Stages of the cerebral mechanisms of deceptive responses

Cerebral mechanisms of perceiving and telling lies were studied by recording event-related potentials (ERPs) both after an actual deceptive response and during the time interval when the subject decided to tell a lie. Ten healthy volunteers participated in the study. The test consisted of their playing a game against a computer. The subjects could choose between deceptive and truthful answers so as to win the game. The subjects gave a deceptive answer intentionally, the structure of the test ensuring equal numbers of deceptive and truthful answers. The relaxation times in the cases of truthful and deceptive answers did not differ significantly from each other. The comparison of ERPs accompanying deceptive and truthful answers showed the existence of a negativity with a latent period of 90 ms in the regions of the right frontal, central, and right parietal derivations. This negativity indicated that the brain reacted to a deceptive answer even if this a priori “erroneous” act ensured reaching the goal and, in this sense, was subjectively relevant. In terms of the cerebral error detector mechanism, this phenomenon may be regarded as a special case of a general response of the brain to giving an incorrect (deceptive) answer, rather than a response to a lie per se. The interval of time when, presumably, the decision on a deceptive answer was being made was found to contain the late positive component P540, which is most likely to be involved in the preparation of the deceptive answer and the intention to tell a lie.     

Driving actin dynamics under the influence of alcohol

The actin cytoskeleton plays a pivotal role in regulating neuronal development and activity, and dysregulation of actin dynamics has been linked to impaired cognitive function. In this issue of Cell Rothenfluh et al. (2006) , and Offenh?user et al. (2006) show that actin dynamics can also affect the cellular and behavioral responses of flies and mice to alcohol.     

Cerebral responses to exercise and the influence of heat stress in human fatigue

There are a number of mechanisms thought to be responsible for the onset of fatigue during exercise-induced hyperthermia. A greater understanding of the way in which fatigue develops during exercise could be gleaned from the studies which have examined the maintenance of cerebral blood flow through the process of cerebral autoregulation. Given that cerebral blood flow is a measure of the cerebral haemodynamics, and might reflect a level of brain activation, it is useful to understand the implications of this response during exercise and in the development of fatigue. It is known that cerebral blood flow is significantly altered under certain conditions such as altitude and exacerbated during exercise induced – hyperthermia. In this brief review we consider the processes of cerebral autoregulation predominantly through the measurement of cerebral blood flow and contrast these responses between exercise undertaken in normothermic versus heat stress conditions in order to draw some conclusions about the role cerebral blood flow might play in determining fatigue.     

Cerebral responses evoked by stimulation of the vesico-urethral junction in normal subjects

Following the bipolar stimulation of the vesico-urethral junction (VUJ), evoked potentials (EPs) with a late and prominent negativity (mean latency 91.4 ± 11.0 msec) were recorded from scalp in 22 male subjects. Although remarkable intersubject variations occurred, no peak variation could be seen in any given subject. Maximum amplitude of the EPs was recorded from Cz and CzP points. Stimuli with various frequencies did not lead to any differences in shape and latency of EPs.The differences between the EPs by bipolar stimulation of the VUJ and the responses elicited by distal urethal and pudendal nerve stimulation suggest that, during bipolar stimulation of VUJ, the somatic afferents were not excited. Therefore, these responses were most likely due to the excitement of the visceral afferents arising from the VUJ separately. This method may be a useful technique for evaluating the physiological condition of the afferent nerves arising from VUJ.     

Nitric oxide is involved in light-specific responses of tomato during germination under normal and osmotic stress conditions

Background and Aims Nitric oxide (NO) is involved in the signalling and regulation of plant growth and development and responses to biotic and abiotic stresses. The photoperiod-sensitive mutant 7B-1 in tomato (Solanum lycopersicum) showing abscisic acid (ABA) overproduction and blue light (BL)-specific tolerance to osmotic stress represents a valuable model to study the interaction between light, hormones and stress signalling. The role of NO as a regulator of seed germination and ABA-dependent responses to osmotic stress was explored in wild-type and 7B-1 tomato under white light (WL) and BL. Methods Germination data were obtained from the incubation of seeds on germinating media of different composition. Histochemical analysis of NO production in germinating seeds was performed by fluorescence microscopy using a cell-permeable NO probe, and endogenous ABA was analysed by mass spectrometry. Key Results The NO donor S-nitrosoglutathione stimulated seed germination, whereas the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) had an inhibitory effect. Under WL in both genotypes, PTIO strongly suppressed germination stimulated by fluridone, an ABA inhibitor. The stimulatory effect of the NO donor was also observed under osmotic stress for 7B-1 seeds under WL and BL. Seed germination inhibited by osmotic stress was restored by fluridone under WL, but less so under BL, in both genotypes. This effect of fluridone was further modulated by the NO donor and NO scavenger, but only to a minor extent. Fluorescence microscopy using the cell-permeable NO probe DAF-FM DA (4-amino-5-methylamino-2',7'-difluorofluorescein diacetate) revealed a higher level of NO in stressed 7B-1 compared with wild-type seeds. Conclusions As well as defective BL signalling, the differential NO-dependent responses of the 7B-1 mutant are probably associated with its high endogenous ABA concentration and related impact on hormonal cross-talk in germinating seeds. These data confirm that light-controlled seed germination and stress responses include NO-dependent signalling.     

Cerebral metabolic and pressure-flow responses during sustained hypoxia in awake sheep.

Conscious sheep (n = 6), exposed to 3.5 h of normobaric hypoxia (arterial PO2 = 40 Torr) while allowed varying arterial PCO2, showed striking early increments of cerebral blood flow (CBF; +200-250%, by radiolabeled microspheres) and decrements of cerebral vascular resistance (CVR) in association with an early temporary elevation of cerebral O2 consumption (CMRO2; +25-60%). After 2 h, CMRO2 returned to normoxic levels, while CBF declined to a lower but still elevated level (+150%). CBF/CMRO2 increased twofold, while cerebral fractional extraction of O2 was unchanged. Mean arterial pressure was unchanged, but cerebral venous pressure rose (+11 mmHg) in a stable fashion such that cerebral perfusion pressure declined by 13%. Cerebral venous hematocrit and hemoglobin concentration were both elevated (+2.2-2.7% Hct units; +1.0-1.3 g/dl, respectively) above the corresponding arterial values between 150 and 210 min of hypoxia, suggesting venous hemoconcentration in possible association with a transcapillary fluid shift. CBF, and especially CVR, were well correlated with arterial O2 content.     

Histofunctional state of mouse ovaries in normal conditions and during hypervitaminosis A

Morphometry was used to analyze different histofunctional structures of mouse ovaries (follicles of varying maturation grades, yellow and atretic bodies, interstitial tissue) in health and hypervitaminosis A (80 000 IU). It was noticed that in the ovaries of female mice in health, there occurred consistent cyclic processes marked by the changes in the number and size of the morphofunctional structures during different stages of the estrous cycle. In hypervitaminosis A, female mice had no estrous cycle. The ovaries showed the impairment of the growth of the follicles and enhancement of atresia. As a result, the follicles did not reach the final stages of development, which led to the cessation of ovulation and formation of yellow bodies.     

The influence of the initial state of hydration on endocrine responses to exercise in the heat

This study examines the effect of the initial state of hydration on hormone responses to prolonged exercise in the heat. Five subjects at two initial hydration levels (hypohydrated and hyperhydrated) were exposed to a 36 degrees C environment for 3 h of intermittent exercise. During exercise, the subjects were either fluid-deprived, or rehydrated with water or an isotonic electrolyte sucrose solution (ISO). Both the stress hormones, adrenocorticotropic hormone and cortisol, and the main fluid regulatory hormones, aldosterone, renin activity (PRA) and arginine vasopressin (AVP), were measured in blood samples taken every hour. Prior hyperhydration significantly reduced initial AVP, aldosterone and PRA levels. However, except for AVP, which responded to exercise significantly less in previously hyperhydrated subjects (p less than 0.05), the initial hydration state did not influence the subsequent vascular and hormonal responses when the subjects were fluid-deprived while exercising. Concurrent rehydration, either with water or with ISO, reduced or even abolished the hormonal responses. There were no significant differences according to the initial hydration state, except for PRA responses, which were significantly lower (p less than 0.01) in previously hyperhydrated subjects who also received water during exercise. These results indicate that prior hydration levels influence only slightly the hormonal responses to prolonged exercise in the heat. Progressive rehydration during exercise, especially when extra electrolytes are given, is more efficient in maintaining plasma volume and osmolarity and in reducing the hormonal responses.