LOVE: AN EMERGENT PROPERTY OF THE MAMMALIAN AUTONOMIC NERVOUS SYSTEM

The evolution of the autonomic nervous system provides an organizing principle to interpret the adaptive significance of mammalian affective processes including courting, sexual arousal, copulation, and the establishment of enduring social bonds. According to the Polyvagal Theory (Porges, 1995; Porges, 1996 and Porges, 1997), the well-documented phylogenetic shift in the neural regulation of the autonomic nervous system passes through three stages, each with an associated behavioral strategy. The first stage is characterized by a primitive unmyelinated visceral vagus that fosters digestion and responds to threat by depressing metabolic activity. Behaviorally, the first stage is associated with immobilization behaviors. The second stage is characterized by the sympathetic nervous system that is capable of increasing metabolic output and inhibiting the visceral vagus to foster mobilization behaviors necessary for ‘fight or flight’. The third stage, unique to mammals, is characterized by a myelinated vagus that can rapidly regulate cardiac output to foster engagement and disengagement with the environment. The mammalian vagus is neuroanatomically linked to the cranial nerves that regulate social engagement via facial expression and vocalization. The Polyvagal Theory provides neurobiological explanations for two dimensions of intimacy: courting and the establishment of enduring pair-bonds. Courting is dependent upon the social engagement strategies associated with the mammalian vagus. The establishment of enduring pair-bonds is dependent upon a co-opting of the visceral vagus from an immobilization system associated with fear and avoidance to an immobilization system associated with safety and trust. The theory proposes that the phylogenetic development of the mammalian vagus is paralleled by a specialized communication, via oxytocin and vasopressin, between the hypothalamus and the medullary source nuclei of the visceral vagus, which facilitates sexual arousal, copulation, and the development of enduring pair-bonds. © 1998 Elsevier Science Ltd. All rights reserved.     

THE EFFECTS OF LOSARTAN AND IMMOBILIZATION STRESS ON HEART RATE VARIABILITY AND PLASMA CORTICOSTERONE LEVELS IN RATS

In this study, the effects of losartan, an angiotensin II receptor antagonist, on heart rate variability and the changes of plasma corticosterone levels caused by immobilization stress were investigated. Losartan (3 mg/kg, p.o.) significantly prevented increases in plasma corticosterone levels in both losartan+acute stress and losartan+chronic stress groups. But, losartan did not prevent the diminution of the power of heart rate variability caused by stress. Our results supported the idea that the renin-angiotensin system is also involved in the stress--induced cardiovascular response, besides the autonomic nervous system. But, the effects of losartan on heart rate variability remained controversial     

Brief Communication EFFECTS OF UNILATERAL NOSTRIL BREATHING ON BLOOD PRESSURE AND HEART RATE IN RIGHT-HANDED HEALTHY SUBJECTS

The effects of unilateral forced nostril breathing (UFNB) on systolic and diastolic blood pressures and heart rate (HR) were studied in 88 male and 41 female right-handed subjects. In men, both the right and left unilateral forced nostril breathings significantly increased the systolic blood pressure (SBP) and HR, but had no effect on the diastolic blood pressure (DBP). In women, the right UFNB increased, but the left UFNB slightly decreased the SBP and DBP. The results suggested that there may be a nostril laterality affecting the autonomous nervous system differentially.     

Activation of peripheral opioid receptors has no effect on heart rate variability

Opioid receptors involved in regulating the motility of the gastrointestinal tract have been localized in both contractile and neuronal tissues. Trimebutine, a peripheral opioid receptor agonist, modulates gastrointestinal motor activity in both directions and also may act on cardiac tissue. This study investigated the effects of trimebutine in clinical doses on cardiac autonomic functions with heart rate variability. The effect of trimebutine on cardiac autonomic outflows was evaluated in 11 healthy subjects. Trimebutine (200 mg) or placebo was administered orally at random in a double-blind, cross-over manner. Continuous electrocardiography recordings were obtained before and after drug administration during three states: rest, controlled breathing, and a hand grip exercise. Heart rate variability analysis showed that there was no significant difference between subjects administered with placebo or trimebutine throughout rest, controlled breathing, or the hand grip exercise. We concluded that trimebutine, in clinical doses, has no significant effect on cardiac autonomic functions.     

AGE AND SEX DIFFERENCES IN NEUROBEHAVIORAL PERFORMANCE: A STUDY OF PORTUGUESE ELEMENTARY SCHOOL CHILDREN

In this study normative data were obtained on measures of IQ, visual/motor, motor and memory functions among Portuguese elementary school children. Subjects were 228 females and 275 males, 8.0 to 11.9 years of age, in grades 2 through 4, who participated in a dental study. Performance on all tests improved with increasing age. Females performed better in rote verbal learning, psychomotor speed, and speed of information processing. Males had higher scores on tests of visual learning, visual memory, and fine motor speed and coordination. Nonverbal IQ had a significant impact on all tests except motor speed and coordination. Results represent an initial attempt to evaluate Portuguese children in educational and medical settings.     

微量注射L—精氨酸及L—NMMA至延髓头端腹外侧区对血压,心率的影响

微量注射一氧化氮（NO）前体L-精氨酸至用乌拉坦和氯醛糖混合麻醉的雄性SD大鼠的延髓头端腹外侧区（rVLM），可引起血压（BP）和心率（HR）的快速明显下降．电刺激中脑中央导水管周围灰质背侧部（dPAG）诱发的防御性升压反应受到明显抑制。相反，微量注射NO合成抑制剂L-NG-单甲基-L-精氨酸（L—NMMA）至rVLM，则引起BP和HR的快速明显升高，电刺激dPAG诱发的防御性升压反应明显增强。结果提示，NO参与rVLM神经元调节心血管活动的信息传递过程，并在其中起抑制性作用。     

INCREASED PREVALENCE OF A POLYMORPHISM IN THE GENE CODING FOR HUMAN PROTHROMBIN IN PATIENTS WITH CORONARY HEART DISEASE

A number of genetic risk factors for the development of coronary heart disease has been identified in the past. Some of these represent polymorphisms in genes of proteins which are associated with the process of blood clotting. We investigated the distribution of a recently described G/A polymorphism in the 3′untranslated region of the human prothrombin gene (nt 20210) in 98 patients (19 female age: 53+12 SD years and 79 male, age: 49+8.5 SD years) with coronary heart disease and in 102 healthy newborns by enzymatic amplification of the genomic DNA carrying the polymorphic site and by subsequent restricition digest. The diagnosis of coronary heart disease was established by coronary angiography in all patients. The frequency of the A allele in the healthy newborns was 0.98 % (0.2 % – 3.5 %; CI 0.95) with the G/A genotype occurring in 1.96% (0.24 % – 6.9 %; CI 0.95).

In the group of patients with coronary heart disease the G/A genotype was found in 5.1 % (1.7 % – 11.4 %; CI 0.95). 94.9 % of the patients studied showed a G/G genotype. The A/A genotype was neither detected in the newborns nor in the patients with coronary heart disease. This preliminary study strongly suggest that the presence of the G/A polymorphism in the 3′untranslated region of the gene coding for human prothrombin is associated with the occurrence of coronary heart disease. © 1997 Elsevier Science Ltd     

谷氨酸载体在中枢神经系统中的作用

自１９９２ 年以来,随着各亚型谷氨酸载体氨基酸顺序逐渐被阐明,有关它们在中枢神经系统中的作用研究越来越深入,本文就谷氨酸载体的分布和结构、耦联的离子流、在中枢神经系统发育中的表达变化以及它们的生理作用和病理意义等几方面作一介绍     

COMPARATIVE NEUROPHYSIOLOGICAL STUDY FOR THE DIAGNOSIS OF MILD POLYNEUROPATHY IN PATIENTS WITH DIABETES MELLITUS AND GLUCOSE INTOLERANCE

This article evaluates diagnostic sensitivity of minimal F-wave latency, sural/radial amplitude ratio (SRAR), dorsal sural/radial amplitude ratio (DSRAR), sympathetic skin response (SSR), and R-R interval variability (RRIV) for detecting early polyneuropathy in patients with glucose intolerance and diabetic patients. F-wave latencies were more prolonged in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). SRAR was lower, SSR latency was more prolonged, and RRIV was lower in diabetic patients with abnormal nerve conduction studies than healty controls (p < .001). SSR latency was more prolonged and RRIV was lower in diabetic patients with normal nerve conduction studies than healty controls (p < .01, p < .05, respectively). DSRAR was lower in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). DSRAR was also lower in patients with glucose intolerance than control subjects (p < .01). DSRAR was the most sensitive and specific test in either of diabetic patients with normal nerve conduction studies (sensitivity 66%, specificity 90%) and diabetic patients with abnormal nerve conduction studies (sensitivity 100%, specificity 90%). DSRAR is the most reliable method for detection of early nerve pathology. Patients with glucose intolerance might have subclinical neuropathy that can be demonstrated with DSRAR analysis.     

Dysfunctions in circadian behavior and physiology in mouse models of Huntington's disease

Many patients with Huntington's disease (HD) exhibit disturbances in their daily cycle of sleep and wake as part of their symptoms. These patients have difficulty sleeping at night and staying awake during the day, which has a profound impact on the quality of life of the patients and their care-givers. In the present study, we examined diurnal and circadian rhythms of four models of HD including the BACHD, CAG 140 knock-in and R6/2 CAG 140 and R6/2 CAG 250 lines of mice. The BACHD and both R6/2 lines showed profound circadian phenotypes as measured by wheel-running activity. Focusing on the BACHD line for further analysis, the amplitude of the rhythms in the BACHD mice declined progressively with age. In addition, the circadian regulation of heart rate and body temperature in freely behaving BACHD mice were also disrupted. Furthermore, the distribution of sleep as well as the autonomic regulation of heart rate was disrupted in this HD model. To better understand the mechanistic underpinnings of the circadian disruption, we used electrophysiological tools to record from neurons within the central clock in the suprachiasmatic nucleus (SCN). The BACHD mice exhibit reduced rhythms in spontaneous electrical activity in SCN neurons. Interestingly, the expression of the clock gene PERIOD2 was not altered in the SCN of the BACHD line. Together, this data is consistent with the hypothesis that the HD mutations interfere with the expression of robust circadian rhythms in behavior and physiology. The data raise the possibility that the electrical activity within the central clock itself may be altered in this disease.     

AT1 antagonism by eprosartan lowers heart rate variability and baroreflex gain

INTRODUCTION: Blockade of the renin-angiotensin system (RAS) by ACE inhibitors has been demonstrated to reduce total mortality in cardiovascular diseases. This advantage was attributed in part to changes of autonomic cardiovascular control, exemplified by an increase of heart rate variability (HRV) and baroreflex gain (BRG). We sought to assess the effects of the angiotensin type 1 (AT1) receptor blocker eprosartan on HRV and BRG. MATERIALS AND METHODS: In a double-blind randomized cross-over design 25 young males took eprosartan (600 mg/day) and placebo each for a period of 7 days with a wash-out period of at least 4 weeks in between. At the end of the intake phases simultaneous recordings of arterial blood pressure (AP; Finapres) and electrocardiogram (ECG) were taken. Power spectra of HRV and arterial blood pressure variability (APV) were calculated by fast Fourier transform (FFT) and served to calculate BRG. Ang-II levels were measured by radioimmunoassay. RESULTS: Eprosartan tended to lower mean AP, it slightly increased heart rate (HR) (p<0.05), and markedly increased circulating Ang-II levels (p<0.01). Eprosartan diminished the total power of HRV (p<0.05) and the BRG (p<0.01). The low/high frequency (LF/HF) ratio of HRV and the APV were not altered. CONCLUSIONS: AT1 antagonism by eprosartan lowers heart rate variability and baroreflex gain. We speculate that these findings are due to the marked increase in circulating angiotensin II (Ang II). Further studies are needed to clarify whether angiotensin type 1 (AT1) blockers with potential actions inside the blood-brain barrier (BBB) may have different effects on HRV and BRG.     

Will daytime occupational noise exposures induce nighttime sleep disturbance?

BackgroundNighttime environmental noise affects sleep quality. However, the effects of daytime occupational noise remain unclear.MethodsA quasi-experiment of 48 participants who had been employed for at least six months in two hospital cafeterias. The participants were randomly designated to be assessed on high- and low-noise workdays for 8 h or low- and high-noise workdays, separated by a washout period of 14 days. Subsequently, pure tone audiometry, autonomic nervous system (ANS) function tests, serum cortisol tests, and polysomnography were conducted.ResultsFor the 40 participants in the study, the 8-h time-weighted average of personal noise exposed on high- and low-noise workdays was 76.8 dBA (standard deviation, SD: 6.2) and 61.0 dBA (SD: 7.1), respectively. Participants with higher personal noise exposure during the day were found to have a lower percentage of slow wave sleep (percent change of mean value: −1.287%; 95% CI: −2.602%, −0.037%) and lower sleep efficiency (−0.267%; 95% CI: −0.525%, −0.008%). In addition, after work, personal noise exposure was revealed to be related to increased serum cortisol levels (1.698%; 95% CI: 0.887%, 2.528%), and sympathetic activity as measured by low frequency/high frequency (3.000%; 95% CI: 1.294%, 4.706%) and blood pressures by cold pressor test (systolic: 5.163%; 95% CI: 2.780%, 7.537%) (diastolic: 3.109%; 95% CI: 1.604%, 4.614%).ConclusionsDaytime occupational noise exposure had sustained effects on nighttime sleep quality, specifically on slow wave sleep and sleep efficiency. These disturbances could be partially explained by post-shift elevated cortisol and ANS activity. The psychosocial and metabolic consequences of poorer sleep quality induced by occupational noise exposure warrant further investigation.