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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A decrease in amplitude and conduction speed in the compound action potential is observed with time in gar olfactory and rabbit vagus nerve when it is stimulated between 4 and 15 Hz at 26 degrees C in vitro. The amplitude decays exponentially for 1-3 min before reaching a steady state. Recs 15 s for gar olfactory nerve and 50 s for rabbit vagus nerve. The steady state values are 14% and 36% of the original amplitude, respectively, and conduction speeds are reduced by 25 % in both nerves. The effect results from completion between ion flow during the action potential and active transport. The accumulation of K+ions and depletion of Na+ ions in the restricted extracellular space contributes to the amplitude fatigue while the depletion of Na+ ions alone causes the decrease in conduction speed. Ouabain increases the fatigue rate in both preparations, but more so for gar. The fatigue and recovery measurements may provide a useful method to investigate active pumping, including both the total pumping rate and the electrogenic component.
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PMID:Action potential fatigue in nonmyelinated nerve fibers: garfish olfactory and rabbit vagus nerve. 97 77

The effect of hemodialysis (HD) on olfactory recognition and memory function was investigated in people receiving chronic HD treatment. Fifteen subjects were given an olfactory recognition task 0.5 h before and 0.5 h after a dialysis session in counterbalanced order. Ten dialysis patients received a verbal recall task twice. Ten age-matched normal subjects received the olfactory task twice. Results were: (1) olfactory scores in the HD group were significantly lower than control subjects scores; (2) within the dialysis sample, olfactory identification scores were significantly lower after treatment than before, and (3) there were no parallel decreases in memory performance of the dialysis group after a HD treatment. We therefore conclude that those subjects receiving HD treatment demonstrate acute and chronic deficits in olfactory recognition which are unlikely to be due to fatigue, cognitive disequilibrium, anticoagulant treatment or high levels of uremic toxins.
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PMID:Olfaction and hemodialysis: baseline and acute treatment decrements. 369 14

Sick-building syndrome is an illness characterized by fatigue, headache, and upper-respiratory complaints. It is usually associated with modern office buildings, structures with an impervious outer shell and inoperable windows. Poor air quality, specific pollutants, and inadequate ventilation are considered common causes. The ability to smell faint odors requires air that is free of contamination. Human evolutionary ancestors depended on odors for survival. Even the slightest increase in the ability to smell a predator conveyed a distinct, immediate survival advantage. Conversely, an enormous survival advantage would also accrue to the animal that sought protection or avoided activity when this vital olfactory information was unavailable. Such would be the case with fire on the savannah. The foraging, olfactory dependent animal, unable to smell predators because of contaminated air, would be quickly snatched by a keen-sighted carnivore. There exist, however, well-described reflexes from the nose mediated through the trigeminal nerve that discourage activity when these free nerve endings are irritated. This mechanism may serve as a defense against predation. In adulterated atmosphere the animal, subdued by these reflexes, would be less likely to venture forth and, therefore, less vulnerable to predators. Similar reflexes may persist in humans, activated by poor air quality, air ill-suited for the dissemination of odors. I suggest that the human perception of these inhibitory reflexes is the feeling of fatigue associated with the sick building syndrome.
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PMID:Sick-building syndrome fatigue as a possible predation defense. 779 87

An encounter between rats results in bouts of social investigation consisting mainly of sniffing, nosing, following and grooming. The assessment of social recognition is based on the tendency of rodents to investigate unfamiliar conspecifics more intensely, than familiar ones. In the laboratory an immature conspecific is normally used as the social stimulus because the use of juveniles eliminates possible sexual and/or aggressive behaviors of the rat whose memory is assessed. When a juvenile is presented for the first time, it is intensely investigated. A second presentation shortly after the first one elicits less attention. This is not due to satiation or fatigue, since the presentation of a novel juvenile triggers the full sequence of investigation. Social recognition is defined as a specific decrease in social investigation during the second encounter of the same individual. This form of memory is short lasting (< 40 min) and based on the olfactory characteristics of the stimulus animal. Social memory is prolonged by repeated exposure to the stimulus juvenile rat and is impaired by retroactively interfering stimuli. It can be facilitated by vasopressin and derivatives as well as by several other memory facilitating compounds, and, depending on the dose, attenuated or facilitated by oxytocin and derivatives. Ethologically oriented memory tests, that are based on olfactory characteristics of the information to-be-remembered, have an advantage over 'classical' ones: they estimate behavioral patterns which are important to an animal and not only to the investigator. Social memory paradigms can reveal information about memory processes in animals that is relevant for memory deficits in humans.
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PMID:Neurohypophyseal peptides and social recognition in rats. 1007 4

Five experiments examined recognition memory for sequentially presented odors. Participants were presented with a sequence of odors and then had to identify an odor from the list in a test probe containing 2 odors. All experiments demonstrated enhanced recognition of odors presented at the start and end of a series, compared with those presented in the middle of the series when a 3-s retention interval between list termination and test was used. In Experiments 2 and 3, when a 30-s or 60-s retention interval was used, participants performed at slightly lower levels, although the serial position function was similar to that obtained with the 3-s retention interval. These results were noted with a 5-item (Experiments 1 and 4), 7-item (Experiment 2), 6-item (Experiment 3), and 4-item (Experiment 5) list of odors. As the number of test trials increased, recognition performance decreased, indicating a strong role for olfactory fatigue or interference in these procedures. A verbal suppression task, used in Experiments 4 and 5, had little influence on serial-position-based performance.
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PMID:Serial position effects in recognition memory for odors. 1076 3

Continuous presentation of an olfactory stimulus causes a decrement of the chemotaxis response in the nematode Caenorhabditis elegans. However, the differences between the learning process of habituation (a readily reversible decrease in behavioral response) and other types of olfactory plasticity such as adaptation (a decrement in response due to sensory fatigue, which cannot be dishabituated) have not been addressed. The volatile odorant diacetyl (DA) was used within a single paradigm to assess the distinct processes of olfactory adaptation and habituation. Preexposing and testing worms to 100% DA vapors caused a chemotaxis decrement that was not reversible despite the presentation of potentially dishabituating stimuli. This DA adaptation was abolished in worms with an odr-10 mutation (encoding a high-affinity DA receptor on the AWA neuron), even though naive chemotaxis remained unaffected. Conversely, DA adaptation remained intact in odr-1 mutants (defective in AWC neuron-mediated olfactory behavior), even though naive chemotaxis to DA decreased. Surprisingly, exposure to vapors of intermediate concentrations of DA (0.01% and 25%) did not cause worms to exhibit any response decrement. In contrast to preexposure to high DA concentrations, preexposure to low DA concentrations (0.001%) produced habituation of the chemotaxis response (a dishabituating stimulus could reverse the response decrement back to baseline levels). The distinct behavioral effects produced by DA preexposure highlight a concentration-dependent dissociation between two decremental olfactory processes: adaptation at high DA concentrations versus habituation at low DA concentrations.
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PMID:A behavioral and genetic dissection of two forms of olfactory plasticity in Caenorhabditis elegans: adaptation and habituation. 1094 Mar 20

The effects of opioids on human subjective olfactory function have rarely been investigated. This is despite the fact that opioid receptors are widely distributed throughout the olfactory systems. Using an established validated test of subjective olfactory function, olfactory threshold, odor discrimination and odor identification performance were tested in 16 healthy volunteers before opioid administration and at steady state after 3 hours remifentanil infusion. Each one man and one women were assigned randomly to one out of eight predefined remifentanil target plasma concentrations: 0, 1.2, 1.8, 2.4, 3, 3.6, 4.8, and 6 ng/ml. In the thirteen subjects that had completed the tests, olfactory thresholds were elevated with increasing remifentanil dose, and this correlated statistically significant with the remifentanil dose. Remifentanil plasma concentrations were linearly related to changes in olfactory thresholds. In contrast, effects of remifentanil on odor discrimination and identification were not statistically significant. However, remifentanil target plasma concentrations were also significantly correlated with the subjects' ratings of tiredness and drowsiness, although only drowsiness was significantly correlated with the differences in odor thresholds. We conclude that opioid administration leads to impaired olfactory function expressed in raised olfactory thresholds. This is compatible with previously reported opioidergic effects at the level of the olfactory bulb.
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PMID:Effects of the opioid remifentanil on olfactory function in healthy volunteers. 1166 70

The equivalent mixture of cis-3-hexenol and trans-2-hexenal (hexenol/hexenal), 'green odor', is known to have a healing effect on the psychological damage caused by stress. Behavioral studies in humans and monkeys have revealed that hexenol/hexenal prevents the prolongation of reaction time caused by fatigue. In the present study, we investigated which brain regions are activated by the odor of hexenol/hexenal using positron emission tomography with alert monkeys. Regional cerebral blood flow (rCBF) in the prepyriform area (the primary olfactory cortex) was commonly increased by the passive application of odor: acetic acid, isoamylacetate or hexenol/hexenal. We observed rCBF increases in the orbitofrontal cortex (the secondary olfactory cortex) by these olfactory stimuli in two of three monkeys, and found no predominance of laterality of the activated hemisphere. Furthermore, rCBF increase in the cerebellum was observed in two of three monkeys, and the odor of acetic acid increased rCBF in the substantia innominata in all monkeys. In addition to these olfactory related regions, the anterior cingulate gyrus was activated by the odor of hexenol/hexenal. These findings suggest that the increase of rCBF in the anterior cingulate gyrus by the odor of hexenol/hexenal may contribute the healing effects of this mixture observed in the monkey.
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PMID:Activation of the anterior cingulate gyrus by 'Green Odor': a positron emission tomography study in the monkey. 1457 18

Olfactory loss can occur through accidental exposure, poor industrial hygiene, or exposure to low levels of toxins in the ambient air over long periods. This loss can lead to transient olfactory disorders, irreversible anosmia, temporary olfactory fatigue, or industrial anosmia. Inevitably, a practicing otolaryngologist will encounter a patient with complaints of decreased smell and taste that initially may be difficult to diagnose and treat. Much of the challenge in evaluating a patient with disturbances of olfaction is in obtaining adequate quantitative measurements of sensory dysfunction and identifying a source for the olfactory loss. Although there is no particular test for environmental toxins as a source of olfactory loss, an accurate cause can be determined by obtaining a careful, detailed history. A significant exposure history and lack of more common causes of olfactory loss strengthens an argument for environmental toxins as an etiology. Unfortunately, no available treatments can reverse permanent damage caused by toxic exposure, but removal from the source of toxins may allow for repair of the olfactory system and return of normal function, especially in acute exposures. Despite the increasing number of studies investigating toxic exposure on olfactory function, these effects are understood poorly. With continued study of human exposure to these substances and the use of animal models, the mechanisms by which damage occurs will be understood better and new approaches for diagnosis and treatment will be developed. Furthermore, with increasing regulations of occupational environments and stricter policies on industrial air pollution, olfactory dysfunction secondary to toxicity should become less prevalent.
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PMID:Olfactory loss as a result of toxic exposure. 1556 10

The purpose of this study was to establish if early chronic oral breathing could induce an ultra-structural adaptation of the diaphragm and orofacial muscles related to oral or nasal breathing. Therefore, we performed a bilateral nasal obstruction at day 8 on rat pups and the myosin heavy chain (MHC) composition of the muscles was analyzed at day 21. Nasal obstruction and the related switch to chronic oral breathing were associated with impaired growth, atrophy of olfactory bulbs, hypertrophy of adrenal glands and reduced muscle growth for all muscles studied except the diaphragm. Furthermore, we detected a smaller decrease of MHC 2b compared to MHC 2a and 2x in levator nasolabialis, a muscle involved with nasal breathing. In masseter superficialis and anterior digastric involved with oral breathing, we observed a smaller decrease of MHC 2a compared to MHC 2b or 2x, respectively. No difference was detected in the diaphragm MHC expression of oral breathing animals. Since the relative expression of fatigue resistant MHC fiber types increased in muscles involved with oral breathing, orofacial muscles seem to present a profile in MHC adapted to the transition from nasal to oral breathing, facilitating respiration.
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PMID:Myosin heavy chain expression and muscle adaptation to chronic oral breathing in rat. 1646 73


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