Stimuli release

Diuretics This indicates the unique property of capsaicin-sensitive primary afferent neurons to release mediators (neuropeptides and others) from both peripheral and central nervous system terminals upon adequate stimulation. Capsaicin and other chemical (protons) or physical (heat) stimuli release mediators from both peripheral and... 

Hudson, R. (1985) Do newborn rabbits learn the odor stimuli releasing nipple-search behavior Dev. Psychobiol. 18, 575-585. 

Appleton, R.D. and Palmer, A.R., Water-borne stimuli released by predatory crabs and damaged prey induce more predator-resistant shells in amarine gastropod, Proc. Nat. Acad. Sci. USA, 85,4387, 1988. 

Recently, we have completed a series of studies comparing the effect of Pavlovian stimuli conditioned to morphine and food on DA relase in the NAc shell, NAc core and PFCX (Bassareo et al., in preparation). A more detailed account of these studies will be given in the Section Drug-induced stimulation of DA transmission and abnormal Pavlovian incentive learning. Here it will suffice to say that while drug-conditioned stimuli elicit a sustained release of DA in the NAc shell but not in the NAc core, food-conditioned stimuli release DA in the NAc core but not in the shell (Figs. 6-8). 

DA plays a fundamental role in behavior motivated by rewards and reward-related stimuli. Release of DA in the NAc shell by Pavlovian stimuli induces an appetitive state of incentive arousal (state-hedonia, euphoria) that facilitates the rate of current instrumental... 

Q8 Dehydration reduces ECF volume, venous return, cardiac output and BP, leading to both a reflex vasoconstrictor response and to the stimulation of the renin-angiotensin system. Angiotensin stimulates the release of aldosterone from the adrenal cortex, which causes salt and water retention in the distal tubule and collecting ducts of the nephron. The same stimuli release ADH... 

The inflammatory response is initiated by stimuli released from sites of tissue injury that results in the expression of selectins on the endothelial layer. These selectins (E(endothelial)-selectin and P(platelet)-selectin) function through recognition of oligosaccharides on the opposing leukocyte cell surface [194]. This interaction eventually weakly tethers the leukocyte to the endothelial layer, at which point integrin binding events lead to firm adhesion and extravasation of the leukocyte into the tissue. In certain disease processes, excessive leukoc)4e infiltration becomes deleterious to the body, and inhibitors of this process are desirable. Rheumatoid arthritis, asthma, organ transplant rejection, and reperfusion injury are just a few of the cases in which these events occur [27]. 

Free, J.B. (1961). The stimuli releasing the stinging response of honeybees. Anim. Behav. 9,193-196. 

In conclusion, stress or other stimuli release CRF from the hypothalamus. CRF probably binds to receptors in special hypophyseal cells and causes the release of ACTH which binds to the membrane of the cells of the inner portion of the adrenal stimulating adenyl cyclase activity and raising the intracellular concentrations of cyclic AMP with resultant corticosteroi-dogenesis. 

Pardosa milvina E Contact stimulus releases change in behavior in males Kaston, 1936... 

So now we know that both sensation and movement mechanisms evince the same external dampening and internal stimulus release in both states. We therefore can t help wondering if the same kinds of neural processes underlie these strikingly parallel and reciprocal phenomena. 

As has been indicated earlier the function of the azide in an explosive train is to respond to an external mechanical, thermal, or electrical stimulus release more energy and transfer this with sufficient power and intensity to initiate the next element in the train. Each of the functions must be performed within a limited geometry (fractions of an inch), with minimal input energies, and with the maximum of assurance that the sequence will function upon demand but will remain quiescent until then. 

They antagonize the positive inotropic and chronotropic effects of catecholamines. Cardiac arrhythmias associated with excessive adrenergic stimulus, released endogenous catecholamines or sensitization of the heart by anes-thetics or cardiac glycosides may effectively be treated by 6-blockade. Some B-blockers also possess membrane or local anesthetic action and are effective against arrhythmias due to ischemia or cardiac glycoside toxicity as well. This membrane action was shown to be independent of 6-blockade since resolved isomers of B-blockers possessed equal antiarrhythmic potency but unequal B-blocking action. 

An alternative approach to stimulate cholinergic function is to enhance the release of acetylcholine (ACh). Compounds such as the aminopyridines increase the release of neurotransmitters (148). The mechanism by which these compounds modulate the release of acetylcholine is likely the blockade of potassium channels. However, these agents increase both basal (release in the absence of a stimulus) and stimulus-evoked release (148). 4-Aminopyridine [504-24-5] was evaluated in a pilot study for its effects in AD and found to be mildly effective (149). 

Kidney Function. Prostanoids influence a variety of kidney functions including renal blood flow, secretion of renin, glomerular filtration rate, and salt and water excretion. They do not have a critical role in modulating normal kidney function but play an important role when the kidney is under stress. Eor example, PGE2 and -I2 are renal vasodilators (70,71) and both are released as a result of various vasoconstrictor stimuli. They thus counterbalance the vasoconstrictor effects of the stimulus and prevent renal ischemia. The renal side effects of NSAIDS are primarily observed when normal kidney function is compromised. 

Finally, receptor stimulus can be measured through membrane assays directly monitoring G-protein activation (group IV assays). In these assays, radiolabeled GTP (in a stable form for example, GTPj/S) is present in the medium. As receptor activation takes place, the GDP previously bound to the inactive state of the G-protein is released and the radiolabeled GTP/S binds to the G-protein. This is quantified to yield a measure of the rate of GDP /GTP j/S exchange and hence receptor stimulus. 

Autacoids are literally self-medicating agents that are liberated from or produced by cells in response to a stimulus. They differ from hormones in that they usually act locally after release, rather than reaching their target organ via the bloodstream. 

IP3 Receptors. Figure 1 Interplay between Ca2+ channels. Ca2+ signals are initiated when an extracellular stimulus (red) directly opens a Ca2+ channel in the plasma membrane or indirectly, via a signalling pathway (green), opens an intracellular Ca2+ channel. Ca2+ signals may then be propagated across the cell by Ca2+-induced Ca2+ release mediated by IP3R or RyR. 

Possible mechanisms responsible for the decreased Ca release are changes in the sensitivity of the voltage sensor in the T-tubular system or in the SR Ca channel to the sensor stimulus. A third possibility would be a decreased availability... 

Hundt W, Holter SM, Spanagel R Discriminative stimulus effects of glutamate release inhibitors in rats trained to discriminate ethanol. Pharmacol Biochem Behav 59 691-695, 1998... 

In 2000, the first example of ELP diblock copolymers for reversible stimulus-responsive self-assembly of nanoparticles was reported and their potential use in controlled delivery and release was suggested [87]. Later, these type of diblock copolypeptides were also covalently crossUnked through disulfide bond formation after self-assembly into micellar nanoparticles. In addition, the encapsulation of l-anilinonaphthalene-8-sulfonic acid, a hydrophobic fluorescent dye that fluoresces in hydrophobic enviromnent, was used to investigate the capacity of the micelle for hydrophobic drugs [88]. Fujita et al. replaced the hydrophilic ELP block by a polyaspartic acid chain (D ). They created a set of block copolymers with varying... 

Fig. 1.—Diagrammatic Representation of the Three Steps in the Taste-cell Transduction. Step 1, interaction of stimulus (S) with membrane-bound receptor (R) to form stimulus-receptor complex (SR) step 2, conformational change (SR) to (SR), brought about by interaction of S with R (this change initiates a change in plasma-membrane conformation of taste cells, probably below the level of the tight junction) and step 3, conformational changes of the membrane result in lowered membrane resistance, and the consequential influx on intracellular ionic species, probably Na. This influx generates the receptor potential which induces synaptic vesicular release to the innervating, sensory nerve, leading to the generator potential.

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