Neurotransmitter characteristics of brain grafts: striatal and septal tissues form the same laminated input to the hippocampus

In previous experiments we have studied the development of grafts of embryonic septal tissues implanted alongside the hippocampal formation of neonatal rats. In the present study we examined intracerebral implants of corpus striatum, a brain region that contains acetylcholinesterase-positive cells and does not normally project to the hippocampal formation, in order to evaluate the possibility that neurotransmitter identity may be involved in mechanisms guiding patterns of afferent growth and connectivity. Implant cavities were made in the entorhinal cortices of neonatal rat recipients and 3-6 days later embryonic striatal tissues were grafted to these preformed cavities. Implants were examined with acetylcholinesterase histochemistry one month after implantation. Grafts of embryonic striatal tissues did not survive implantation when the implant was introduced at the same time as the cavity was made. Grafts of corpora striata containing acetylcholinesterase-positive neurons were found in 7 of 11 rats in the delayed implant paradigm and, in all but one of these animals, acetylcholinesterase was present within those terminal laminae in the ipsilateral hippocampus and dentate gyrus that normally receive cholinergic input from the septal area. These findings suggest that cues underlying the development of specific connections between native (and implanted) septal efferents and hippocampal target neurons may be recognized by ingrowing acetylcholinesterase-reactive fibers from striatal implants.     

High-resolution analysis of locomotor activity rhythms indisconnected,a visual-system mutant ofDrosophila melanogaster

Free-running locomotor activity and eclosion rhythms ofDrosophila melanogaster, mutant at thedisconnected (disco) locus, are substantially different from the wild-type phenotype. Initial periodogram analysis revealed little or no rhythmicity (Dushayet al., 1989). We have reanalyzed the locomotor activity data using high-resolution signal analysis (maximum-entropy spectral analysis, or MESA). These analyses, corroborated by autocorrelograms, uncovered significant residual circadian rhythmicity and strong ultradian rhythms in most of the animals tested. In this regard thedisco mutants are much like flies expressing mutant alleles of theperiod gene, as well as wild-type flies reared throughout life in constant darkness. We hypothesize that light normally triggers the coupling of multiple ultradian oscillators into a functional circadian clock and that this process is disrupted indisco flies as a result of the neural lesion.This work was supported in part by NIH Grant FM-33205.     

Inhalation anesthetic-induced neuroinvasion by an attenuated strain of West Nile virus in mice

There are contradictory reports regarding the effects of inhalation anesthetics on the immune system. Measurable immune responses have been studied in vitro, but little is known about the in vivo effects in the intact organism. We used an attenuated, non-neuroinvasive, nonlethal strain of the encephalitic West Nile virus, termed WN-25, which can become lethal in combination with environmental stressors, to study possible modulatory immune effects of inhalation anesthetics in mice. Both single short-term exposure and repeated exposure to halothane and nitrous oxide were studied. Exposure to 30% CO2 served as a positive control. Mortality, brain invasion, spleen weight, and antiviral antibodies served as the experimental endpoints. Halothane and nitrous oxide led to viral brain invasion, increased mortality, and suppressed immune response in a concentration- and time-dependent manner. Repeated exposures had a cumulative effect. Assessment of the stability of the viral attenuation did not demonstrate any alteration in the character of the virus, suggesting an increased access to the brain by inhalation anesthetics that led to the fatal encephalitis. These findings may be of special concern to populations at risk, such as operating room staff and patients undergoing general anesthesia in endemic areas of encephalitic virus species, in which subclinical infection may develop into an overt disease.     

Disturbances of Haemostasis in Diabetes Mellitus

Diabetes mellitus is associated with disturbances in haemostasis that could contribute to the development of thrombotic complications.The present study was undertaken to determine the behavior of coagulation variables and fibrinolytic system in diabetes mellitus. Forty five diabetic patients and forty five matched controls were evaluated by doing the following haemostatic parameter, prothrombin time, partial thromboplastin time, thrombin time, coagulation factors assay II, VII, IX, & plasma fibrinogen, ADP-induced platelet aggregation, protein C, a₂- antiplasmin, PAI and FDPs. Generally diabetic patients have high levels of fibrinogen, a₂- antiplasmin, & PAI and lower level of protein C. Other haemostatic parameters did not show statistically significant difference between diabetic patients and control group. Significantally elevated levels of PAI, a₂- antiplasmin together with low protein C level in diabetic patients may result in the disturbance of haemostatic balance favoring thrombotic events. Conclusion: High levels of plasma fibrinogen, a₂A- antiplasmin with low plasma protein C activity could lead to a prothrombotic tendency in insulin dependent diabetic patients. Moreover, in non-insulin dependent diabetic patients, the above mentioned parameters together with high levels of ADP-induced platelet aggregation and plasminogen activator inhibitor may increase the risk of thrombotic complications. Obesity can be considered as an additional risk factor for development of thrombosis in diabetic patients.     

Effects of signaled and unsignaled stressor on ECG T-wave amplitude

Thirty-six human subjects were exposed to noise (noxious US) under one of the following signal (CS) conditions: signaled stressor (SS), unsignaled stressor (NS) and a truly random control group (RS). Changes in ECG T-wave amplitude were used to index the stress response and the greatest change in amplitude occurred in the SS group. T-wave amplitude change was compared to HR change as an index of sympathetic stimulation and the former proved the more sensitive. The increased sympathetic responding in the SS condition suggests that a reliable signal may serve a physiologically adaptive purpose.     

人胎儿中枢神经系统星形胶质细胞形态发育的观察

为观察人胎儿中枢神经系统星形胶质细胞形态发育。用胶质原纤维酸性蛋白抗体进行免疫组织化学染色。结果表明；１．以颈段脊髓，脑干，海马和小脑蚓部于胚胎２５周其ＧＦＡＰ染色强度，细胞密度接近出生时水平。而此时期大脑皮层Ａｓｔ密度约为出生时的四分之一。２．在同一胎龄ＣＮＳ的不同部位，ＧＦＡＰ阳性Ａｓｔ分布不均匀。３．Ａｓｔ不仅在毛细胞血管周围，而且在小血管周围密度大染色深，环绕血管呈辐射状排列。     

Frequent expression of the multi-drug resistance-associated protein BCRP/MXR/ABCP/ABCG2 in human tumours detected by the BXP-21 monoclonal antibody in paraffin-embedded material

The expression and cellular localization of angiotensin II (Ang II) and AT(1) receptor proteins were examined in the normal human prostate and benign prostatic hyperplasia (BPH) by immunohistochemistry. In the normal prostate, Ang II immunoreactivity was localized to the basal layer of the epithelium and AT(1) receptor immunostaining was found predominantly on stromal smooth muscle and also on vascular smooth muscle of prostatic blood vessels. Ang II immunoreactivity was markedly increased in hyperplastic acini in BPH compared with acini in the normal prostate (normal: 7.4+/-0.2%, n=5 vs. BPH: 22.7+/-1.9%, n=5, p<0.001). However, AT(1) receptor immunoreactivity was significantly decreased in BPH compared with the normal prostate [normal: 16.4+/-2.2%, n=4 vs. BPH: 9.4+/-1.3%, n=5, p<0.05 (p=0.025)]. The present study demonstrates the presence of Ang II peptide in the basal layer of the epithelium and AT(1) receptors on stromal smooth muscle, suggesting that Ang II may mediate paracrine functions on cellular growth and smooth muscle tone in the human prostate. Furthermore, AT(1) receptor down-regulation in BPH may be due to receptor hyperstimulation by increased local levels of Ang II in BPH. These data extend previous findings in support of the novel concept that overactivity of the renin-angiotensin system (RAS) may be involved in the pathophysiology of BPH.