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Physiological mechanisms of onset adaptation and contralateral suppression of DPOAEs in the rat.

An investigation was undertaken to measure medial olivocochlear (MOC) reflexes in anesthetized rats before and after sectioning of the middle-ear muscles. Distortion product otoacoustic emission (DPOAE) magnitude and phase temporal responses were measured ipsilaterally to study MOC-mediated "DPOAE onset adaptation" and in the presence of a contralateral noise to study MOC-mediated contralateral "suppression" (terms as used by previous researchers). Distortion product otoacoustic emission onset adaptation and contralateral suppression had predictable changes in direction of magnitude and phase that were dependent on the input-output function. After sectioning of the middle-ear muscles (MEMs), DPOAE onset adaptation and contralateral suppression were greatly reduced, and there were little, if any, changes in phase. These "residual" changes were interpreted as a result of the MOC reflex. The results suggest that what appears to be DPOAE onset adaptation and contralateral suppression can be mediated primarily by MEM reflexes. When studying MOC effects on otoacoustic emissions (OAEs) using acoustic stimulation, it is necessary to make recordings over a span of stimulus levels. In addition, looking at both magnitude and phase of the OAE may help separate what is due to the MOC reflex from MEM reflex.

Acoustic Stimulation↗

A new intrinsic thermal parameter for enzymes reveals true temperature optima.

Two established thermal properties of enzymes are the Arrhenius activation energy and thermal stability. Arising from anomalies found in the variation of enzyme activity with temperature, a comparison has been made of experimental data for the activity and stability properties of five different enzymes with theoretical models. The results provide evidence for a new and fundamental third thermal parameter of enzymes, T(eq), arising from a subsecond timescale-reversible temperature-dependent equilibrium between the active enzyme and an inactive (or less active) form. Thus, at temperatures above its optimum, the decrease in enzyme activity arising from the temperature-dependent shift in this equilibrium is up to two orders of magnitude greater than what occurs through thermal denaturation. This parameter has important implications for our understanding of the connection between catalytic activity and thermostability and of the effect of temperature on enzyme reactions within the cell. Unlike the Arrhenius activation energy, which is unaffected by the source ("evolved") temperature of the enzyme, and enzyme stability, which is not necessarily related to activity, T(eq) is central to the physiological adaptation of an enzyme to its environmental temperature and links the molecular, physiological, and environmental aspects of the adaptation of life to temperature in a way that has not been described previously. We may therefore expect the effect of evolution on T(eq) with respect to enzyme temperature/activity effects to be more important than on thermal stability. T(eq) is also an important parameter to consider when engineering enzymes to modify their thermal properties by both rational design and by directed enzyme evolution.

Acid Phosphatase↗

THERMOREGULATORY AND ADAPTIVE BEHAVIOR OF BROWN ADIPOSE TISSUE.

Brown adipose tissue has been shown to be a strongly thermogenic effector organ in homeothermic animals exposed to cold and in hibernators during cold-induced arousal from deep hibernation. Because of the anatomical distribution of brown fat and the utilization of vascular countercurrent heat exchange, this cold-induced thermogenic response protects the animal by contributing heat to the vital organs of the thorax, the cervical and thoracic segments of the spinal cord, and the sympathetic chain. Evidence indicates that control of thermogenic activity of brown fat is mediated by the sympathetic nervous system.

Acclimatization↗