FMP study of pilot workload. Qualification of workload via instrument scan

Various methods of measuring a pilot's mental workload are discussed. Scanning the various flight instruments with good scan pattern and other verbal tasks during instrument landings is given special attention for measuring pilot workload

Visual scanning behavior and pilot workload

Sophisticated man machine interaction often requires the human operator to perform a stereotyped scan of various instruments in order to monitor and/or control a system. For situations in which this type of stereotyped behavior exists, such as certain phases of instrument flight, scan pattern was shown to be altered by the imposition of simultaneous verbal tasks. A study designed to examine the relationship between pilot visual scan of instruments and mental workload is described. It was found that a verbal loading task of varying difficulty causes pilots to stare at the primary instrument as the difficulty increases and to shed looks at instruments of less importance. The verbal loading task also affected the rank ordering of scanning sequences. By examining the behavior of pilots with widely varying skill levels, it was suggested that these effects occur most strongly at lower skill levels and are less apparent at high skill levels. A graphical interpretation of the hypothetical relationship between skill, workload, and performance is introduced and modelling results are presented to support this interpretation

Entropy, instrument scan and pilot workload

Correlation and information theory which analyze the relationships between mental loading and visual scanpath of aircraft pilots are described. The relationship between skill, performance, mental workload, and visual scanning behavior are investigated. The experimental method required pilots to maintain a general aviation flight simulator on a straight and level, constant sensitivity, Instrument Landing System (ILS) course with a low level of turbulence. An additional periodic verbal task whose difficulty increased with frequency was used to increment the subject's mental workload. The subject's looppoint on the instrument panel during each ten minute run was computed via a TV oculometer and stored. Several pilots ranging in skill from novices to test pilots took part in the experiment. Analysis of the periodicity of the subject's instrument scan was accomplished by means of correlation techniques. For skilled pilots, the autocorrelation of instrument/dwell times sequences showed the same periodicity as the verbal task. The ability to multiplex simultaneous tasks increases with skill. Thus autocorrelation provides a way of evaluating the operator's skill level

Elevations of intracellular calcium reflect normal voltage-dependent behavior, and not constitutive activity, of voltage-dependent calcium channels in gastrointestinal and vascular smooth muscle

In smooth muscle, the gating of dihydropyridine-sensitive Ca2+ channels may either be stochastic and voltage dependent or coordinated among channels and constitutively active. Each form of gating has been proposed to be largely responsible for Ca2+ influx and determining the bulk average cytoplasmic Ca2+ concentration. Here, the contribution of voltage-dependent and constitutively active channel behavior to Ca2+ signaling has been studied in voltage-clamped single vascular and gastrointestinal smooth muscle cells using wide-field epifluorescence with near simultaneous total internal reflection fluorescence microscopy. Depolarization (−70 to +10 mV) activated a dihydropyridine-sensitive voltage-dependent Ca2+ current (ICa) and evoked a rise in [Ca2+] in each of the subplasma membrane space and bulk cytoplasm. In various regions of the bulk cytoplasm the [Ca2+] increase ([Ca2+]c) was approximately uniform, whereas that of the subplasma membrane space ([Ca2+]PM) had a wide range of amplitudes and time courses. The variations that occurred in the subplasma membrane space presumably reflected an uneven distribution of active Ca2+ channels (clusters) across the sarcolemma, and their activation appeared consistent with normal voltage-dependent behavior. Indeed, in the present study, dihydropyridine-sensitive Ca2+ channels were not normally constitutively active. The repetitive localized [Ca2+]PM rises (“persistent Ca2+ sparklets”) that characterize constitutively active channels were observed rarely (2 of 306 cells). Neither did dihydropyridine-sensitive constitutively active Ca2+ channels regulate the bulk average [Ca2+]c. A dihydropyridine blocker of Ca2+ channels, nimodipine, which blocked ICa and accompanying [Ca2+]c rise, reduced neither the resting bulk average [Ca2+]c (at −70 mV) nor the rise in [Ca2+]c, which accompanied an increased electrochemical driving force on the ion by hyperpolarization (−130 mV). Activation of protein kinase C with indolactam-V did not induce constitutive channel activity. Thus, although voltage-dependent Ca2+ channels appear clustered in certain regions of the plasma membrane, constitutive activity is unlikely to play a major role in [Ca2+]c regulation. The stochastic, voltage-dependent activity of the channel provides the major mechanism to generate rises in [Ca2+]

Optical Control of Metabotropic Glutamate Receptors

G-protein coupled receptors (GPCRs), the largest family of membrane signaling proteins, respond to neurotransmitters, hormones and small environmental molecules. The neuronal function of many GPCRs has been difficult to resolve because of an inability to gate them with subtype-specificity, spatial precision, speed and reversibility. To address this, we developed an approach for opto-chemical engineering native GPCRs. We applied this to the metabotropic glutamate receptors (mGluRs) to generate light-agonized and light-antagonized “LimGluRs”. The light-agonized “LimGluR2”, on which we focused, is fast, bistable, and supports multiple rounds of on/off switching. Light gates two of the primary neuronal functions of mGluR2: suppression of excitability and inhibition of neurotransmitter release. The light-antagonized “LimGluR2block” can be used to manipulate negative feedback of synaptically released glutamate on transmitter release. We generalize the optical control to two additional family members: mGluR3 and 6. The system works in rodent brain slice and in zebrafish in vivo, where we find that mGluR2 modulates the threshold for escape behavior. These light-gated mGluRs pave the way for determining the roles of mGluRs in synaptic plasticity, memory and disease