Physiological reactivity to infant crying: a behavioral genetic study

In this study, we examined adults' cardiac reactivity to repeated infant cry sounds in a genetically informative design. Three episodes of cry stimuli were presented to a sample of 184 adult twin pairs. Cardiac reactivity increased with each cry episode, indicating that subjects were increasingly sensitized to repeated infant distress signals. Non‐parents showed more cardiac reactivity than parents, and males displayed a larger increase in heart rate (HR) in response to repeated cry sounds than females. Multivariate genetic modeling showed that the genetic component of adults' HR while listening to infant crying was substantial. Genetic factors explained 37–51% of the variance in HR and similar genes influenced HR at baseline and HR reactivity to infant crying. The remaining variance in HR across the cry paradigm was accounted for by unique environmental influences (including measurement error). These results point to genetic and experiential effects on HR reactivity to infant crying that may contribute to the explanation of variance in sensitive and harsh parenting.     

Alpha1 desensitization of the heart during adaptation to stress]

Results of the experiments evidence that a combination of three factors, limiting the Ca2+ concentration increase in myocardial cell, can play a role in the cardioprotective effect of adaptation of rats to short-term immobilization stress (every second day for a month) are presented. Those factors are as follows: desensitization of alpha 1-adrenoreceptors, M-cholinoreceptors up-regulation and reduced number of voltage-dependent Ca2+ channels in the myocardial membranes.     

A method to soothe and promote sleep in crying infants utilizing the transport response

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Fast desensitization of the response to InsP3 in Limulus ventral photoreceptors.

In Limulus ventral photoreceptor cells the time-course of the desensitization of InsP3 response was measured by an injection-pair paradigm. Pressure pulses of InsP3 were delivered into the cell with various interpulse intervals. The desensitization of the response to the second injection of each pair approached totality at 200 ms, which is the duration of the response to a single pressure pulse of InsP3. Lowering extracellular calcium did not affect the time-course of the desensitization. Lowering the temperature slowed down both the time-course of the response to InsP3 and the time-course of the desensitization to the same extent. These findings suggest that the desensitization is powerful enough and its onset fast enough to contribute to the transience of the InsP3 response. The time-course of the desensitization suggests it may influence light adaptation.     

Characteristics of the infant arousal response

Arousal is considered to be an importantresponse to a life-threatening stimulus. Recently, it has been shownthat the infant arousal response to an elevated inspiredCO₂ level occurs as a sequence ofevents involving presumptive brain stem responses before awakening (A. Lijowska, N. Reed, B. Chiodini, and B. T. Thach. Am.J. Respir. Crit. Care Med. 151: A151, 1995; A. S. Lijowska, N. W. Reed, B. A. Mertins Chiodini, and B. T. Thach.J. Appl. Physiol. 83: 219-228,1997). We wanted to further evaluate the relationship ofsubcortical reflexes to cortical arousal in infants. We used anonrespiratory (tactile) stimulus to elicit arousal in infants duringnon-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. Wefound that a tactile stimulus elicited an arousal sequence thatcommenced with a spinal withdrawal reflex, was followed by brain stemresponses (respiratory and startle responses), and ended in a corticalarousal. The entire pathway or part of it in the order of spinal tocortical responses could be elicited. REM and NREMresponses were similar except for significant differences in thelatencies of spinal and subcortical reflexes. These observations suggest that the infant arousal response to a tactile stimulus involvesa progression of central nervous system activation from the spinal tocortical levels. The different components of the arousal pathway may beimportant for an infant to respond appropriately to stimuli duringsleep without necessarily disturbing sleep.

     

Synaptosomal response to oxidative stress: Effect of vinpocetine

It has been suggested that reactive oxygen species (ROS) play a role in the neuronal damage occurring in ischemic injury and neurodegenerative disorders and that their neutralization by antioxidant drugs may delay or minimize neurodegeneration. In the present study we examine whether vinpocetine can act as an antioxidant and prevent the formation of ROS and lipid peroxidation in rat brain synaptosomes. After ascorbate/Fe²⁺ treatment a significant increase in oxygen consumption (about 5-fold) and thiobarbituric acid reactive substances (TBARS) formation (about 7-fold) occurred as compared to control conditions. Vinpocetine inhibited the ascorbate/Fe²⁺ stimulated consumption of oxygen and TBARS accumulation, an indicator of lipid peroxidation, in a concentration-dependent manner. The ROS formation was also prevented by vinpocetine. Oxidative stress increased significantly the fluorescence of the probes 2′,7′-dichlorodihydrofluorescein (DCFH₂-DA) (about 6-fold) and dihydrorhodamine (DHR) 123 (about 10-fold), which is indicative of intrasynaptosomal ROS generation. Vinpocetine at 100 μM concentration decreased the fluorescence of DCFH₂-DA and DHR 123 by about 50% and 83%, respectively. We conclude that the antioxidant effect of vinpocetine might contribute to the protective role exerted by the drug in reducing neuronal damage in pathological situations.     

Synaptosomal response to oxidative stress: effect of vinpocetine

It has been suggested that reactive oxygen species (ROS) play a role in the neuronal damage occurring in ischemic injury and neurodegenerative disorders and that their neutralization by antioxidant drugs may delay or minimize neurodegeneration. In the present study we examine whether vinpocetine can act as an antioxidant and prevent the formation of ROS and lipid peroxidation in rat brain synaptosomes. After ascorbate/Fe²⁺ treatment a significant increase in oxygen consumption (about 5-fold) and thiobarbituric acid reactive substances (TBARS) formation (about 7-fold) occurred as compared to control conditions. Vinpocetine inhibited the ascorbate/Fe²⁺ stimulated consumption of oxygen and TBARS accumulation, an indicator of lipid peroxidation, in a concentration-dependent manner. The ROS formation was also prevented by vinpocetine. Oxidative stress increased significantly the fluorescence of the probes 2',7'-dichlorodihydrofluorescein (DCFH₂-DA) (about 6-fold) and dihydrorhodamine (DHR) 123 (about 10-fold), which is indicative of intrasynaptosomal ROS generation. Vinpocetine at 100 μM concentration decreased the fluorescence of DCFH₂-DA and DHR 123 by about 50% and 83%, respectively. We conclude that the antioxidant effect of vinpocetine might contribute to the protective role exerted by the drug in reducing neuronal damage in pathological situations.     

Glial response to polyglutamine-mediated stress

Neurodegenerative trinucleotide (CAG) repeat disorders are caused by the expansion of polyglutamine tracts within the disease proteins. Some of these proteins have an unknown function. How expanded polyglutamine causes target neurons to degenerate is not clear. Recent evidence suggests that intercellular miscommunication may contribute to polyglutamine pathogenesis in CAG repeat disorders. Polyglutamine induced degeneration of the target neuron can be mediated via glia-neuron interactions. Here we hypothesize that during the neurodegenerative process the failure of cell-cell interactions have more severe consequences than alterations in intracellular neuron biology. We further believe that bidirectional communication between neurons and glia is a prerequisite for the normal development and function of either cell type. Understanding intercellular signaling mechanisms such as glial trophic factors and their receptors, cell adhesion or other well-defined signaling molecules provides opportunities for developing potential therapies.     

Spermatozoal response to osmotic stress

The process of sperm cryopreservation imparts on sperm cells the stress of low-temperature and drastic osmotic change. Damage to the cell plasma membrane results in cell injury in a number of cellular structures and associated functions. Studies in the author's laboratory have focused upon the various mechanisms of osmotic and thermal injury including plasma membrane lipid structure, mitochondrial membrane potential, and intracellular signaling. We have determined that cryoinjury to sperm, as for somatic cells, is a multi-factorial event and some of these events are reversible while some are not.     

Lisianthus response to salinity stress

The effect of salinity on some morpho-physiological characteristics in lisianthus cultivars was investigated. Cultivars namely, Blue Picotee (C1), Champagne (C₂), Lime Green (C₃), and Pure White (C₄), were subjected to salt stress (0–60 mM NaCl) in a sand culture and their responses were measured. Our results showed that as a salinity level increased, growth parameters, relative water content, photosynthetic pigments, and gas-exchange characteristics decreased in all cultivars, while root fresh mass, root/shoot length ratio, electrolyte leakage, and a malondialdehyde content increased. However, the changes were less pronounced in C₃ and C₄ compared to C1 and C₂. The regression analysis of the relationship between salinity levels and seedling height or root/shoot length ratio defined two groups with different slope coefficients: C1 and C₂ as salt-sensitive cultivars and C₃ and C₄ as salt-tolerant cultivars. Shoot dry mass and leaf area tolerance indices were less affected by salinity in C₃ and C₄ compared to those in C1 and C₂. Further, C₃ and C₄ showed higher photosynthetic rates, greater stomatal conductances, and accumulated greater K+ and Ca2+ contents and K+/Na+ ratios in roots and shoots compared to those in C1 and C₂. The results suggests that C₃ and C₄ could be recommended as resistant cultivars due to maintaining higher growth, water balance, leaf gas exchange, ion compartmentalization, and lower lipid peroxidation in response to salinity compared to C1 and C₂.     

Venous response to orthostatic stress

Head-up tilt (HUT) induces a reduction in preload, which is thought to be restored through sympathetic venoconstriction, reducing unstressed volume (V(u)) and venous compliance (VeC). In this study, we assessed venous inflow and outflow responses and their reproducibility and determined the relation with autonomic function during HUT. Eight healthy non-pregnant women were subjected to 20 degrees head-down tilt to 60 degrees HUT at 20 degrees intervals. At each rotational step, we randomly assessed forearm pressure-volume (P-V) curves (venous occlusion plethysmography) during inflow (VeC(IN)) and outflow [venous emptying rate (VER(OUT))]. VeC(IN) was defined as the ratio of the slope of the volume-time curve and pressure-time curve, with direct intravenous pressure measurement. VER(OUT) was determined using the derivate of a quadratic regression model using cuff pressure. We defined V(u) as the y-intercept of the P-V curve. We calculated, for both methods, the coefficients of reproducibility (CR) and variation (CV). Vascular sympathetic activity was determined by spectral analysis. VeC(IN) decreased at each rotational step compared with the supine position (P<0.05), whereas VER(OUT) increased. CR of VeC(IN) was higher in the supine position than VER(OUT) but lower during HUT. CV varied between 19% and 25% (VeC(IN)) and between 12% and 21% (VER(OUT)). HUT decreased V(u). The change in VeC(IN) and VER(OUT) correlated with the change in vascular sympathetic activity (r= -0.36, P<0.01, and r=0.48, P<0.01). This is the first study in which a reproducible reduction in VeC(IN) and V(u) and a rise in VER(OUT) during HUT are documented. The alterations in venous characteristics relate to changes in vascular sympathetic activity.     

Measuring a cell's response to stress: the p53 pathway

The characterization of complex cellular responses to diverse stimuli can be studied by the use of emerging chip-based technologies.     

Stretching the stress boundary: Linking air pollution health effects to a neurohormonal stress response

Inhaled pollutants produce effects in virtually all organ systems in our body and have been linked to chronic diseases including hypertension, atherosclerosis, Alzheimer's and diabetes. A neurohormonal stress response (referred to here as a systemic response produced by activation of the sympathetic nervous system and hypothalamus–pituitary–adrenal (HPA)-axis) has been implicated in a variety of psychological and physical stresses, which involves immune and metabolic homeostatic mechanisms affecting all organs in the body. In this review, we provide new evidence for the involvement of this well-characterized neurohormonal stress response in mediating systemic and pulmonary effects of a prototypic air pollutant — ozone. A plethora of systemic metabolic and immune effects are induced in animals exposed to inhaled pollutants, which could result from increased circulating stress hormones. The release of adrenal-derived stress hormones in response to ozone exposure not only mediates systemic immune and metabolic responses, but by doing so, also modulates pulmonary injury and inflammation. With recurring pollutant exposures, these effects can contribute to multi-organ chronic conditions associated with air pollution. This review will cover, 1) the potential mechanisms by which air pollutants can initiate the relay of signals from respiratory tract to brain through trigeminal and vagus nerves, and activate stress responsive regions including hypothalamus; and 2) the contribution of sympathetic and HPA-axis activation in mediating systemic homeostatic metabolic and immune effects of ozone in various organs. The potential contribution of chronic environmental stress in cardiovascular, neurological, reproductive and metabolic diseases, and the knowledge gaps are also discussed. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.     

Psychosocial modifiers of response to stress

The impact of stress upon an organism is far more complex than the simple design of most stress research implies. We offer an expanded model for studying the relation of stressors to pathological outcomes, which takes into account both the adaptive capacity of the organism before the stressor occurs and the defenses marshalled in response to the stressor. The model also distinguishes among the initial responses of alarm, sustained defensive behaviors, and the relatively irreversible endstates which remain after resistance has ended. Realizing that only a multidiscomplinary approach can begin to capture the wholeness of human experience, this research paradigm anticipates that stressors, adaptive capacities, defenses, alarm reactions, and pathologial end-states will take place at the biological, psychological, interpersonal and sociocultural levels simultaneously and successively. Data on life change stress and psychological health outcomes gathered as part of the Air Traffic Controller Health Change Study are analyzed to illustrate the use of the model in identifying psychosocial and biological modifiers of response to stress.     

Physiological stress response to video-game playing: the contribution of built-in music

Recent studies on video game playing have uncovered a wide range of measurable physiological effects on the organism, such as increases in cardiovascular activity and breathing responses. However, the exact source of these effects remains unclear. Given the well-known effects of sound on physiological activity, especially those of noise and of music, and on the secretion of the stress hormone cortisol in particular, we hypothesized that music may be a major source of stress during video game playing. We thus examined the effect of built-in music on cortisol secretion as a consequence of video game playing. Players were assigned quasi-randomly to either a Music or a Silence condition. Four saliva samples were taken, that is, after practice (T1), immediately after having played for 10 minutes (T2), 15 minutes after the end of the experiment (T3), and 30 minutes after the end of the experiment (T4). The results show that the Music group had significantly higher cortisol levels at T3, that is, when cortisol levels are assumed to reflect the stress induced by the game. These findings suggest for the first time that the auditory input contributes significantly to the stress response found during video game playing.     

Cellular stress response: From homeostatic to allostatic perspective

For the vertebrates the more flexible allostasis frameworks tend to overlap the homeostatic model in the study of stress-induced physiological changes and whole-body adaptation. I hypothesise the possibility to extend this paradigm to stress-induced rearrangements of cellular networks.