scholarly journals Effector system-specific sequential modulations of congruency effects

2017 ◽  
Vol 25 (3) ◽  
pp. 1066-1072 ◽  
Author(s):  
Markus Janczyk ◽  
Hartmut Leuthold
Keyword(s):  
1991 ◽  
Vol 33 (3) ◽  
pp. 287-297 ◽  
Author(s):  
María J. Carmena ◽  
Consolación Hueso ◽  
Luis G. Guijarro ◽  
Juan C. Prieto

1963 ◽  
Vol 16 (2) ◽  
pp. 323-359 ◽  
Author(s):  
David S. Smith

The organization of the luminescent organ of an adult firefly has been studied with the electron microscope, and particular attention has been given to the disposition of nerve terminals within the organ. The cytological structure of the cells of the tracheal system, the peripheral and terminal axons, the photocytes and the cells of the dorsal ("reflecting") layer is described. Previous observations on the peripheral course of nerve branches alongside the tracheal trunks at the level of the dorsal layer and photocyte epithelium have been confirmed, and specialised nerve endings containing axoplasmic components structurally identical with "synaptic vesicles" and "neurosecretory droplets" have been identified, not in association with the surface of the photocytes, but lying between the apposed surfaces of two components of the tracheal epithelium: the tracheal end-cell and the tracheolar cell. These cytological findings are discussed in terms of available biochemical and physiological evidence concerning the mechanism of light emission in the firefly, especially with respect to the possible role of chemical "transmitter" action in triggering a response in a luminescent effector system.


1984 ◽  
Vol 58 (2) ◽  
pp. 619-624 ◽  
Author(s):  
Robert M. Kohl ◽  
Daniel L. Roenker ◽  
Paul E. Turner

Payne and others, within a Hullian framework, have analytically defined reactive inhibition in terms of a negative drive occurring within the effector system. In strong support, they have demonstrated that the maintenance of work decrement is dependent upon limb, but not task, specificity. However, equally creditable research by Adams allows interpretations of inhibition based on the processing of information. These contrasting arguments are evaluated, and an initial model integrating the two is proposed.


2010 ◽  
Vol 298 (3) ◽  
pp. F502-F509 ◽  
Author(s):  
K. Mutig ◽  
T. Saritas ◽  
S. Uchida ◽  
T. Kahl ◽  
T. Borowski ◽  
...  

Vasopressin influences salt and water transport in renal epithelia. This is coordinated by the combined action of V2 receptor-mediated effects along distinct nephron segments. Modulation of NaCl reabsorption by vasopressin has been established in the loop of Henle, but its role in the distal convoluted tubule (DCT), an effective site for fine regulation of urinary electrolyte composition and the target for thiazide diuretics, is largely unknown. The Na+-Cl− cotransporter (NCC) of DCT is activated by luminal trafficking and phosphorylation at conserved NH2-terminal residues. Here, we demonstrate the effects of short-term vasopressin administration (30 min) on NCC activation in Brattleboro rats with central diabetes insipidus (DI) using the V2 receptor agonist desmopressin (dDAVP). The fraction of NCC abundance in the luminal plasma membrane was significantly increased upon dDAVP as shown by confocal microscopy, immunogold cytochemistry, and Western blot, suggesting increased apical trafficking of the transporter. Changes were paralleled by augmented phosphorylation of NCC as detected by antibodies against phospho-threonine and phospho-serine residues (2.5-fold increase at Thr53 and 1.4-fold increase at Ser71). dDAVP-induced phosphorylation of NCC, studied in tubular suspensions in the absence of systemic effects, was enhanced as well (1.7-fold increase at Ser71), which points to the direct mode of action of vasopressin in DCT. Changes were more pronounced in early (DCT1) than in late DCT as distinguished by the distribution of 11β-hydroxysteroid dehydrogenase 2 in DCT2. These results suggest that the vasopressin-V2 receptor-NCC signaling cascade is a novel effector system to adjust transepithelial NaCl reabsorption in DCT.


1995 ◽  
Vol 145 (2) ◽  
pp. 227-234 ◽  
Author(s):  
G Muñoz-Acedo ◽  
I Alvaro-Alonso ◽  
E Arilla

Abstract To date, it is unknown whether intrapancreatic serotonergic nerves can influence pancreatic somatostatin (SS) content and the SS receptor/effector system in the exocrine pancreas. In this study, the intrapancreatic serotonergic nerves were chemically ablated by injecting a specific serotonin (5-HT) neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into the substance of the gland. Three days after the injection, the 5-HT-like immunoreactive levels in the pancreas were reduced by more than 85% whereas somatostatin-like immunoreactive levels had increased (86%). The number of SS receptors in the pancreatic acinar cell membranes of the 5,7-DHT-treated rats was also increased (72%). No significant differences were seen in basal or forskolin-stimulated adenylate cyclase (AC) enzyme activities in the control and the 5,7-DHT-treated groups. In spite of the increase in the number of SS receptors in the pancreatic acinar cell membranes of 5,7-DHT-treated rats, SS caused a significantly lower inhibition of AC activity in these membranes. This finding is related to the observed decrease of a 41 kD pertussis toxin-sensitive substrate, presumably the αi subunit of the guanine nucleotide inhibitory protein, in pancreatic acinar cell membranes 3 days after intrapancreatic 5,7-DHT administration when compared with the corresponding controls. The functions of pancreatic serotonergic nerves seem to be associated with enteropancreatic communication. These data together with the present results suggest that pancreatic SS content and the SS receptor/effector system in the exocrine pancreas may be regulated by enteropancreatic serotonergic nerve fibers and may participate in enteropancreatic reflexes. Journal of Endocrinology (1995) 145, 227–234


2007 ◽  
Vol 98 (5) ◽  
pp. 2887-2902 ◽  
Author(s):  
Timothy J. Fort ◽  
Vladimir Brezina ◽  
Mark W. Miller

We are studying the functional “logic” of neuromodulatory actions in a simple central pattern generator (CPG)-effector system, the heart of the blue crab Callinectes sapidus. The rhythmic contractions of this heart are neurogenic, driven by rhythmic motor patterns generated by the cardiac ganglion (CG). Here we used anatomical and physiological methods to examine the sources and actions on the system of the FMRFamide-like peptides (FLPs) TNRNFLRFamide (F1), SDRNFLRFamide (F2), and GYNRSFLRFamide, an authentic Callinectes FLP. Immunohistochemical localization revealed a plexus of FLP-immunoreactive fibers in the pericardial organs (POs), from which modulators are released to reach the heart as circulating neurohormones. Combined backfill and immunohistochemical experiments indicated that the FLPs in the POs originated in the CNS, from large neurosecretory cells in the B cluster of the first thoracic neuromere. In physiological experiments, we examined the actions of the FLPs on the intact working heart, on the semi-intact heart in which we could record the motor patterns as well as the muscle contractions, on the isolated CG, and in a preparation developed to assess direct actions on the muscle with controlled patterns of motor neuron spikes. The FLPs had strong positive chronotropic and inotropic effects. Dissection of these effects suggested that they were produced through at least two primary actions of the FLPs exerted both on the heart muscle and on the CG. These primary actions elicited numerous secondary consequences mediated by the feedforward and feedback interactions that integrate the activity of the complete, coupled CPG-effector system.


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