Pilot Perceptions of Wire Strikes in Agricultural Aviation Operations.

INTRODUCTION: Agricultural aircraft operations are associated with unique challenges. In particular, these include maintaining awareness of obstacles associated with flight at very low altitudes. Wire strikes are a common cause of accidents in these operations.METHODS: Focus groups were completed during the 2022 Ag Aviation Expo hosted by the National Agricultural Aviation Association with pilots who had experienced wire-strike events (N = 22). The researchers coded the transcripts using a human factors framework.RESULTS: Notably, unplanned "trim passes" were a key stage of flight during wire-strike events. Cognitive risk factors that may have affected their performance included situation awareness, decision-making choices, and pressure to perform. Over half of subjects reported being aware of the wire before collision. Possible prevention strategies include not spraying the field due to safety risks, paying better attention to where they were in the field, and avoiding deviation from the planned route.DISCUSSION: Wire-strike events often occur due to momentary lapses in attention, even when the pilot is already aware of the wire. This study shows that targeted approaches to prevent wire strikes in agricultural aviation operations require addressing a number of cognitive risks and human factors, rather than implementing increased preflight surveillance. These results have implications for preventing future wire-strike accidents based directly on pilot perceptions, both within agricultural operations and general aviation more broadly.Baumgartner HM, DiDomenica R, Hu PT, Thomas S. Pilot perceptions of wire strikes in agricultural aviation operations. Aerosp Med Hum Perform. 2024; 95(6):305-312.

Wire Strikes and In-Air Obstacle Collisions During Agricultural Aviation Operations.

INTRODUCTION: Wire strikes and in-air collisions with obstacles are a leading cause of accidents in the aerial application industry. While some of these collisions occur due to unseen obstacles, some pilots report being previously aware of the obstacles that they collide with. Whether or not pilots are aware of obstacles pre-collision is an important factor to inform methods of accident prevention.METHODS: Final reports from the National Transportation Safety Board were analyzed for Part 137 Agricultural Operation accidents that took place between January 2020 and December 2022. A deeper analysis of cases that involved an in-air collision with an obstacle was performed, excluding cases that were attributable to an external cause (e.g., aerodynamic stall). The pilot's awareness of the obstacle pre-accident was inferred from accident narratives if available.RESULTS: Nearly half of all accidents (N = 45 of 107) involved an in-air collision with an obstacle (e.g., wire, tree, pole) as the defining event. In cases where pilot awareness of the obstacle was determinable through the accident report, over half of pilots (N = 21 of 39) had previously seen this obstacle yet still made contact with it.DISCUSSION: In-air obstacle collisions make up a substantial portion of accidents within Part 137 Agricultural Operations. Nearly half of pilots were already aware of the obstacle before collision, indicating that inadequate preparation in scoping the field is not a predominant driver of these events. Instead, these findings suggest that other factors including distractions, high task difficulty, and errors in decision-making may contribute.Baumgartner HM. Wire strikes and in-air obstacle collisions during agricultural aviation operations. Aerosp Med Hum Perform. 2023; 94(11):852-856.

Corticotropin releasing factor (CRF) systems: Promoting cocaine pursuit without distress via incentive motivation.

Corticotropin releasing factor (CRF) systems in limbic structures are posited to mediate stress-induced relapse in addiction, traditionally by generating distress states that spur drug consumption as attempts at hedonic self-medication. Yet evidence suggests that activating CRF-expressing neurons in the central amygdala (CeA) or nucleus accumbens (NAc) can magnify incentive motivation in absence of distress, at least for sucrose rewards. However, traditional CRF hypotheses in addiction neuroscience are primarily directed toward drug rewards. The question remains open whether CRF systems can similarly act via incentive motivation mechanisms to promote pursuit of drug rewards, such as cocaine. Here we tested whether optogenetic excitation of CRF-containing neurons in either NAc medial shell, lateral CeA, or dorsolateral BNST of transgenic Crh-Cre+ rats would spur preference and pursuit of a particular laser-paired cocaine reward over an alternative cocaine reward, and whether excitation served as a positively-valenced incentive itself, through laser self-stimulation tests. We report that excitation of CRF-containing neurons in either NAc or CeA recruited mesocorticolimbic circuitry to amplify incentive motivation to pursue the laser-paired cocaine: focusing preference on the laser-paired cocaine reward in a two-choice task, and spurred pursuit as doubled breakpoint in a progressive ratio task. Crucially indicating positive-valence, excitation of CRF neurons in NAc and CeA also was actively sought after by most rats in self-stimulation tasks. Conversely, CRF neuronal activation in BNST was never self-stimulated, but failed to enhance cocaine consumption. Collectively, we find that NAc and CeA CRF-containing neurons can amplify pursuit and consumption of cocaine by positively-valenced incentive mechanisms, without any aversive distress.

Activating Corticotropin-Releasing Factor Systems in the Nucleus Accumbens, Amygdala, and Bed Nucleus of Stria Terminalis: Incentive Motivation or Aversive Motivation?

BACKGROUND: Corticotropin-releasing factor (CRF) neural systems are important stress mechanisms in the central amygdala (CeA), bed nucleus of stria terminalis (BNST), nucleus accumbens (NAc), and related structures. CRF-containing neural systems are traditionally posited to generate aversive distress states that motivate overconsumption of rewards and relapse in addiction. However, CRF-containing systems may alternatively promote incentive motivation to increase reward pursuit and consumption without requiring aversive states. METHODS: We optogenetically stimulated CRF-expressing neurons in the CeA, BNST, or NAc using Crh-Cre+ rats (n = 37 female, n = 34 male) to investigate roles in incentive motivation versus aversive motivation. We paired CRF-expressing neuronal stimulations with earning sucrose rewards in two-choice and progressive ratio tasks and investigated recruitment of distributed limbic circuitry. We further assessed valence with CRF-containing neuron laser self-stimulation tasks. RESULTS: Channelrhodopsin excitation of CRF-containing neurons in the CeA and NAc amplified and focused incentive motivation and recruited activation of mesocorticolimbic reward circuitry. CRF systems in both the CeA and NAc supported laser self-stimulation, amplified incentive motivation for sucrose in a breakpoint test, and focused "wanting" on laser-paired sucrose over a sucrose alternative in a two-choice test. Conversely, stimulation of CRF-containing neurons in the BNST produced negative valence or aversive effects and recruited distress-related circuitry, as stimulation was avoided and suppressed motivation for sucrose. CONCLUSIONS: CRF-containing systems in the NAc and CeA can promote reward consumption by increasing incentive motivation without involving aversion. In contrast, stimulation of CRF-containing systems in the BNST is aversive but suppresses sucrose reward pursuit and consumption rather than increase, as predicted by traditional hedonic self-medication hypotheses.

Desire or Dread from Nucleus Accumbens Inhibitions: Reversed by Same-Site Optogenetic Excitations.

Microinjections of a glutamate AMPA antagonist (DNQX) in medial shell of nucleus accumbens (NAc) can cause either intense appetitive motivation (i.e., 'desire') or intense defensive motivation (i.e., 'dread'), depending on site along a flexible rostrocaudal gradient and on environmental ambience. DNQX, by blocking excitatory AMPA glutamate inputs, is hypothesized to produce relative inhibitions of NAc neurons. However, given potential alternative explanations, it is not known whether neuronal inhibition is in fact necessary for NAc DNQX microinjections to generate motivations. Here we provide a direct test of whether local neuronal inhibition in NAc is necessary for DNQX microinjections to produce either desire or dread. We used optogenetic channelrhodopsin (ChR2) excitations at the same local sites in NAc as DNQX microinjections to oppose relative neuronal inhibitions induced by DNQX in female and male rats. We found that same-site ChR2 excitation effectively reversed the ability of NAc DNQX microinjections to generate appetitive motivation, and similarly reversed ability of DNQX microinjections to generate defensive motivation. Same-site NAc optogenetic excitations also attenuated recruitment of Fos expression in other limbic structures throughout the brain, which was otherwise elevated by NAc DNQX microinjections that generated motivation. However, to successfully reverse motivation generation, an optic fiber tip for ChR2 illumination needed to be located within <1 mm of the corresponding DNQX microinjector tip; that is, both truly at the same NAc site. Thus, we confirm that localized NAc neuronal inhibition is required for AMPA-blocking microinjections in medial shell to induce either positively-valenced 'desire' or negatively-valenced 'dread'.SIGNIFICANCE STATEMENT A major hypothesis posits neuronal inhibitions in nucleus accumbens generate intense motivation. Microinjections in nucleus accumbens of glutamate antagonist, DNQX, which might suppress local neuronal firing, generate either appetitive or defensive motivation, depending on site and environmental factors. Is neuronal inhibition in nucleus accumbens required for such pharmacologically-induced motivations? Here we demonstrate that neuronal inhibition is necessary to generate appetitive or defensive motivations, using local optogenetic excitations to oppose putative DNQX-induced inhibitions. We show that excitation at the same site prevents DNQX microinjections from recruiting downstream limbic structures into neurobiological activation, and simultaneously prevents generation of either appetitive or defensive motivated behaviors. These results may be relevant to roles of nucleus accumbens mechanisms in pathological motivations, including addiction and paranoia.

Glucagon-Like Peptide-1 (GLP-1) and 5-Hydroxytryptamine 2c (5-HT2c) Receptor Agonists in the Ventral Tegmental Area (VTA) Inhibit Ghrelin-Stimulated Appetitive Reward.

Current literature indicates that the orexigenic peptide ghrelin increases appetitive motivation via signaling in the mesolimbic reward system. Another gastric peptide, glucagon-like peptide-1 (GLP-1), and the neurotransmitter 5-hydroxytryptamine (5-HT), are both known to suppress operant responding for food by acting on key mesolimbic nuclei, including the ventral tegmental area (VTA). In order to investigate the interaction effects of ghrelin, GLP-1, and 5-HT within the VTA, we measured operant responding for sucrose pellets after the administration of ghrelin, the GLP-1 receptor agonist exendin-4 (Ex-4), and the 5-HT2c receptor agonist Ro60-0175 in male Sprague-Dawley rats. Following training on a progressive ratio 3 (PR3) schedule, animals were first injected with ghrelin into the VTA at doses of 3 to 300 pmol. In subsequent testing, separate rats were administered intraperitoneal (IP) Ex-4 (0.1⁻1.0 µg/kg) or VTA Ex-4 (0.01⁻0.1 µg) paired with 300 pmol ghrelin. In a final group of rats, the 5-HT2c agonist Ro60-0175 was injected IP (0.25⁻1.0 mg/kg) or into the VTA (1.5⁻3.0 µg), and under both conditions paired with 300 pmol ghrelin delivered into the VTA. Our results indicated that ghrelin administration increased operant responding for food reward and that this effect was attenuated by IP and VTA Ex-4 pretreatment as well as pre-administration of IP or VTA Ro60-0175. These data provide compelling evidence that mesolimbic GLP-1 and serotonergic circuitry interact with the ghrelinergic system to suppress ghrelin's effects on the mediation of food reinforcement.

Does spatial attention modulate the C1 component? The jury continues to deliberate.

The thoughful comments on our study (Baumgartner et al., this issue) that failed to replicate the C1 attention effect reported by a previous study roughly fall into three broad categories. First, the commentators identified specific differences between the two studies that may have contributed to the discrepant results. Second, they highlighted some of the theoretical and methodological problems that are encountered when trying to demonstrate attention effects on the initial evoked response in primary visual cortex. Third, they offered a number of proposals for optimizing experimental designs and analysis methods that may increase the likelihood of observing attention-related modulations of the C1. We consider each of these topics in turn.

Does spatial attention modulate the earliest component of the visual evoked potential?

Whether visual spatial attention can modulate feedforward input to human primary visual cortex (V1) is debated. A prominent and long-standing hypothesis is that visual spatial attention can influence processing in V1, but only at delayed latencies suggesting a feedback-mediated mechanism and a lack of modulation during the initial afferent volley. The most promising challenge to this hypothesis comes from an event-related potential (ERP) study that showed an amplitude enhancement of the earliest visual ERP component, called the 'C1', in response to spatially attended relative to spatially unattended stimuli. In the Kelly et al. study, several important experimental design modifications were introduced, including tailoring the stimulus locations and recording electrodes to each individual subject. In the current study, we employed the same methodological procedures and tested for attentional enhancements of the C1 component in each quadrant of the visual field. Using the same analysis strategies as Kelly et al., we found no evidence for an attention-based modulation of the C1 (measured from 50-80 ms). Attention-based amplitude enhancements were clear and robust for the subsequent P1 component (90-140 ms). Thus, despite using methods specifically designed to reveal C1 attention effects, the current study provided no confirmatory evidence for such effects.