NGF prevents the changes induced by monocular deprivation during the critical period in rats

Photic evoked responses were recorded from the striate cortex of Long-Evans hooded intact, monocular visual deprivation (MD) and MD treated with NGF rats. The averaged visual evoked responses (AVER) were obtained from both hemispheres and provided comparison after binocular photic stimuli between the contralateral and the ipsilateral striate cortex with relation to the MD eye. One month of monocular visual deprivation at the critical period of development resulted in marked reduction of the amplitudes of AVER components as compared to the control recordings (P < 0.001). These changes of the AVER could be prevented by NGF infusion to lateral ventricle at the dosage of 2.0–2.4 μg/day for four weeks during the monocular deprivation. In conclusion, the change of AVER amplitudes induced by monocular visual deprivation during the critical period of development can be prevented by NGF infusion to lateral ventricle.     

Effect of forward rapidly rotating shift work on circadian rhythms of arterial pressure, heart rate and oral temperature in air traffic controllers

Twenty-four-hour records of arterial pressure (AP), heart rate(HR), oral temperature (OT) and physical and mental performancewere obtained in air traffic controllers during morning (n=16),afternoon (n=17) and night (n=19) shifts. Data were analyzedby the cosinor method. The results obtained during the morningshift were as follows (mesor/amplitude/;acrophase): systolicAP (mm Hg)—113.6/10.0/16:03 h; diastolic AP—71.1/8.2—15:19h; mean AP—85.6/8.8/15:41 h; HR (beats/min)—77.5/8.9/16:00h; OT (dg C)—36.71/0.21/15:49 h; right-hand grip strength(kg)—49.8/2.0/17:43 h; left-hand grip strength—46.1/2.0/16.08h; mental performance (calculations/min)—14.9/1.1/16:39h. During the night shift either no change of the circadianacrophases (HR, right-hand grip strength) or acrophase delaysranging from about 2 h (systolic AP, OT, mental performance)up to 3 h (diastolic and mean AP, left-hand grip strength) wereobserved. Our data suggest that the shift system studied doesnot significantly alter the circadian rhythms, and does notinduce a desynchronization, particularly as concerns arterialpressure and oral temperature.     

Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?

Summary In the present study a single case observation of myoclonus during sleep-wave transition was monitored in a depressed patient treated with the monoamine oxidase inhibitor, phenelzine. The myoclonus had a rhythm of 1 c/second and lasted for two years, the duration of phenelzine treatment. Myoclonus appeared neither during wakefulness nor during sleep, but at wake-sleep-wake transitions. This switch myoclonus was associated with phasic muscle hyperactivity during REM sleep.Methysergide a 5-HT suppressor, decreased the switch myoclonus frequency and the REM muscle hyperactivity, indicating serotoninergic involvement in the mechanism of phenelzine induced myoclonus.     

香萱解郁方对血清剥夺诱导HT22细胞损伤模型的神经保护作用

探讨香萱解郁方含药血清对血清剥夺致小鼠海马神经元HT22细胞损伤模型的影响。方法 采用血清剥夺培养HT22细胞建立神经损伤体外模型,实验分为对照组、模型组和中药组［中药组A（含药血清15%浓度）、中药组B（含药血清20%浓度）］,各组血清剥夺12 h后,通过CCK8法检测各组细胞活力,确定15%浓度含药血清干预后细胞的存活率最高,设定为后续实验中药组的药物浓度。免疫荧光染色法检测神经元特异性微管蛋白（β-Tubulin Ⅲ）在各组中的表达,蛋白质免疫印迹法及qPCR法检测脑源性神经营养因子（BDNF）蛋白及其mRNA在各组中的表达。结果 在加药后培养12 h,中药组的细胞活力明显高于对照组与模型组（P＜0.001）。培养24 h,模型组细胞活力较对照组明显下降（P＜0.001）,中药组较模型组明显提高（P＜0.001）。培养36 h,模型组细胞活力较对照组显著下降（P＜0.001）,中药组较模型组明显提高（P＜0.001）。模型组BDNF蛋白含量及 BDNF mRNA表达量较对照组显著降低（P＜0.05,P＜0.001）,模型组少数神经元长出突起;中药组BDNF蛋白含量及BDNF mRNA表达量较模型组显著增加（P＜0.05）,中药组HT22细胞轴突突起长度和分支增加,β-Tubulin Ⅲ阳性表达明显增多。结论 香萱解郁方含药血清对血清剥夺诱导小鼠海马神经元HT22细胞损伤具有神经保护作用,可能与促进BDNF蛋白表达有关     

Human slow-wave sleep and the cerebral cortex

SUMMARY  Recent hypotheses about the roles of human slow-wave sleep (hSWS—delta EEG activity) are appraised. The possible linkage between hSWS and the functions of the prefrontal cortex (PFC) are explored with respect to normal subjects and to disorders involving PFC deficits.     

The effects of short-term smokeless tobacco deprivation on performance

Several past studies have reported reliable changes in reaction time performance and self-rated withdrawal scores as a consequence of cigarette deprivation. The purpose of the present study was to determine, prospectively, the effect 24 h of smokeless tobacco deprivation in regular users has on performance and the associated withdrawal symptomology. Forty smokeless tobacco users (Copenhagen brand) were randomly divided evenly into two groups gen brand) were randomly divided evenly into two groups (N=20)24 h of deprivation and no deprivation. A third group of ten nonchewers was added as another control group. The results indicated that behavioral, subjective and physiological changes are associated with smokeless tobacco deprivation in regular users. These include increased craving scores, reaction time, self-rated withdrawal symptoms and decreased heart rate.     

Sleep and its homeostatic regulation in mice lacking the adenosine A1 receptor

Sleep deprivation (SD) increases extracellular adenosine levels in the basal forebrain, and pharmacological manipulations that increase extracellular adenosine in the same area promote sleep. As pharmacological evidence indicates that the effect is mediated through adenosine A1 receptors (A1R), we expected A1R knockout (KO) mice to have reduced rebound sleep after SD. Male homozygous A1R KO mice, wild-type (WT) mice, and heterozygotes (HET) from a mixed 129/C57BL background were implanted during anesthesia with electrodes for electroencephalography (EEG) and electromyography (EMG). After 1 week of recovery, they were allowed to adapt to recording leads for 2 weeks. EEG and EMG were recorded continuously. All genotypes had a pronounced diurnal sleep/wake rhythm after 2 weeks of adaptation. We then analyzed 24 h of baseline recording, 6 h of SD starting at light onset, and 42 h of recovery recording. Neither rapid eye movement sleep (REM sleep) nor non-REM sleep (NREMS) amounts differed significantly between the groups. SD for 6 h induced a strong NREMS rebound in all three groups. NREMS time and accumulated EEG delta power were equal in WT, HET and KO. Systemic administration of the selective A1R antagonist 8-cyclopentyltheophylline (8-CPT) inhibited sleep for 30 min in WT, whereas saline and 8-CPT both inhibited sleep in KO. We conclude that constitutional lack of adenosine A1R does not prevent the homeostatic regulation of sleep.     

Control of feeding during saline consumption and fluid deprivation in hamsters

Cellular dehydration induced by water deprivation or hypertonic saline injection reduces feeding in a variety of species. Normal feeding in rats is maintained during isotonic saline consumption by increasing the intake of saline compared to the usual intake of water. Hamsters do not show the spontaneous preference for isotonic saline noted in rats, even after adrenalectomy. In the present investigation, feeding by hamsters was depressed during both isotonic and hypertonic saline consumption compared to the usual feeding with water. Saline intakes did not exceed water intakes under similar conditions. When fluid intakes were elevated by prior fluid deprivation, feeding rates increased at all concentrations of saline after a delay proportional to the osmolality of the solution. Positive 24-hr sodium balances were always associated with saline consumption. Water and hypertonic saline injections reduced feeding, and the fluid loads were excreted very slowly. When hamsters were fluid deprived prior to injections, saline totally suppressed feeding, while water increased feeding compared to sham injected controls. It is concluded that cellular dehydration produces a reduction of feeding in hamsters drinking isotonic or hypertonic saline. Reduced feeding with isotonic saline consumption results from the failure of hamsters to increase their ad lib intake of that solution. The prolonged retention of both sodium and fluid after saline consumption or injection suggests that further saline intake may be inhibited by an expansion of the extracellular space.     

How do topical nasal corticosteroids improve sleep and daytime somnolence in allergic rhinitis?

Therapy for rhinitis improves sleep quality and symptoms of daytime sleepiness. This improvement with therapy may be secondary to anti-inflammatory effects, leading to a reduction of inflammatory mediators, or to a mechanical reduction of congestion directly leading to improvement in sleep disturbance. We combined our data from 3 placebo-controlled studies of intranasal corticosteroids in patients with perennial rhinitis to determine whether a correlation between the reduction of congestion and improved sleep and daytime somnolence existed. The pooled data of budesonide, flunisolide, and fluticasone demonstrated significantly decreased nasal congestion, sleep problems, and sleepiness in treated patients. The data demonstrated a correlation between a reduction in nasal congestion and an improvement of sleep (P < .01) and daytime somnolence (P = .01). Thus, topical intranasal corticosteroids should be used to decrease nasal congestion and to improve sleep and daytime somnolence in patients manifesting these symptoms.     

Genotypic influences on lead-induced hyperactivity in mice

Male mice, genetically selected for differences in brain weight or from a heterogeneous (HET) stock, were used to explore potential interactions between genotype and exposure to lead as manifested in activity. At the time of birth dams and their pups were given either water or a 0.5% lead acetate solution as the sole source of fluid. Fluid conditions remained constant throughout the experiment. The effects of chronic lead on activity in young adult mice depended on the genotype of the individual. Specifically, in an open field, HET mice exposed to lead tended to be more active than their control counterparts. Low-and high-brain weight lead-exposed mice at times were hypoactive but this effect depended on the specific nature of the measure.This research was supported in part by National Science Foundation Grant DAR7911233 to Peter J. Donovick and Richard G. Bruggight and by Biomedical Research Support Group Grant 5S077RR07149 to Peter J. Donovick.