Behavioral response and erythrocyte chromophilia of rats in experimental traumatic brain injury

Введение. Патогенетические основы изменения микроциркуляции крови в головном мозге вследствие черепно-мозговой травмы (ЧМТ) изучены не в полной мере по причине высокой инвазивности нейроморфологических методов. Цель исследования - изучение поведенческого статуса и информативности цитохимических критериев хромофилии эритроцитов в качестве маркеров вазореактивности микрососудов головного мозга при черепно-мозговой травме у крыс. Методика. Объектом исследования являлись 3-месячные аутбредные крысы Wistar массой 250-270 г. Легкую и средней тяжести ЧМТ воспроизводили с применением модифицированной модели падающего груза для взрослых крыс. Через 2 ч, 1, 2, 8 и 14 сут после моделирования ЧМТ проводили неврологическое обследование животных по модифицированной шкале Neurological Severity Scores (mNSS), сенсомоторное - по степени тревожности в тесте «свет-темнота», поведение анализировали с использованием теста условной реакции пассивного избегания. С помощью хромаффинной реакции исследовали функциональное состояние эритроцитов. Срезы тканей головного мозга, окрашивали по Нисслю и гематоксилин-эозином, микроскопировали, проводили морфометрию цифровых изображений. Результаты. Неврологическое обследование при среднетяжелой ЧМТ показало очаговую симптоматику, соответствующую выраженным неврологическим расстройствам, тогда как после ЧМТ легкой степени у крыс отмечались незначительные нарушения координации. В тесте условной реакции пассивного избегания на 7-е сут у этих животных выявлено состояние повышенной тревожности. Морфометрический анализ препаратов головного мозга травмированных животных показал уменьшение диаметра просвета капилляров и выявил признаки гипоксии нейронов. Цитохимическая оценка эритроцитов, с привлечением количественного определения степени флуоресценции, выявила особенности окислительного метаболизма в клетках у травмированных крыс. Эти показатели коррелировали с морфологическими признаками гипоксии головного мозга. Заключение. В начальный посттравматический период отмечено уменьшение диаметра просвета капилляров нервной ткани, наличие морфологических признаков компенсации нейронов, что является локальной ответной реакцией клеток на ишемию головного мозга. В капиллярах определяется нарушение гемореологии, что является следствием изменения окислительно-восстановительных процессов вследствие гипоксии при внутричерепной травме. The pathogenetic basis of changes in blood microcirculation in the brain due to traumatic brain injury (TBI) has not been fully studied due to the highly invasive nature of neuromorphological methods. Aim: To study the behavioral status and informative value of cytochemical criteria for erythrocyte chromophilia as markers of cerebral microvessel vasoreactivity in rats with TBI. Methods. The study was conducted on 3-month-old Wistar albino, outbred rats weighing 250-270 g. Mild to moderate TBI was simulated using a modified falling weight model for adult rats. At 2 hrs, 1, 2, 8, and 14 days after TBI, a neurological examination was performed according to the modified Neurological Severity Score (mNSS) modified scale and a sensorimotor examination was performed according to the degree of anxiety in the light-dark test. Behavior was analyzed using the conditioned passive avoidance response test. The functional state of erythrocytes was studied using the chromaffin reaction. Brain tissue samples stained by Nissl and with hematoxylin-eosin were evaluated under a microscope, digital images were obtained, and morphometric processing was performed. Results. Neurological examination after moderate TBI showed focal symptoms corresponding to severe neurological disorders, while after mild TBI, rats had minor coordination disorders. In the conditioned passive avoidance response test on the 7th day, the rats showed a state of increased anxiety. Morphometric analysis of the brains showed a decrease in the diameter of capillary lumen and changes in neurons, indicating signs of hypoxia. The cytochemical assessment of erythrocytes, involving a quantitative determination of the degree of fluorescence, revealed features of cell oxidative metabolism in injured rats. Moreover, these indicators correlated with morphological signs of hypoxia in brain neural tissue. Conclusion. In the initial post-traumatic period, there was a decrease in the capillary lumen diameter of the brain neural tissue and the presence of morphological signs of neuronal compensation, which is a local response of cells to cerebral ischemia. Disorders of hemorheology were found. These changes were a consequence of altered redox processes due to hypoxia after intracranial injury.

Escape Steering by Cholecystokinin Peptidergic Signaling

Escape is an evolutionarily conserved and essential avoidance response. Considered to be innate, most studies on escape responses focused on hard-wired circuits. We report here that peptidergic signaling is an integral and necessary component of the Caenorhabditis elegans escape circuit. Combining genetic screening, electrophysiology, and calcium imaging, we reveal that a neuropeptide NLP-18 and its cholecystokinin receptor CKR-1 enable the escape circuit to execute a full omega turn, the last motor step where the animal robustly steers away from its original trajectory. We demonstrate in vivo and in vitro that CKR-1 is a Gq protein-coupled receptor for NLP-18. in vivo, NLP-18 is mainly secreted by the gustatory sensory neuron (ASI) to activate CKR-1 in the head motor neuron (SMD) and the turn-initiating interneuron (AIB). Removal of NLP-18, removal of CKR-1, or specific knockdown of CKR-1 in SMD or AIB neurons lead to shallower turns hence less robust escape steering. Consistently, the Ca2+ transients elevation of head motor neuron SMD during escape steering is attenuated upon the removal of NLP-18 or CKR-1. in vitro, synthetic NLP-18 directly evokes CKR-1-dependent currents in oocytes and CKR-1-dependent Ca2+ transients in SMD. Thus, cholecystokinin signaling modulates an escape circuit to generate robust escape steering.

Stress increases impulsive punishment avoidance in unmedicated mood disorders

In an intriguing study designed to test whether and how stress affects learning and decision making in anxious individuals, Aylward et al. (2019)1 used a restless four-armed bandit task, where threat of electric shocks was used to induce stress. They hypothesized that anxious individuals would learn faster from punishments under stress, and as a result, exhibit choices that are more affected by those punishments. Unfortunately, these hypotheses were not confirmed.Here, we re-analyzed the original dataset using behavioral models that incorporate different mechanisms that could account for punishment-related behavioral biases. We found evidence that support the original hypotheses, namely increased punishment-avoidance for anxious individuals during stress. The avoidance-behavior was driven by punishments that were presented following a sequence of neutral outcomes, and in turn increased the tendency to elicit an immediate avoidance response (rather than larger learning rates). This impulsive avoidance bias was particularly pronounced in anxious individuals during stress.

The human olfactory bulb processes odor valence representation and cues motor avoidance behavior

Determining the valence of an odor to guide rapid approach–avoidance behavior is thought to be one of the core tasks of the olfactory system, and yet little is known of the initial neural mechanisms supporting this process or of its subsequent behavioral manifestation in humans. In two experiments, we measured the functional processing of odor valence perception in the human olfactory bulb (OB)—the first processing stage of the olfactory system—using a noninvasive method as well as assessed the subsequent motor avoidance response. We demonstrate that odor valence perception is associated with both gamma and beta activity in the human OB. Moreover, we show that negative, but not positive, odors initiate an early beta response in the OB, a response that is linked to a preparatory neural motor response in the motor cortex. Finally, in a separate experiment, we show that negative odors trigger a full-body motor avoidance response, manifested as a rapid leaning away from the odor, within the time period predicted by the OB results. Taken together, these results demonstrate that the human OB processes odor valence in a sequential manner in both the gamma and beta frequency bands and suggest that rapid processing of unpleasant odors in the OB might underlie rapid approach–avoidance decisions.

Dichlorvos and Paraquat induced spatial avoidance response: A more realistic determinant of population decline of Oreochromis niloticus

The present study evaluated the ability of Dichlorvos and Paraquat to provoke avoidance response in fingerlings of Nile tilapia Oreochromis niloticus and estimate the population immediate decline (PID). The non-forced multi-compartmented system used for non-forced assays, were constructed to allow free movement of fishes along six compartments. Fishes (n=3 per compartment/treatment, totaling 18 per system) were exposed to a gradient of Dichlorvos (1.0, 2.0, 4.0, 5.0 and 6.0 mg L-1) and Paraquat (10.0, 30.0, 50.0, 70.0, 100.0 mg L-1) and their distribution were recorded at 20 min interval for a 3-h period. Mortalities recorded in forced exposures were 17% and 0% at lowest concentrations and, 67% and 83% at highest concentrations for Dichlorvos and Paraquat correspondingly. For non-forced exposure, fishes presented a significant (p < 0.005) gradient-dependent spatial avoidance for both pesticides after 3-h. They avoided the lowest concentrations of Dichlorvos and Paraquat (1.0 and 10.0 mg L-1) by 40% and 90% respectively and 100% at the highest concentrations for both pesticides. The PID was driven by avoidance behavior rather than mortality. This result indicates that the dangers of pesticide contamination is not only in their toxicity to organisms, but also, in habitat selection processes by organism resulting in serious environmental turbulence.

Common and distinct neurofunctional representations of core and social disgust in the brain: An ALE meta-analysis and MACM characterization

ABSTRACTDisgust represents a multifaceted defensive-avoidance response. On the behavioral level, the response includes withdrawal and a disgust-specific facial expression. While both serve the avoidance of pathogens the latter additionally transmits social-communicative information. Given that common and distinct brain representation of the primary defensive-avoidance response (core disgust) and encoding of the social-communicative signal (social disgust) remain debated we employed neuroimaging meta-analyses to (1) determine brain systems generally engaged in disgust processing, and (2) segregate common and distinct brain systems for core and social disgust. Disgust processing, in general, engaged a bilateral network encompassing the insula, amygdala, occipital and prefrontal regions. Core disgust evoked stronger reactivity in left-lateralized threat detection and defensive response network including amygdala, occipital and frontal regions while social disgust engaged a right-lateralized superior temporal-frontal network engaged in social cognition. Anterior insula, inferior frontal and fusiform regions were commonly engaged during core and social disgust suggesting a common neural basis. We demonstrate a common and separable neural basis of primary disgust responses and encoding of associated social-communicative signals.

Explaining preemptive acclimation by linking information to plant phenotype

We review mechanisms for preemptive acclimation in plants and propose a conceptual model linking developmental and evolutionary ecology with the acquisition of information through sensing of cues and signals. The idea is that plants acquire much of the information in the environment not from individual cues and signals but instead from their joint multivariate properties such as correlations. If molecular signalling has evolved to extract such information, the joint multivariate properties of the environment must be encoded in the genome, epigenome and phenome. We contend that multivariate complexity explains why extrapolating from experiments done in artificial contexts into natural or agricultural systems almost never works for characters under complex environmental regulation: biased relationships among the state variables both in time and space create a mismatch between the evolutionary history reflected in the genotype and the artificial growing conditions in which the phenotype is expressed. Our model can generate testable hypotheses bridging levels of organization. In this note we describe the model, its theoretical bases and discuss its implications. We illustrate the hypotheses that can be derived from the model in two cases of preemptive acclimation based on correlations in the environment: the shade avoidance response and acclimation to drought.

Shade-induced WRKY transcription factors restrict root growth during the shade avoidance response

Shade-intolerant plants rapidly elongate their stems, branches, and leaf stalks to compete with their neighboring vegetation to maximize sunlight capture for photosynthesis. This rapid growth adaptation, known as the shade avoidance response (SAR), comes at a cost; reduced biomass, crop yield, and root growth. Significant progress has been made on the mechanistic understanding of hypocotyl elongation during SAR; however, the molecular account of how root growth is repressed is not well understood. Here, we explore the mechanisms by which low red:far-red induced SAR restrict the primary and lateral root (LR) growth. By analyzing whole-genome transcriptome, we identified a core set of shade-induced genes in the roots of Arabidopsis and tomato seedlings grown in the shade. Abiotic and biotic stressors also induce many of these shade-induced genes and are predominantly regulated by the WRKY transcription factors. Correspondingly, a majority of the WRKYs were also among the shade-induced genes. Functional analysis using transgenics of these shade-induced WRKYs revealed their role is essentially to restrict primary root and LR growth in the shade, and captivatingly, they did not affect hypocotyl elongation. Similarly, we also show that ethylene hormone signaling is necessary to limit root growth in the shade. Our study proposes that during SAR, shade-induced WRKY26, 45, and 75, and ethylene reprogram gene expression in the root to restrict its growth and development. The reduced growth of root organs helps the plant divert its critical resources to the elongating organs in the shoot to ensure competitiveness under limiting photosynthetic radiation