This potentiation was blocked by both yohimbine (50 nM) and prazosin (1 μM) but not by propranolol (1 μM). Clonidine (10 nM) potentiated the KH to 113.5 ± 3.4% of control (n = 5), whereas methoxamine (0.1 μM) was ineffective. Several lines of evidence argued against the hypothesis that the AdH may be generated, in whole or in part, by stimulation of the Na+ pump. For example, (i) the AdH was sometimes completely unaffected when the KH was blocked by ouabain, and (ii) the AdH was eliminated by 2 nM Ba2+ even though this cation enhanced membrane hyperpolarization accompanying electrogenic Na+ pumping. These results imply that the electrogenic Na+ pump is not involved in the short-term electrophysiological effects of catecholamines. Despite this, it is possible that the homeostasis of Na+ and K+ in nerve may be regulated by α-adrenergic mechanisms.

scholarly journals Epidermal growth factor, like glucagon, exerts a short-term stimulation of alanine transport in rat hepatocytes

1987 ◽  
Vol 247 (1) ◽  
pp. 233-235 ◽  
Author(s):  
S K Moule ◽  
J D McGivan
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Membrane ◽  
Rat Hepatocytes ◽  
Short Term ◽  
Membrane Hyperpolarization ◽  
Control Value ◽  
Alanine Transport ◽  
Epidermal Growth ◽  
Stimulation Of

Epidermal growth factor causes a transient stimulation of alanine transport in hepatocytes. The stimulation is maximal after 30 min, and the rate returns to the control value after 90 min. These characteristics are very similar to the short-term stimulation of alanine transport by glucagon, which has been attributed to cell membrane hyperpolarization.

The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia

1986 ◽  
Vol 56 (3) ◽  
pp. 823-834 ◽  
Author(s):  
P. A. Smith ◽  
F. F. Weight
Keyword(s):  
B Cells ◽  
Ringer Solution ◽  
Sympathetic Ganglia ◽  
Sympathetic Chain ◽  
C Cells ◽  
Inhibitory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Sucrose Gap ◽  
Paravertebral Sympathetic Ganglia ◽  
Stimulation Of

Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in C cells of the IXth and Xth paravertebral ganglia treated with 70 microM d-tubocurarine chloride (dTC). Under these conditions, local iontophoretic application of acetylcholine (ACh) could produce a slow hyperpolarization of C cell membrane potential. ACh hyperpolarizations or slow IPSPs were not detected in ganglionic B cells. Stimulation of the preganglionic B-fibers in the sympathetic chain produced a fast nicotinic EPSP and a slow muscarinic EPSP in ganglionic B cells. A small population of C cells also received cholinergic B-fiber innervation from the sympathetic chain and exhibited a slow IPSP upon tetanic stimulation of this pathway. When curarized ganglia were examined by means of sucrose gap recording, superfusion of the muscarinic agonist, methacholine (MCh), produced an initial hyperpolarization (MChH) followed by a depolarization (MChD). Both responses were blocked by atropine and therefore presumably reflect the activation of muscarinic receptors involved in the generation of the slow IPSP and the slow EPSP, respectively. Although synaptic transmission was blocked by Ringer solution containing 4 mM Co2+, neither this solution nor 10 microM tetrodotoxin reduced the amplitude of the MChH. The MChH was slightly reduced by Ringer solution containing 0.1 mM Ca2+, however, the response could be restored by the addition of 6 mM Mg2+. These results indicate that the MChH in curarized bullfrog sympathetic ganglia results from a direct muscarinic action on ganglionic cells. This suggests that the slow IPSP is mediated by ACh released from cholinergic preganglionic fibers that make synaptic contact with ganglionic C cells.

scholarly journals Short-term stimulation of Na+-dependent amino acid transport by dibutyryl cyclic AMP in hepatocytes. Characteristics and partial mechanism

1987 ◽  
Vol 241 (3) ◽  
pp. 737-743 ◽  
Author(s):  
S K Moule ◽  
N M Bradford ◽  
J D McGivan
Keyword(s):  
Amino Acid ◽  
Cyclic Amp ◽  
Amino Acid Transport ◽  
Acid Transport ◽  
Short Term ◽  
Membrane Hyperpolarization ◽  
Alanine Transport ◽  
Cell Plasma ◽  
Time Courses ◽  
Stimulation Of

The short-term protein-synthesis-independent stimulation of alanine transport in hepatocytes was further investigated. Cyclic AMP increased the Vmax. of alanine transport. Amino acid transport via systems A, ASC and N was stimulated. A good correlation was found between the initial rate of transport and the cell membrane potential as calculated from the distribution of Cl-. Cyclic AMP increased the rate of alanine transport, stimulated Na+/K+ ATPase (Na+/K+-transporting ATPase) activity and caused membrane hyperpolarization. The time courses and cyclic AMP dose-dependencies of all three effects were similar. Ouabain abolished the effect of cyclic AMP on Cl- distribution and on transport of alanine. The effect of cyclic AMP on alanine transport and Cl- distribution was mimicked by the antibiotic nigericin; the effect of nigericin was also abolished by ouabain. It is concluded that the effect of cyclic AMP on transport is mediated via membrane hyperpolarization. It is suggested that the primary action of cyclic AMP is to increase the activity of an electroneutral Na+/K+-exchange system in the liver cell plasma membrane, thus hyperpolarizing the membrane by stimulating the electrogenic Na+/K+ ATPase.

The α1- and α2-adrenoceptor and muscarinic responses of normal and axotomized bullfrog sympathetic ganglia

1990 ◽  
Vol 68 (9) ◽  
pp. 1189-1193 ◽  
Author(s):  
P. A. Smith ◽  
T. Gordon ◽  
M. P. Kehoe ◽  
K. C. Marshall
Keyword(s):  
B Cells ◽  
Sympathetic Ganglia ◽  
C Cells ◽  
Muscarinic Agonists ◽  
Biphasic Response ◽  
Selective Agonist ◽  
Gap Technique ◽  
Adrenoceptor Agonists ◽  
Sucrose Gap ◽  
Paravertebral Sympathetic Ganglia

When neurones in bullfrog paravertebral sympathetic ganglia are studied by means of the sucrose-gap technique, muscarinic agonists produce a biphasic response (an initial hyperpolarization of ganglionic C cells followed by a depolarization of ganglionic B cells). Activation of ganglionic α2-adrenoceptors promotes hyperpolarization. The present experiments with selective α1- and α2-adrenoceptor agonists and antagonists provided evidence for the existence of hitherto undescribed α1-adrenoceptors, which are responsible for the production of depolarizing responses in these ganglia. Fifteen to twenty-five days after cutting postganglionic axons (axotomy), there was a nonselective depression of both α1- and α2-adrenoceptor mechanisms but little change in muscarinic responses. These results argue against the hypothesis that C cells assume all the properties of B cells after axotomy. Since the α-selective agonist phenylephrine failed to depolarize axotomized ganglia, it is unlikely that an α1-adrenoceptor mechanism is prominent in axotomized neurones as it is in some immature adrenergic neurones. The data are consistent with the idea that axotomy selectively affects the properties of certain types of cation channels and raise questions as to the mechanisms involved in regulating the expression and maintenance of specific neurotransmitter responses on ganglionic neurones.Key words: axotomy, α-adrenoceptor mechanisms, muscarinic receptors, sympathetic ganglion, frog.

Is money the creation of the state or the market? (On the “modern monetary theory” as described in the textbook by W. Mitchell, L. R. Wray and M. Watts “Macroeconomics”)

2020 ◽  
pp. 121-134
Author(s):  
S. A. Andryushin
Keyword(s):  
Public Debt ◽  
Scientific Community ◽  
Full Employment ◽  
Term Effect ◽  
Scientific Concept ◽  
Monetary Theory ◽  
Left Wing ◽  
Medium Term ◽  
Short Term ◽  
Stimulation Of

In 2019, a textbook “Macroeconomics” was published in London, on the pages of which the authors presented a new monetary doctrine — Modern Monetary Theory, MMT, — an unorthodox concept based on the postulates of Post-Keynesianism, New Institutionalism, and the theory of Marxism. The attitude to this scientific concept in the scientific community is ambiguous. A smaller part of scientists actively support this doctrine, which is directly related to state monetary and fiscal stimulation of full employment, public debt servicing and economic growth. Others, the majority of economists, on the contrary, strongly criticize MMT, arguing that the new theory hides simple left-wing populism, designed for a temporary and short-term effect. This article considers the origins and the main provisions of MMT, its discussions with the mainstream, criticism of the basic tenets of MMT, and also assesses possible prospects for the development of MMT in the medium term.

EFFECT OF ACTINOMYCIN D ON TSH-INDUCED STIMULATION OF THYROIDAL PROTEIN SYNTHESIS IN THE RAT

1974 ◽  
Vol 77 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Gustav Wägar
Keyword(s):  
Protein Synthesis ◽  
Actinomycin D ◽  
The Other ◽  
Leucine Incorporation ◽  
Short Term ◽  
Other Hand ◽  
Thyroid Glands ◽  
Translational Level ◽  
Stimulation Of

ABSTRACT Whether the short-term regulation of thyroidal protein synthesis by TSH occurs at the transcriptional or the translational level was tested by measuring the effect of actinomycin D (act D) on the TSH-induced stimulation of L-14C-leucine incorporation into the thyroidal proteins of rats. TSH was injected 6 h before the rats were killed. The thyroid glands were then removed and incubated in vitro in the presence of L-14C-leucine for 2 h. The pronounced stimulation of leucine incorporation in the TSH-treated animals was depressed as compared with controls but still significant even when the animals had been pre-treated with 100 μg act D 24 and 7 h before sacrifice. On the other hand, act D strongly decreased incorporation of 3H-uridine into RNA. Short-term regulation of thyroidal protein synthesis by TSH appears to be partly but not wholly dependent on neosynthesis of RNA. Hence regulation may partly occur at the translation level of protein synthesis.

Electrical stimulation of referred sensation area alleviates phantom limb pain

2021 ◽  
pp. 1-10
Author(s):  
Michihiro Osumi ◽  
Daisuke Shimizu ◽  
Yuki Nishi ◽  
Shu Morioka
Keyword(s):  
Electrical Stimulation ◽  
Single Case ◽  
Phantom Limb Pain ◽  
Phantom Limb ◽  
Long Term Effects ◽  
Limb Pain ◽  
Short Term ◽  
Analgesic Effects ◽  
Stimulation Of

Background: Patients with brachial plexus avulsion (BPA) usually experience phantom sensations and phantom limb pain (PLP) in the deafferented limb. It has been suggested that evoking the sensation of touch in the deafferented limb by stimulating referred sensation areas (RSAs) on the cheek or shoulder might alleviate PLP. However, feasible rehabilitation techniques using this approach have not been reported. Objective: The present study sought to examine the analgesic effects of simple electrical stimulation of RSAs in BPA patients with PLP. Methods: Study 1: Electrical stimulation of RSAs for 60 minutes was conducted for six BPA patients suffering from PLP to examine short-term analgesic effects. Study 2: A single case design experiment was conducted with two BPA patients to investigate whether electrical stimulation of RSAs was more effective for alleviating PLP than control electrical stimulation (electrical stimulation of sites on side opposite to the RSAs), and to elucidate the long-term effects of electrical stimulation of RSAs. Results: Study 1: Electrical stimulation of RSAs evoked phantom touch sensations in the deafferented limb, and significantly alleviated PLP (p <  0.05). Study 2: PLP was alleviated more after electrical stimulation on RSAs compared with control electrical stimulation (p <  0.05). However, the analgesic effects of electrical stimulation on RSAs were observed only in the short term, not in the long term (p >  0.05). Conclusions: Electrical stimulation of RSAs not only evoked phantom touch sensation but also alleviated PLP in the short term. The results indicate that electrical stimulation of RSAs may provide a useful practical rehabilitation technique for PLP. Future studies will be required to clarify the mechanisms underlying immediate PLP alleviation via electrical stimulation of RSAs.

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