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Receptor Sensitivity (receptor + sensitivity)
Selected AbstractsTrying to See Red Through Stickleback Photoreceptors: Functional Substitution of Receptor SensitivitiesETHOLOGY, Issue 3 2006Mickey P. Rowe A key to understanding animal behavior is knowledge of the sensory information animals extract from their environment. For visually motivated tasks, the information animals obtain through their eyes is often assumed to be essentially the same as that perceived by humans. However, known differences in structure and processing among the visual systems of different animals clearly indicate that the world seen by each is different. A well-characterized difference between human and other animal visual systems is the number of types and spectral sensitivities of their photoreceptors. We are developing a technique, functional substitution, that exploits knowledge of these differences to portray for human subjects, colors as they would appear through the photoreceptors of another animal. In a specific application, we ask human subjects to rank hues of male threespine stickleback (Gasterosteus aculeatus) throats viewed through stickleback photopigments. We compare these ranks to ranks of the same throat hues viewed through normal human photoreceptors. We find essentially no difference between the two sets of rankings. This suggests that any differences in human and stickleback rankings of such hues would result from differences in post-receptoral neural processing. Using a previously developed model of stickleback neural processing, we established another ranking of the hues which was again essentially the same as the rankings produced by the human subjects. A growing literature indicates that stickleback do rank such hues in the evaluation of males as potential mates or threats. Although our results do not demonstrate that humans and stickleback use the same mechanisms to assess color, our experiments significantly failed to show that stickleback and human rankings of throat hues should be different. Nevertheless, a comparison of all these rankings to ranks derived from subjective color scoring by human observers suggests that color scoring may utilize other cues and should thus be used cautiously. [source] Mood states, sympathetic activity, and in vivo ,-adrenergic receptor function in a normal populationDEPRESSION AND ANXIETY, Issue 7 2008Bum-Hee Yu M.D. Ph.D. Abstract The purpose of this study was to examine the relationship between mood states and ,-adrenergic receptor function in a normal population. We also examined if sympathetic nervous system activity is related to mood states or ,-adrenergic receptor function. Sixty-two participants aged 25,50 years were enrolled in this study. Mood states were assessed using the Profile of Mood States (POMS). ,-adrenergic receptor function was determined using the chronotropic 25 dose isoproterenol infusion test. Level of sympathetic nervous system activity was estimated from 24-hr urine norepinephrine excretion. Higher tension-anxiety, depression-dejection, and anger-hostility were related to decreased ,-adrenergic receptor sensitivity (i.e., higher chronotropic 25 dose values), but tension-anxiety was the only remaining independent predictor of ,-adrenergic receptor function after controlling for age, gender, ethnicity, and body mass index (BMI). Urinary norepinephrine excretion was unrelated to either mood states or ,-adrenergic receptor function. These findings replicate previous reports that anxiety is related to decreased (i.e., desensitized) ,-adrenergic receptor sensitivity, even after controlling for age, gender, ethnicity, and body mass index. Depression and Anxiety 0:1,6, 2007. © 2007 Wiley-Liss, Inc. [source] Experimental and Clinical Evidence for Loss of Effect (Tolerance) during Prolonged Treatment with Antiepileptic DrugsEPILEPSIA, Issue 8 2006Wolfgang Löscher Summary:, Development of tolerance (i.e., the reduction in response to a drug after repeated administration) is an adaptive response of the body to prolonged exposure to the drug, and tolerance to antiepileptic drugs (AEDs) is no exception. Tolerance develops to some drug effects much more rapidly than to others. The extent of tolerance depends on the drug and individual (genetic?) factors. Tolerance may lead to attenuation of side effects but also to loss of efficacy of AEDs and is reversible after discontinuation of drug treatment. Different experimental approaches are used to study tolerance in laboratory animals. Development of tolerance depends on the experimental model, drug, drug dosage, and duration of treatment, so that a battery of experimental protocols is needed to evaluate fully whether tolerance to effect occurs. Two major types of tolerance are known. Pharmacokinetic (metabolic) tolerance, due to induction of AED-metabolizing enzymes has been shown for most first-generation AEDs, and is easy to overcome by increasing dosage. Pharmacodynamic (functional) tolerance is due to "adaptation" of AED targets (e.g., by loss of receptor sensitivity) and has been shown experimentally for all AEDs that lose activity during prolonged treatment. Functional tolerance may lead to complete loss of AED activity and cross-tolerance to other AEDs. Convincing experimental evidence indicates that almost all first-, second-, and third-generation AEDs lose their antiepileptic activity during prolonged treatment, although to a different extent. Because of diverse confounding factors, detecting tolerance in patients with epilepsy is more difficult but can be done with careful assessment of decline during long-term individual patient response. After excluding confounding factors, tolerance to antiepileptic effect for most modern and old AEDs can be shown in small subgroups of responders by assessing individual or group response. Development of tolerance to the antiepileptic activity of an AED may be an important reason for failure of drug treatment. Knowledge of tolerance to AED effects as a mechanism of drug resistance in previous responders is important for patients, physicians, and scientists. [source] Clonazepam as a therapeutic adjunct to improve the management of depression: a brief reviewHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2009*Article first published online: 27 MAR 200, Shigeru Morishita Abstract Clonazepam, first used for seizure disorders, is now increasingly used to treat affective disorders. We summarize the use of clonazepam to improve the management of depression. Clonazepam is useful for treatment-resistant and/or protracted depression, as well as for acceleration of response to conventional antidepressants. Clonazepam is at this time recommended for use in combination with SSRIs (fluoxetine, fluvoxamine, sertraline) as an antidepressant, and should be used at a dosage of 2.5,6.0,mg/day. If clonazepam is effective, a response should be observed within 2,4 weeks. It is significantly more effective for unipolar than for bipolar depression. Low-dose, long-term treatment with clonazepam exhibits a prophylactic effect against recurrence of depression. Although the mechanism of action of clonazepam has not yet been established, some investigators have been suggested that it involves enhancement of anti-anxiety effects, anticonvulsant effects on subclinical epilepsy, increase in 5-HT/monoamine synthesis or decrease in 5-HT receptor sensitivity mediated through the GABA system, and regulate in GABA activity. Copyright © 2009 John Wiley & Sons, Ltd. [source] | ||||||||||