Effect of stimulation with light on synthesis and release of acetylcholine by an isolated mammalian retina

1976 ◽  
Vol 39 (6) ◽  
pp. 1210-1219 ◽  
Author(s):  
R. H. Masland ◽  
C. J. Livingstone
Keyword(s):  
Initial Rate ◽  
Horizontal Cells ◽  
High Rate ◽  
Cholinergic Synapse ◽  
Pharmacological Agents ◽  
Choline Incorporation ◽  
Rate Acceleration ◽  
Mammalian Retina ◽  
Release Of Acetylcholine ◽  
Stimulation Of

1. Acetylcholine synthesis and release were studied in rabbit retinas isolated from the eye and incubated under conditions in which their electrophysiological function is maintained. ACh synthesized from exogenous [14C] choline appeared in the retina at an initial rate of 16 nmol/g wet wt-h. Incorporation of labeled choline into ACh was accelerated by stimulation of the retina with light. 2. Retinas incubated for 40 min in the presence of labeled choline and then superfused with a medium containing an anticholinesterase released radioactive ACh into the perfusate. The rate of release increased approximately fourfold during stimulation with light. 3. When retinas were incubated with labeled choline and then superfused with medium containing no pharmacological agents, stimulation with light caused an increased release of choline into the perfusate. The recovery of labeled choline following stimulation was enhanced by hemicholinium 3. 4. Neither the light-induced release of ACh (in perfusate containing anticholinesterase) nor the light-induced release of choline (in perfusate containing no anticholinesterase) occurred if the perfusate contained 20 mM Mg2+ and 0.2 mM Ca2+. 5. Synthesis of ACh by the retina at a high rate, acceleration of choline incorporation by stimulation, and Ca2+-dependent release of ACh by stimulation are each presumptive evidence that the retina contains a cholinergic synapse. If this presumption is correct, one such synapse mayx be of an amacrine or bipolar cell since these cells can depolarize during illumination, whereas the predominant response of receptor and horizontal cells is hyperpolarization.

scholarly journals Therapeutic use of botulinum toxin in pain treatment

2018 ◽  
Vol 2 (3) ◽  
Author(s):  
Raj Kumar
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Botulinum Toxin ◽  
Acetylcholine Release ◽  
Pain Treatment ◽  
Muscle Relaxation ◽  
Cholinergic Synapse ◽  
Systems Research ◽  
Release Of Acetylcholine ◽  
Myofascial Syndrome

Botulinum toxin is one of the most potent molecule known to mankind. A neurotoxin, with high affinity for cholinergic synapse, is effectively capable of inhibiting the release of acetylcholine. On the other hand, botulinum toxin is therapeutically used for several musculoskeletal disorders. Although most of the therapeutic effect of botulinum toxin is due to temporary skeletal muscle relaxation (mainly due to inhibition of the acetylcholine release), other effects on the nervous system are also investigated. One of the therapeutically investigated areas of the botulinum neurotoxin (BoNT) is the treatment of pain. At present, it is used for several chronic pain diseases, such as myofascial syndrome, headaches, arthritis, and neuropathic pain. Although the effect of botulinum toxin in pain is mainly due to its effect on cholinergic transmission in the somatic and autonomic nervous systems, research suggests that botulinum toxin can also provide benefits related to effects on cholinergic control of cholinergic nociceptive and antinociceptive systems. Furthermore, evidence suggests that botulinum toxin can also affect central nervous system (CNS). In summary, botulinum toxin holds great potential for pain treatments. It may be also useful for the pain treatments where other methods are ineffective with no side effect(s). Further studies will establish the exact analgesic mechanisms, efficacy, and complication of botulinum toxin in chronic pain disorders, and to some extent acute pain disorders.

Stimulation of phosphate transport in the proximal tubule by metabolic substrates

1984 ◽  
Vol 247 (4) ◽  
pp. F582-F587 ◽  
Author(s):  
S. R. Gullans ◽  
P. C. Brazy ◽  
L. J. Mandel ◽  
V. W. Dennis
Keyword(s):  
Proximal Tubule ◽  
Fluid Transport ◽  
Initial Rate ◽  
Tricarboxylic Acid Cycle ◽  
Phosphate Transport ◽  
Glucose Absorption ◽  
Metabolic Substrates ◽  
Tricarboxylic Acid Cycle Intermediates ◽  
Stimulation Of

Studies of phosphate transport in the proximal tubule have recently focused on interactions with cellular metabolism. The present studies demonstrate that two fatty acids, valerate and butyrate, and two tricarboxylic acid cycle intermediates, succinate and malate, stimulate net phosphate transport in the rabbit proximal tubule by 34-117%. Valerate had no effect on the total uptake of inorganic [32P]phosphate into suspensions of proximal tubules but did enhance the initial rate of influx. Net fluid transport was unaffected by these substrates although glucose absorption increased by 10-15% following the addition of either valerate or succinate. Since valerate, butyrate, and succinate are known to stimulate gluconeogenesis and respiration, we evaluated the role of gluconeogenesis in the stimulation of phosphate transport. The addition of 3-mercaptopicolinate (1 mM), an inhibitor of gluconeogenesis, did not alter phosphate transport, nor did it prevent the valerate-induced stimulation of phosphate transport. We conclude that valerate, butyrate, succinate, and malate enhance phosphate transport by the proximal convoluted tubule. This action appears to be unrelated to effects on gluconeogenesis and may be related to close links between phosphate transport and oxidative metabolism.

Options at the fundamental level for growth regulation in farm livestock

1997 ◽  
Vol 1987 ◽  
pp. 22-22
Author(s):  
P. J. Reeds
Keyword(s):  
Growth Regulation ◽  
Genetic Manipulation ◽  
Growth Promotion ◽  
Cellular Mechanisms ◽  
Pharmacological Agents ◽  
New Developments ◽  
Protein Deposition ◽  
Effective Use ◽  
Farm Livestock ◽  
Stimulation Of

New developments in immunological techniques and increasing expertise in genetic manipulation, especially by gene transfer, have opened up a wide variety of approaches to the manipulation of the growth and metabolism of farm livestock. However, the most effective use of these techniques and the design of new pharmacological agents for growth promotion and nutrient “repartitioning” might well rest on a greater understanding of the factors and cellular mechanisms that coordinate growth and protein anabolism. It is this coordidnation that must be disturbed if persistent gains are to bke made. This greater understanding may well result from an examination of the mechanisms whereby currently available anabolic agents and techniques exert their effects and this paper will draw on these experiences. Growth is clearly a closely coordinated process and this has hampered many attempts to maintain accelerated protein deposition for long periods. For example forced increases in hormonal concentrations often induce hormonal insensitivity. It is possible that understanding and reducing the constraints on growth for example by reducing the levels of suppressive factors rather than concentrating on the active stimulation of anabolic factors may be more effective.

Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

1992 ◽  
Vol 263 (5) ◽  
pp. G709-G718 ◽  
Author(s):  
M. Schemann ◽  
D. Grundy
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Enteric Neurons ◽  
Command Neurons ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine ◽  
Vagal Innervation ◽  
Guinea Pig Stomach ◽  
Stimulation Of

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

Excitation-induced Ca2+uptake in rat skeletal muscle

1999 ◽  
Vol 276 (2) ◽  
pp. R331-R339 ◽  
Author(s):  
H. Gissel ◽  
T. Clausen
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Initial Rate ◽  
Low Frequency ◽  
Channel Blockers ◽  
Ca Uptake ◽  
Edl Muscle ◽  
Isotonic Contractions ◽  
Progressive Accumulation ◽  
Stimulation Of

In isolated rat extensor digitorum longus (EDL) muscle mounted for isometric contractions, chronic low-frequency electrical stimulation was found to lead to an increased uptake of45Ca (154% above control after 240 min) and a progressive accumulation of Ca2+ (85% above control after 240 min). In soleus, however, this treatment led to a small, but significant, increase in 45Ca uptake (30% above control after 180 min) but no significant accumulation of Ca2+. In muscles mounted for isotonic contractions without any external load, electrical stimulation gave rise to a larger45Ca uptake and accumulation of Ca2+ in both EDL and soleus. These uptakes of Ca2+ coincided with an accumulation of Na+. During isometric or isotonic contractions, stimulation at 40 Hz increased the initial (60 s) rate of 45Ca uptake in soleus muscle 15- and 30-fold, respectively. The stimulation-induced increase in 45Ca uptake was only reduced by 17% by the Ca2+-channel blockers nifedipine and verapamil but was blocked by tetrodotoxin. The initial rate of stimulation-induced 22Na and45Ca uptake was correlated ( r = 0.80; P < 0.003). Stimulation of Na+ channels with veratridine increased 45Ca uptake by 93 and 139% in soleus and EDL, respectively ( P < 0.001), effects that were abolished by tetrodotoxin. The results indicate that in skeletal muscle, excitation induces a considerable influx of Ca2+, mediated by Na+ channels.

scholarly journals A new method to determine reflex latency induced by high rate stimulation of the nervous system

2014 ◽  
Vol 8 ◽  
Author(s):  
Ilhan Karacan ◽  
Halil I. Cakar ◽  
Oguz Sebik ◽  
Gizem Yilmaz ◽  
Muharrem Cidem ◽  
...  
Keyword(s):  
Nervous System ◽  
New Method ◽  
High Rate ◽  
Reflex Latency ◽  
Stimulation Of

scholarly journals The Q43L mutant of neuregulin 2β is a pan-ErbB receptor antagonist

2012 ◽  
Vol 443 (1) ◽  
pp. 133-144 ◽  
Author(s):  
Kristy J. Wilson ◽  
Christopher P. Mill ◽  
Richard M. Gallo ◽  
Elizabeth M. Cameron ◽  
Henry VanBrocklin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tyrosine Phosphorylation ◽  
Kinase Activity ◽  
Growth Factor Receptor ◽  
Erbb Receptor ◽  
Pharmacological Agents ◽  
Akt Phosphorylation ◽  
Agonist Stimulation ◽  
Phosphoinositide 3 Kinase ◽  
Stimulation Of

The ErbB4 receptor tyrosine kinase possesses both tumour suppressor and oncogenic activities. Thus pharmacological agents are needed to help elucidate ErbB4 functions. However, limitations of existing ErbB4 agonists and antagonists have led us to seek novel ErbB4 antagonists. The Q43L mutant of the ErbB4 agonist NRG2β (neuregulin 2β) stimulates ErbB4 tyrosine phosphorylation, yet fails to stimulate ErbB4 coupling to cell proliferation. Thus in the present paper we hypothesize that NRG2β/Q43L may be an ErbB4 antagonist. NRG2β/Q43L competitively antagonizes agonist stimulation of ErbB4 coupling to cell proliferation. NRG2β/Q43L stimulates less ErbB4 tyrosine phosphorylation than does NRG2β. In addition, NRG2β stimulation of cell proliferation requires PI3K (phosphoinositide 3-kinase) activity and NRG2β stimulates greater Akt phosphorylation than does NRG2β/Q43L. Moreover, EGFR [EGF (epidermal growth factor) receptor] kinase activity (but not that of ErbB4) is critical for coupling ErbB4 to proliferation. Experiments utilizing ErbB4 splicing isoforms and mutants suggest that NRG2β and NRG2β/Q43L may differentially stimulate ErbB4 coupling to the transcriptional co-regulator YAP (Yes-associated protein). Finally, NRG2β/Q43L competitively antagonizes agonist stimulation of EGFR and ErbB2/ErbB3, indicating that NRG2β/Q43L is a pan-ErbB antagonist. Thus we postulate that NRG2β/Q43L and other antagonistic ligands stimulate ErbB tyrosine phosphorylation on a set of residues distinct from that stimulated by agonists, thus suggesting a novel mechanism of ErbB receptor regulation. Moreover, NRG2β/Q43L and related ligand-based antagonists establish a paradigm for the discovery of anti-ErbB therapeutics.

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