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PubMedDate not supplied

Holoprosencephaly anomaly with nasal and premaxillar agenesis (possibly autosomal recessive type).

A one-day-old male infant with cleft lip and palate, microcephaly, hypotelorism, microphthalmia and absence of the nose is presented. The intermaxillar segment and nasal bone structure were not seen on radiological examination of the skull. Chromosome examination showed a 46, XY karyotype. On postmortem examination, the cerebrum was seen to be a single lobe. Olfactory nerves, corpus callosum and nasal formation, besides the septum were absent. The first and second ventricles were formed as a single ventricle. These findings were compatible with alobar holoprosencephaly.

Abnormalities, Multiple↗
PubMed1994

Multiple types of ryanodine receptor/Ca2+ release channels are differentially expressed in rabbit brain.

The neuronal Ca2+ signal is induced by a rise in the intracellular free Ca2+ concentration ([Ca2+]i), and is thought to be important for higher brain function. Dynamic changes in [Ca2+]i are affected by the spatial distributions of various Ca(2+)-increasing molecules (channels and receptors). The ryanodine receptor (RyR) is an intracellular channel through which Ca2+ is released from intracellular stores. To define the contribution of neuronal Ca2+ signaling via the RyR channel, we examined RyR type-specific gene expression in rabbit brain by in situ hybridization histochemistry. The neuronal RyR was composed of three distinct types, two types dominant in skeletal (sRyR) and cardiac (cRyR) muscle, respectively, and a novel brain type (bRyR). sRyR was distinguished by its high level of expression in cerebellar Purkinje cells. cRyR was predominantly expressed throughout nearly the entire brain, and was characterized by its markedly high level of expression in the olfactory nerve layer, layer VI of the cerebral cortex, the dentate gyrus, cerebellar granule cells, the motor trigeminal nucleus, and the facial nucleus. bRyR expression was the least widely distributed throughout the brain, and was high in the hippocampal CA1 pyramidal layer, caudate, putamen, and dorsal thalamus. This investigation demonstrates that the heterogeneous distribution of neuronal RyRs may be implicated in distinct Ca(2+)-associated brain functions. Moreover, it should be noted that cRyR, a typical CICR channel, is distributed widely throughout the brain, suggesting that in a variety of cell types, the amplification of neuronal Ca2+ signals is functionally accompanied by a rise in [Ca2+]i, such as Ca2+ influx stimulated by neuronal activity. This widespread distribution of the neuronal RyR family indicates that Ca2+ signals via the intracellular stores should be considered in studies of neuronal Ca2+ dynamics.

Animals↗
PubMed1994

[Effects of zuzhongping on ischemic volume in the rat model of middle cerebral artery occlusion].

Using the middle cerebral artery occlusion model, we studied the effects of Zuzhongping on experimental focal cerebral ischemia. Twenty-eight adult male Wistar rats were randomly divided into three groups: (1) Zuzhongping group (n = 9), (2) Saline control group (n = 10), and (3) Blank control group (n = 9). Group 1 and group 2 received via a gastric tube 1 1ml/kg/day of Zuzhongping and normal saline, respectively. The cerebral middle arteries on the right side of 28 rats were occluded with a bipolar electro-coagulater at sites 1-2 mm from the right olfactory nerve tract. Ischemic volumes were measured by an image analytic system when the cerebral ischemia had lasted 24 h. The results showed that the ischemic volume of Zuzhongping group was significantly smaller than that of group 2 and group 3, suggesting a protective effect of Zuzhongping.

Animals↗
PubMed1993

Free-living amebas of the genera Acanthamoeba and Naegleria: an overview and basic microbiologic correlates.

Free-living amebas of the genera Acanthamoeba and Naegleria are allied in basic cell biology, ecology, and human disease-producing potential. However, several enigmas surrounding these amebas need further intellectual and scientific scrutiny. For instance, a clearer differentiation is needed of factors delineating pathogenic species--those most frequently associated with human infections--from nonpathogenic species. Further, have the pathogenic species bridged the gap in a step-wise fashion between their habitat and the human host to express their disease-producing potential? Second, what attributes of amebas account for the spectrum of disease caused by Acanthamoeba and Naegleria? In the brain, Naegleria is highly destructive of tissue in the course of a rapidly evolving, hemorrhagic primary meningoencephalitis in normal individuals. Central nervous system invasion by Acanthamoeba, however, occurs only in compromised hosts, and is a more slowly evolving subacute to chronic encephalitis. Further, the epidemiology of the infections are disparate. Naegleria is acquired from exposure to contaminated fresh water; this epidemiologic link is absent in Acanthamoeba meningoencephalitis. Naegleria invades the central nervous system via the olfactory nerve; Acanthamoeba is deposited in the central nervous system via hematogenous spread from a pulmonary or cutaneous focus. Additionally, Naegleria is apparently restricted to the brain; Acanthamoeba is not so bridled, and invades more sites in the human body. Finally, Acanthamoeba are beginning to appear opportunistically more frequently in patients infected with the human immunodeficiency virus. To avoid the same lack of effective therapeutics we still face in treating cryptosporidium infections in these patients, more emphasis must be placed on clinical trials dealing with the management of Acanthamoeba infections in patients with AIDS.

Acanthamoeba↗
PubMed1994

[Technical tactics to preserve cortical venous drainage in interhemispheric approach for anterior communicating artery aneurysms].

The interhemispheric approach has been selected for clipping of the anterior communicating artery aneurysm located high above the sphenoidal plate, and in a posterior direction. However, this approach is sometimes complicated with postoperative hemorrhagic infarction due to excess brain retraction combined with damages of the cortical bridging veins. We have devised a modification in this approach to eliminate these complications. Our newly devised methods include the following; 1) Small bifrontal craniotomy performed, 2) Continuous ventricular drainage performed to minimize the effect of compression by the spatula during resection of interhemispheric fissure, 3) Bifrontal dural incision made along the frontal skull base, 4) Mobilization of the major cortical vein in the operated field, if necessary, by resection of the overlying arachnoid membrane with or without sacrificing its small tributaries, 5) Gradual dissection of the olfactory nerves according to the process of operation. We analysed the incidence of operative complications in thirteen consecutive cases with this approach. Major frontal ascending veins were carefully preserved in all cases. None showed hemorrhagic infarction, regardless of the cortical venous drainage patterns. The degree of smell preserved in 10% of the examined 11 cases was more than unilateral. In conclusion, this method is useful for the elimination of perioperative complications even in the acute stage of subarachnoid hemorrhage.

Adult↗
PubMed1996

[Postoperative olfactory dysfunction in interhemispheric approach for ruptured anterior communicating artery aneurysms].

Between 1969 and 1994 we treated 450 patients with ruptured anterior communicating artery aneurysms, of which 434 cases (96.4%) were operated on via the interhemispheric approach (IH), namely, until 1979 mainly, via bifrontal craniotomy, subfrontal and interhemispheric approach (SIH) and, since 1979, via posterior interhemispheric approach (PIH). Postoperative olfactory dysfunction is one of the main disadvantages of IH. The mechanisms and the incidence of this disadvantage were studied in both approaches. The causes of postoperative anosmia in SIH were as follows: sectioning of olfactory tracts intentionally or not, avulsion of olfactory bulbs and probability of ischemic or minor mechanical insults to olfactory tracts. However, these matters rarely occur in PIH because of little exposure of olfactory nerves. The mechanisms of postoperative anosmia in PIH were considered to be as follows: sinking of frontal lobes due to excessive drainage of cerebrospinal fluid and over-retraction of frontal lobes. The incidence of postoperative anosmia decreased from 27.0% via SIH to 5.5% via PIH.

Aneurysm, Ruptured↗
PubMedDate not supplied

[Surface of the olfactory region in man observed by scanning electron microscope].

This report describes the surface of the regio olfactoria of a 25-year-old man as observed in the scanning electron-microscope. Corresponding to the distal ends of the receptor cells, the surface displays various planes: (a) Upper-most is a film of mucus of varying thickness. (b) The olfactory hairs, which are arranged closely together, mostly in a parallel fashion in layers, dip into this mucus film. The long, distal parts of the olfactory hairs are of a rather uniform shape and form, together with the mucus film, a single functional unit. (c) Now follows a layer consisting of the short parts of the olfactory hairs. They branch from the olfactory vesiculae, mostly in a stellar fashion (5-12 on one vesicula) and arch themselves, after a short course, into the mucus film. (d) There then follows the plane of the olfactory vesiculae, mostly bulbous, partly club- and pyramidal in shape. (e) After that comes the plane of the microvilli receptors, which have about 100 or more villi on one cell. (f) Right at the bottom is the apical surface of the supporting cells, different in size, showing microvilli in a regularly arranged pattern. Because of the various planes of the surface of the olfactory region and because of the close situation of the long, distal parts of the olfactory hairs and their rather uniform shape, one could assume, from observations in the scanning electron microscope, that the olfactory-active molecules react immediately with the functional unit of mucus film and long distal parts of the olfactory hairs, so that for the different sense of smell, a quite different structure of the olfactory-active molecules must be assumed as a different shape of the distal ends of the olfactory receptors.

Adult↗
PubMed1997

Developmentally regulated masking of an intracellular epitope of the 180 kDa isoform of the neural cell adhesion molecule NCAM.

The neural cell adhesion molecule NCAM is a cell surface glycoprotein that occurs in several isoforms. It was previously shown that the largest 180-kDa isoform of NCAM (NCAM 180) accumulates at sites of cell contact and in postsynaptic densities and may be responsible for the stabilization of cell contacts by its interaction with the membrane-cytoskeleton linker protein brain spectrin. In immunohistochemical studies on the expression of the NCAM 180, we noticed that two NCAM 180 specific monoclonal antibodies, termed 481 and D3, showed different patterns of immunoreactivity in sections of fresh-frozen adult mouse brain. Here we show that the D3-specific, but not the 481-specific epitope becomes inaccessible to the antibody during development of the hippocampal formation, coincident with the establishment of stable cell-cell contacts. In contrast, in the olfactory bulb with its continually regenerating olfactory nerve fibers, both NCAM 180 antibodies remain fully immunoreactive throughout development and adulthood. We also show that the D3-specific epitope becomes inaccessible in primary cerebellar neuron cultures with time in culture. Electrophoretic separation of hippocampal membrane proteins under nondenaturating conditions showed NCAM to be present in protein complexes of different molecular weights at different developmental stages. We propose that NCAM is involved in the formation of developmentally regulated, noncovalent complexes with as yet unknown partner molecules that could be responsible for the masking of the D3-specific epitope.

Animals↗
PubMed1998

[A case of transethmoidal meningocele showing increased activity of 99mTcHM-PAO at seizure attack].

A case of transethmoidal meningocele presenting seizure attack is reported. A 59-year-old man was admitted to our hospital because of seizure attack. On admission, he was neurologically free without right olfactory dysfunction. T2-weighted image of MRI showed high intensity signal area in right frontal base, and this signal increase herniated into the ethmoidal sinus. Then 3 DCT image clearly showed right frontal base bony defect. After admission, we compared brain activity in this patient during a seizure attack and resting state using SPECT. And we found increased activity in right frontal base using 99mTc HM-PAO. So it was suspected that indicated the focus of the seizure. During the operation a unilateral bony defect and hypoplastic olfactory nerve were observed, but there was no herniated brain tissue. The association of seizure with frontobasal meningoencephalocele is reported only two cases. In one of two cases, it is presumed that reactive gliosis was epileptogenesis. On the other hand, the relationship of the temporal meningoencephalocele to the genesis of temporal lobe seizure is suggested by the extension of gliosis to the amygdalohippocampal lesion. In our case, it is possible that reactive gliosis or scar of the cyst wall may be the focus of seizure. In terms of diagnosis, 3 DCT is useful to identify the bony defect. It makes easy to diagnose the front-basal encephaloceles.

Ethmoid Sinus↗
PubMed1977

Denervation in the primary olfactory pathway of mice. IV. Biochemical and morphological evidence for neuronal replacement following nerve section.

Unilateral olfactory nerve section was performed in the mouse. Three biochemical markers of the olfactory chemoreceptor neurons: carnosine, carnosine synthetase activity and the olfactory marker protein, were measured in the olfactory bulb and epithelium. Parallel observations were made by light microscopy as well as at the ultrastructural level. The specific biochemical markers decrease rapidly in both bulb and epithelium and reach a minimum by the end of the first week after surgery. They then slowly return to 80% of control values by one month. Carnosinase activity in epithelium was essentially unaffected. These biochemical observations coincide temporally with the onset of degenerative changes seen morphologically, in both the bulb and epithelium. The degenerative changes persist for up to two weeks in the bulb and for about one week in the epithelium. At this time basal cell division and differentiation begins in the epithelium with subsequent regrowth of olfactory axons into the glomerular layer of the olfactory bulb with ther reappearance of olfactory axon terminals. The temporal coincidence of these biochemical and morphological observations suggests they are manifestations of the same process, and is consistent with the idea that the olfactory chemoreceptor neurons are perhaps unique in being able to be replaced from undifferentiated stem cells.

Animals↗
PubMed2001

Cultured olfactory ensheathing cells express nerve growth factor, brain-derived neurotrophic factor, glia cell line-derived neurotrophic factor and their receptors.

In the primary olfactory pathway axons of olfactory neurons (ONs) are accompanied by ensheathing cells (ECs) as the fibres course towards the olfactory bulb. Ensheathing cells are thought to play an important role in promoting and guiding olfactory axons to their appropriate target. In recent years, studies have shown that transplants of ECs into lesions in the central nervous system (CNS) are able to stimulate the growth of axons and in some cases restore functional connections. In an attempt to identify a possible mechanism underlying EC support for olfactory nerve growth and CNS axonal regeneration, this study investigated the production of growth factors and expression of corresponding receptors by these cells. Three techniques immunohistochemistry, enzyme linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) were used to assess growth factor expression in cultured ECs. Immunohistochemistry showed that ECs expressed nerve growth factor (NGF), brain derived neurotrophic factor (BDNF) and glial cell-line derived neurotrophic factor (GDNF). ELISA confirmed the intracellular presence of NGF and BDNF and showed that, compared to BDNF, about seven times as much NGF was secreted by ECs. RT-PCR analysis demonstrated expression of mRNA for NGF, BDNF, GDNF and neurturin (NTN). In addition, ECs also expressed the receptors trkB, GFRalpha-1 and GFRalpha-2. The results of the experiments show that ECs express a number of growth factors and that BDNF in particular could act both in a paracrine and autocrine manner.

Animals↗
PubMed1998

[Study of the function of nerve growth factor in the olfactory tract of the mouse].

The aim of this study was to examine the function of nerve growth factor (BGF) in the olfactory tract of mice. Using the mice which had received unilateral olfactory bulbectomy and in which antibodies to NGF had been continuously infused with into the contralateral olfactory blub, three kinds of analysis were performed: histological analysis of the olfactory epithelium by HE staining, immunohistochemical analysis of the olfactory epithelium using polyclonal antibodies to trk which forms the NGF receptor, and olfactory-mediated behavioral analysis with cycloheximide. These animals had been sacrificed at day 1, 3, 7, 14, 21 or 28. Several findings were obtained as a result of the above analysis. Degeneration of the olfactory epithelium and trk expression by the olfactory cells were observed on day 7, and the olfactory epithelium was incompletely regenerated on day 28. However, trk expression by the olfactory cell was still recognized and the olfactory function was not restored by day 28. These examinations suggest that NGF produced in the olfactory bulb was transported retrogradely to olfactory cells through the olfactory nerves, and was associated with sustaining the existence of those cells and with regenerating the olfactory tract after injury.

Animals↗
PubMed2000

Patterning of olfactory sensory connections is mediated by extracellular matrix proteins in the nerve layer of the olfactory bulb.

In early rat embryos when axons from sensory neurons first contact the olfactory bulb primordium, lactosamine-containing glycans (LCG) are detected on neurons that are broadly distributed within the olfactory epithelium, but that project axons to a very restricted region of the ventromedial olfactory bulb. LCG(+) axons extend through channels defined by the coexpression of galectin-1 and beta2-laminin. These two extracellular matrix molecules are differentially expressed, along with semaphorin 3A, by subsets of ensheathing cells in the ventral nerve layer of the olfactory bulb. The overlapping expression of these molecules creates an axon-sorting domain that is capable of promoting and repelling subsets of olfactory axons. Specifically, LCG(+) axons preferentially grow into the region of the nerve layer that expresses high amounts of galectin-1, beta2-laminin, and semaphorin 3A, whereas neuropilin-1(+) axons grow in a complementary pattern, avoiding the ventral nerve layer and projecting medially and laterally. These studies suggest that initial patterning of olfactory epithelium to olfactory bulb connections is, in part, dependent on extracellular components of the embryonic nerve layer that mediate convergence and divergence of specific axon subsets.

Age Factors↗
PubMed1988

Primary olfactory projections and the nervus terminalis in the African lungfish: implications for the phylogeny of cranial nerves.

Primary olfactory and central projections of the nervus terminalis were investigated by injections of horseradish peroxidase into the olfactory epithelium in the African lungfish. In addition, gonadotropin-releasing hormone (GnRH) immunoreactivity of the nervus terminalis system was investigated. The primary olfactory projections are restricted to the olfactory bulb located at the rostral pole of the telencephalon; they do not extend into caudal parts of the telencephalon. A vomeronasal nerve and an accessory olfactory bulb could not be identified. The nervus terminalis courses through the dorsomedial telencephalon. Major targets include the nucleus of the anterior commissure and the nucleus praeopticus pars superior. some fibers cross to the contralateral side. A few fibers reach the diencephalon and mesencephalon. No label is present in the "posterior root of the nervus terminalis" (= "Pinkus's nerve" or "nervus praeopticus"). GnRH immunoreactivity is lacking in the "anterior root of the nervus terminalis," whereas it is abundant in nervus praeopticus (Pinkus's nerve). These findings may suggest that the nervus terminalis system originally consisted of two distinct cranial nerves, which have fused-in evolution-in most vertebrates. Theories of cranial nerve phylogeny are discussed in the light of the assumed "binerval origin" of the nervus terminalis system.

Animals↗
PubMed1983

Association of substance-P-immunoreactive nerves with the murine olfactory mucosa.

Location and distribution of nerve fibers immunoreactive to substance P were studied in the mouse olfactory mucosa. A moderately dense plexus of fibers is present at the interface of the olfactory epithelium and the connective tissue of the lamina propria. In addition, many immunoreactive nerve fibers are noted in close association with Bowman's glands and blood vessels in the lamina propria. However, such fibers were not observed in olfactory epithelium proper nor in the fila olfactoria. Substance-P-immunoreactivity is almost totally abolished by treatment of animals with capsaicin, an agent known to deplete substance P from primary sensory neurons. It is suggested that the substance-P-immunoreactive fibers are of sensory origin, with their perikarya most likely located in the trigeminal ganglia. Functionally, they might influence local blood flow and/or the secretion of Bowman's glands.

Animals↗
PubMed2004

Selective neuroinhibitory effects of taurine in slices of rat main olfactory bulb.

Taurine is abundant in the main olfactory bulb, exceeding glutamate and GABA in concentration. In whole-cell patch-clamp recordings in rat olfactory bulb slices, taurine inhibited principal neurons, mitral and tufted cells. In these cells, taurine decreased the input resistance and caused a shift of the membrane potential toward the chloride equilibrium potential. The taurine actions were sustained under the blockade of transmitter release and were reversible and dose-dependent. At a concentration of 5 mM, typically used in this study, taurine showed 90% of its maximal effect. GABA(A) antagonists, bicuculline and picrotoxin, blocked the taurine actions, whereas the glycine receptor antagonist strychnine and GABA(B) antagonists, CGP 55845A and CGP 35348, were ineffective. These findings are consistent with taurine directly activating GABA(A) receptors and inducing chloride conductance. Taurine had no effect on periglomerular and granule interneurons. The subunit composition of GABA(A) receptors in these cells, differing from those in mitral and tufted cells, may account for taurine insensitivity of the interneurons. Taurine suppressed olfactory nerve-evoked monosynaptic responses of mitral and tufted cells while chloride conductance was blocked. This action was mimicked by the GABA(B) agonist baclofen and abolished by CGP 55845A; CGP 35348, which primarily blocks postsynaptic GABA(B) receptors, was ineffective. The taurine effect most likely was due to GABA(B) receptor-mediated inhibition of presynaptic glutamate release. Neither taurine nor baclofen affected responses of periglomerular cells. The lack of a baclofen effect implies that functional GABA(B) receptors are absent from olfactory nerve terminals that contact periglomerular cells. These results indicate that taurine decreases the excitability of mitral and tufted cells and their responses to olfactory nerve stimulation without influencing periglomerular and granule cells. Selective effects of taurine in the olfactory bulb may represent a physiologic mechanism that is involved in the inhibitory shaping of the activation pattern of principal neurons.

Animals↗