Forebrain and lower brainstem participation in facilitatory and inhibitory regulation of the display of lordosis in female rats

Neural transection of the dorsal extrahypothalamic descending afferents by means of an L-shaped Halász knife at the anterior commissure (anterior roof deafferentation. ARD) markedly potentiated the display of lordosis and soliciting behaviors. Bilateral lesions of the ventromedial hypothalamus (VMH) attenuated lordotic activity in the ARD sham females but not in the ARD females. In contrast, the lesions in the pontine central gray concurrently with ARD effectively inhibited the display of lordosis but not soliciting behaviors. These results suggest that the VMH may not be a primary focus of the dorsal extrahypothalamic inhibitory influence on lordosis. The influence of this inhibitory system seems to be dominant in regulating the expression of lordosis behavior, compared to that of the hypothalamic lordosis facilitating system. Furthermore, the dorsal extrahypothalamic inhibitors influence which could be removed by ARD must be modified by the neural mechanism in the lower brain stem in which the pontine central gray may be actively involved.     

Genotoxicity and physicochemical characteristics of traffic-related ambient particulate matter

Exposure to ambient particulate matter (PM) has been linked to several adverse health effects. Since vehicular traffic is a PM source of growing importance, we sampled total suspended particulate (TSP), PM(10), and PM(2.5) at six urban locations with pronounced differences in traffic intensity. The mutagenicity, DNA-adduct formation, and induction of oxidative DNA damage by the samples were studied as genotoxicological parameters, in relation to polycyclic aromatic hydrocarbon (PAH) levels, elemental composition, and radical-generating capacity (RGC) as chemical characteristics. We found pronounced differences in the genotoxicity and chemical characteristics of PM from the various locations, although we could not establish a correlation between traffic intensity and any of these characteristics for any of the PM size fractions. Therefore, the differences between locations may be due to local sources of PM, other than traffic. The concentration of total (carcinogenic) PAHs correlated positively with RGC, direct and S9-mediated mutagenicity, as well as the induction of DNA adducts and oxidative DNA damage. The interaction between total PAHs and transition metals correlated positively with DNA-adduct formation, particularly from the PM(2.5) fraction. RGC was not associated with one specific PM size fraction, but mutagenicity and DNA reactivity after metabolic activation were relatively high in PM(10) and PM(2.5), when compared with TSP. We conclude that the toxicological characteristics of urban PM samples show pronounced differences, even when PM concentrations at the sample sites are comparable. This implies that emission reduction strategies that take chemical and toxicological characteristics of PM into account may be useful for reducing the health risks associated with PM exposure.     

Use of a high-throughput umu-microplate test system for rapid detection of genotoxicity produced by mutagenic carcinogens and airborne particulate matter

In the present study, we developed a rapid umu-microplate test system that uses the nitroreductase- and O-acetyltransferase-overproducing Salmonella typhimurium strain NM3009 and the O-acetyltransferase-overproducing S. typhimurium strain NM2009 to detect genotoxic activity in small volume samples. The assay was used to test the genotoxicity of several standard mutagens and environmental samples. Exponentially growing cultures of NM3009, NM2009, and the parental strain TA1535/pSK1002 were incubated in 96-well microplates with test chemicals both in the presence and in the absence of rat liver S9. The relative beta-galactosidase activities were then determined colorimetrically using either chlorophenol red-beta-D-galactopyranoside (CPRG) or O-nitrophenyl-beta-D-galactopyranoside (ONPG) as a measure of umuC gene induction activity. The sensitivities of NM3009 without S9 mix and NM2009 with S9 mix to nitroarenes and aromatic amines were up to 24- to 75-fold higher than those of the parent strain. Induction of umuC gene expression was detected more readily with CPRG than ONPG. The umu-microplate assay also detected genotoxicity in organic extracts of particulate matter from air samples collected in Osaka City, Japan. The pattern of the responses suggested that the genotoxic activity of the particulate extract was due primarily to nitrated polycyclic aromatic hydrocarbons. Our results indicate that the umu-microplate assay may be a useful way of carrying out rapid screens for genotoxicity in small-volume environmental samples.     

Laminar distribution and morphology of NADPH-diaphorase containing neurons in the superior colliculus and underlying periaqueductal gray of the rat

Summary We have studied the laminar distribution of reduced nicotinamide dinucleotide phosphate diaphorase (NADPH-d) activity and the morphology of positive neurons in the superior colliculus (SC) and the underlying periaqueductal gray (PAG) of the rat. The morphology of NADPH-d-positive neurons has been compared to that of Golgi-impregnated cells. The highest activity occurs in the stratum zonale and stratum griseum superficiale, contrasting with the pale neuropil in the stratum opticum, where only a few positive neurons are found. In the stratum griseum intermedium positive neurons are grouped in patches separated by narrow, NADPH-d-negative bands. In the deeper layers, the neuropil is NADPH-d-negative, and few neurons show enzymatic activity. In contrast, numerous neurons in the dorsolateral part of the PAG are intensely positive. They are continuous with the positive neurons in the stratum album profundum, with no clear border between the two centers. In both SC and PAG, only small and medium sized neurons are NADPH-d-positive. In comparison with Golgi material, all types of small neurons in the superficial layers show NADPH-d activity; NADPH-d histochemistry, however, does not visualize the characteristic dendritic appendages of these neurons. The large neurons of the SC and PAG, probably representing the long-projecting neurons of these centers, do not contain the enzyme.     

Changes in central serotoninergic transmission affect clonidine analgesia in monkeys

Summary 1. The effects of changes in central serotoninergic transmission on clonidine analgesia were assessed in monkeys. The minimum electrical current required for producing jaw opening is referred to as the pain threshold. Pain was induced by electrical stimulation of tooth pulp afferents. 2. In the first series of studies, intracerebroventricular administration of clonidine (5–30 g) produced dose-dependent analgesia in monkeys. The clonidine-induced analgesia was abolished or attenuated by prior injection of the animals with p-chlorophenylalanine or 5,7-dihydroxytryptamine into the third cerebral ventricle. On the other hand, pretreatment of the animals by injecting 5-HT or its precursor 5-hydroxytryptophan into the cerebral ventricle potentiated the clonidine-induced analgesia in monkeys. 3. In the second series of experiments, administration of clonidine (1–10 g) into the diencephalic periventricular gray (of the anterior hypothalamic portion), the periaqueductal gray, or the dorsal raphe nuclei also produced dose-dependent analgesia in monkeys. The analgesia induced by clonidine injection into the diencephalic periventricular gray or the periaqueductal gray was effectively antagonized by pretreatment of the animals by injecting two 5-HT receptor antagonists (such as ketanserine and methysergide) into the diencephalic periventricular gray or the periaqueductal gray. The clonidine-induced analgesia in monkeys was not affected by pretreatment of the animals with injections of either ketanserine or methysergide into the dorsal raphe nuclei. 4. The results suggest that the functional activity of central 5-HT neurons correlate well with the analgesic sensitivity of clonidine microinjected centrally. In addition, the analgesia induced by clonidine microinjected into the diencephalic periventricular gray or the periaqueductal gray was mediated by the 5-HT receptors at the site of injection.This study was supported by grants from the National Science Council of the Republic of China and the Student Summer Fellowship of National Cheng Kung University Medical College (1986) Send offprint requests to Mao-Tsun Lin at the above address     

Morphology and distribution of Alzheimer neuritic (senile) and amyloid plaques in striatum and diencephalon

Summary Mapping of striatal and diencephalic plaque distribution was conducted in 25 cases of dementia of the Alzheimer type. This analysis was carried out by fluorescence microscopy of paraffinembedded tissue sections treated with Thioflavine S as fluorochrome. Consistent differences in plaque morphology and density between nuclei and fiber tracts were observed. Striatal and pallidal distribution was uneven, with plaque aggregation near and within certain fiber tracts: capsules, medullary laminae, and radial fasciculi. Diencephalic plaques showed also preferred aggregation near and within fiber tracts and within the intralaminar nuclei.The different subcortical plaque morphologies observed according to the nuclear or fiber tract location of the amyloid plaque, indicates that the peripheral (halo) portion of the plaque is determined by the neuropil response to the primary event: the amyloid deposit.No correlation was observed between the distribution of plaques and any particular neurotransmitter system. In that respect, plaques were present within the nucleus basalis. Neurofibrillary tangle distribution was also seen to be dissociated from plaque distribution.     

中脑导水管周围灰质内注射抗强啡肽血清对神经降压素镇痛作用的影响

目的：探讨大鼠中脑导水管周围灰质（PAG）内内源性强啡肽对神经降压素（NT）镇痛作用的影响。方法：以钾离子透入法引起大鼠甩尾反应的电流强度（mA)为痛行为反应的指标,观察向PAG内注入NT,抗神经降压素血清和抗强啡肽A1－13血清对动物痛阈的影响。结果：PAG内注入NT后,大鼠痛阈明显升高;注入抗神经降压素血清后,大鼠痛阈则明显降低,而注入抗强啡肽血清后,对NT的镇痛效应无显著影响,结论：PAG内NT在痛觉调制中发挥着重要的作用,且其作用不依赖于PAG内的内源性强啡肽。     

Neurological prognosis correlated with variations over time in the number of subependymal nodules in tuberous sclerosis

In tuberous sclerosis (TS), brain CT reveals subependymal nodules, cortical tubers and white matter lesions. This study is a retrospective analysis of the relationship between the variations over time in the number of subependymal nodules and the clinical course in cases of tuberous sclerosis. Twenty-four children with tuberous sclerosis, who attended the National Children's Hospital as outpatients, were followed by means of brain CT examinations for 7 years and 1 month on average. Cranial MRI was also performed in 22 cases. Brain CT disclosed subependymal nodules already in early infancy. In almost all cases, the number of subependymal nodules gradually increased with age, especially around the frontal horn of the lateral ventricle. The increase stopped at around age 10. The cases with five or more subependymal nodules at the initial or subsequent CT examination (17 patients; Group A) exhibited a significantly greater number of cortical tubers than those with less than five (five patients; Group B) and had white matter lesions unlike Group B. In addition, the number of cases with either infantile spasms or mental retardation was significantly higher in Group A than Group B (P<0.005). In conclusion, the number of ventricular subependymal nodules may allow prediction of the severity of the cerebral dysfunction in TS. Our results suggest that its variation may reflect the degree of the embryologic disorder when neuronal cells grow in the early gestational period.