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PubMedDate not supplied

A rapid screening measure for the identification of visuospatial learning disability in schools.

Verbal and nonverbal forms of developmental learning disabilities have been reported. Whereas there are several instruments for evaluating children for the presence of verbal learning disabilities at school, no screening tool is available to identify children who have nonverbal learning disabilities. This study aimed at devising and validating a short screening questionnaire that can be used by teachers in primary schools to identify those children who need to be referred for clinical services because they have a visuospatial learning disability (VSLD). An 18-item Shortened Visuospatial Questionnaire (SVS) was derived from an earlier, longer version. Its validation procedure was twofold and was achieved by (a) verifying that children who had been identified with the SVS questionnaire as having a VSLD actually showed visuospatial deficits on psychometric evaluation and by (b) rating with the SVS a clinically identified population of children with VSLD. The results of the validation procedure showed that the SVS is a quick, reliable, and valid instrument that may be helpful in identifying children with VSLD in primary school.

Adolescent↗

PubMed2006

How neurosecretory vesicles release their cargo.

Neurons and related cell types often contain two major classes of neurosecretory vesicles, synaptic vesicles (SVs) and dense-core granules (DCGs), which store and release distinct cargo. SVs store and release classic neurotransmitters, which facilitate propagation of action potentials across the synaptic cleft, whereas DCGs transport, store, and release hormones, proteins, and neuropeptides, which facilitate neuronal survival, synaptic transmission, and learning. Over the past few years, there has been a major surge in our understanding of many of the key molecular mechanisms underlying cargo release from SVs and DCGs. This surge has been driven largely by the use of fluorescence microscopy (especially total internal reflection fluorescence microscopy) to visualize SVs or DCGs in living cells. This review highlights some of the recent insights into cargo release from neurosecretory vesicles provided by fluorescence microscopy, with emphasis on DCGs.

Animals↗

PubMed2003

Autosomal dominant growth hormone deficiency disrupts secretory vesicles in vitro and in vivo in transgenic mice.

Autosomal dominant GH deficiency type II (IGHDII) is often associated with mutations in the human GH gene (GH1) that give rise to products lacking exon-3 ((Deltaexon3)hGH). In the heterozygous state, these act as dominant negative mutations that prevent the release of human pituitary GH (hGH). To determine the mechanisms of these dominant negative effects, we used a combination of transgenic and morphological approaches in both in vitro and in vivo models. Rat GC cell lines were generated expressing either wild-type GH1 (WT-hGH-GC) or a genomic GH1 sequence containing a G->A transition at the donor splice site of IVS3 ((Deltaexon3)hGH-GC). WT-hGH-GC cells grew normally and produced equivalent amounts of human and rGH packaged in dense-cored secretory vesicles (SVs). In contrast, (Deltaexon3)hGH-GC cells showed few SVs but accumulated secretory product in amorphous cytoplasmic aggregates. They produced much less rGH and grew more slowly than WT-hGH-GC cells. When cotransfected with an enhanced green fluorescent protein construct (GH-eGFP), which copackages with GH in SVs, WT-hGH-GC cells showed normal electron microscopy morphology and SV movements, tracked with total internal reflectance fluorescence microscopy. In contrast, coexpression of (Deltaexon3)hGH with GH-eGFP abolished the vesicular targeting of GH-eGFP, which instead accumulated in static aggregates. Transgenic mice expressing (Deltaexon3)hGH in somatotrophs showed an IGHD-II phenotype with mild to severe pituitary hypoplasia and dwarfism, evident at weaning in the most severely affected lines. Hypothalamic GHRH expression was up-regulated and somatostatin expression reduced in (Deltaexon3)hGH transgenic mice, consistent with their profound GHD. Few SVs were detectable in the residual pituitary somatotrophs in (Deltaexon3)hGH transgenic mice, and these cells showed grossly abnormal morphology. A low copy number transgenic line showed a mild effect relatively specific for GH, whereas two severely affected lines with higher transgene copy numbers showed early onset, widespread pituitary damage, macrophage invasion, and multiple hormone deficiencies. These new in vitro and in vivo models shed new light on the cellular mechanisms involved in IGHDII, as well as its phenotypic consequences in vivo.

Animals↗

PubMed2002

Expression of growth hormone-releasing hormone and its receptor splice variants in human prostate cancer.

Antagonists of GHRH inhibit the growth of various human tumors, including prostate cancer, but the tumoral receptors mediating the antiproliferative effect of GHRH antagonists have not been clearly identified. Recently, we demonstrated that human cancer cell lines express splice variants (SVs) of receptors for GHRH, of which SV1 exhibits the greatest similarity to the pituitary GHRH receptors. In this study we investigated the expression of GHRH and SVs of GHRH receptor and the binding characteristics of the GHRH receptor isoform in 20 surgical specimens of organ-confined and locally advanced human prostatic adenocarcinomas. The mRNA expression of GHRH and SVs of GHRH receptor was investigated by RT-PCR. The affinity and density of receptors for GHRH were determined by ligand competition assays based on binding of (125)I-labeled GHRH antagonist JV-1-42 to tumor membranes. Twelve of 20 tumors (60%) exhibited specific, high affinity binding for JV-1-42, with a mean dissociation constant (K(d)) of 0.81 nmol/liter and a mean maximal binding capacity of 185.2 fmol/mg membrane protein. The mRNA of SV1 was detected in 13 of 20 (65%) prostate cancer specimens and was consistent with the presence of GHRH binding. RT-PCR analyses also revealed the expression of mRNA for GHRH in 13 of 15 (86%) prostatic carcinoma specimens examined. The presence of GHRH and its tumoral receptor SVs in prostate cancers suggests the possible existence of an autocrine mitogenic loop. The antitumor effects of GHRH antagonists in prostate cancer could be exerted in part by interference with this local GHRH system.

Adenocarcinoma↗

PubMed2001

Relationship between expression of sex steroid receptors and structure of the seminal vesicles after neonatal treatment of rats with potent or weak estrogens.

In this study we evaluated the effect of manipulating the estrogen and androgen environment of the neonatal male rat on subsequent immunoexpression of sex steroid receptors in the seminal vesicles (SVs) at age 18 days. The aim was to establish to what extent such changes were associated with and predictive of changes in SV structure/composition. Treatments were either diethylstilbestrol (DES; 10, 1, or 0.1 microg/injection), ethinyl estradiol (EE; 10 microg/injection), tamoxifen (2 mg/kg/day), flutamide (50 mg/kg), a gonadotropin-releasing hormone antagonist (GnRHa; 10 mg/kg), genistein (4 mg/kg/day), octylphenol (2 mg/injection), or bisphenol A (0.5 mg/injection). Compared with controls, treatment with DES (10 microg) induced loss of epithelial and stromal androgen receptor (AR) immunoexpression coincident with induction of stromal progesterone receptor (PR) immunoexpression and upregulation of stromal immunoexpression of estrogen receptor-alpha (ERalpha). These changes were associated with gross distortion (increase) of the normal stromal:epithelial tissue proportions in the SVs. DES (1 microg) and EE induced similar but less pronounced changes, and DES (0.1 microg) had no noticeable effect. Tamoxifen and flutamide induced PR and slightly upregulated ERalpha immunoexpression but had only a minor or no effect on AR expression and the stromal:epithelial ratio, though flutamide retarded normal development of the SVs. The latter was also evident in GnRHa-treated males, but otherwise this treatment had no effect on AR and PR immunoexpression. None of the foregoing treatments had any detectable effect on the immunoexpression of ERss in stromal or epithelial cells. The major treatment-induced changes in immunoexpression of AR, PR, and ERalpha and lack of change in ERss were confirmed by Western blots of SV protein extracts. None of the three weak (environmental) estrogens tested caused any detectable change in sex steroid receptor immunoexpression or SV tissue composition. We conclude that treatment-induced loss of AR is a prerequisite for altered stromal:epithelial proportions in the SVs and that such loss is always associated with induction of PR and upregulation of ERalpha; the latter two changes are insufficient on their own to bring about such a change. Nevertheless, induction of PR expression was always associated with altered SV development and is a potentially useful marker because it is not normally expressed in male reproductive tissues.

Animals↗

PubMed1995

Combined cisternal drainage and intrathecal urokinase injection therapy for prevention of vasospasm in patients with aneurysmal subarachnoid hemorrhage.

The effect of cisternal drainage and intrathecal urokinase injection in preventing symptomatic vasospasm (SVS) after aneurysmal subarachnoid hemorrhage was studied in 60 patients with uniform background (Hunt & Kosnik grade III, younger than 70 yrs, undergoing surgery within 72 hrs after hemorrhage). The incidence of permanent neurological deficits caused by vasospasm was 5/16 without cisternal drainage, 5/34 with drainage alone, and 1/10 with drainage and urokinase injection. Analysis of patients without postoperative cisternal drainage showed the amount of subarachnoid clot on the initial computed tomographic scan was closely related to the occurrence of SVS (p < 0.05, unpaired t test). Analysis of patients with cisternal drainage showed the amount of bloody cerebrospinal fluid (CSF) drained during the 10 days after surgery and the duration of drainage placement were critical in preventing vasospasm (p < 0.05, unpaired t test). Greater CSF drainage significantly reduced the incidence of permanent neurological deficits caused by vasospasm (p < 0.01, chi 2), but significantly increased the incidence of hydrocephalus requiring shunt procedures (p < 0.01, chi 2). Urokinase injection via cisternal drainage achieved a further reduction in the occurrence of SVS. Intrathecal thrombolytic therapy after aneurysmal surgery is an effective method for SVS prophylaxis, and CSF drainage (> 1500 ml for 10 days) enhances the effect.

Brain↗

PubMed1983

A comparative study of neurotic depression in symptomatic volunteers and psychiatric patients.

A comparative study of neurotic depression in 66 symptomatic community volunteers (SVs) and 43 formal psychiatric patients is reported. Compared to the psychiatric patients the SVs were older and there was a less marked female preponderance. Thier depression was of a longer duration and vegetative symptoms (e.g. appetite and weight loss) were less marked. They were less likely to have made a suicide attempt in the past, less likely to be single or divorced, and much less likely to have experienced a disruption in an intimate relationship in the preceding year. On personality measures the SVs rated as having a more internal locus of control and a higher self-esteem. An Index of Definition cut-off point of 5 or more on the PSE for a neurotic depressive 'case' is supported by the finding that only 2% of the patients, compared with 26% of the SVs, did not rate as 'cases'.

Adult↗

PubMedDate not supplied

Evaluation of the evidence for ion channels in synaptic vesicles.

Synaptic vesicles (SVs) have been the focus of much research for many years, however only recently have ion channels from SV membranes been reported. There is now convincing evidence that SVs contain ion channels. This conclusion is based on direct experimental results from several different laboratories using the patch clamp or planar lipid bilayer technique on SVs and neurosecretory granules (NSG). Some limitations of patch clamping and of fusing synamptic vesicles to a bilayer are described and the advantages of the nystatin/ergosterol fusion method are presented. Six different channels appear to exist in SV (or NSG) membranes. Two large channels (250 and 154 pS) have been observed in SVs isolated from mammalian brain, two channels (180 and 13 pS) from Torpedo electric organ, and two channels (130 and 30-40 pS) from NSG. The three larger channels from each set (250, 180 and 130 pS7) are novel in that they have a subconductance state. The 154 pS channel has been identified as synaptophysin but the identity and function of the other channels is unknown. Although some of the channels are gated by voltage, only the 130 pS channel is modulated by Ca2+. Further knowledge of what regulates these channels is mandatory if we are to determine the physiological significance of these channels.

Animals↗

PubMed2002

Serotonin stimulates phosphorylation of Aplysia synapsin and alters its subcellular distribution in sensory neurons.

Only a small fraction of neurotransmitter-containing synaptic vesicles (SVs), the readily releasable pool, is available for fast Ca(2+)-induced release at any synapse. Most SVs are sequestered at sites away from the plasma membrane and cannot be exocytosed directly. Recruitment of SVs to the releasable pool is thought to be an important component of short-term synaptic facilitation by serotonin (5-HT) at Aplysia sensorimotor synapses. Synapsins are associated with SVs and hypothesized to play a central role in the regulation of SV mobilization in nerve terminals. Aplysia synapsin was cloned to examine its role in synaptic plasticity at the well characterized sensorimotor neuron synapse of this animal. Acute 5-HT treatment of ganglia induced synapsin phosphorylation. Immunohistochemical analyses of cultured Aplysia neurons revealed that synapsin is distributed in distinct puncta in the neurites. These puncta are rapidly dispersed after treatment of the neurons with 5-HT. The dispersion of synapsin puncta by 5-HT was fully reversible after washout of the modulator. Both 5-HT-induced phosphorylation and dispersion of synapsin were mediated, at least in part, by cAMP-dependent protein kinase and mitogen-activated protein kinase. These experiments indicate that synapsin and its regulation by 5-HT may play an important role in the modulation of SV trafficking in short-term synaptic plasticity.

Animals↗

PubMed2005

[Syndromes of overdrainage of ventricular shunting in childhood hydrocephalus].

Overdrainage in ventricular shunting constitutes a difficult to prevent and to treat complication. The authors reviewed a retrospective series of 512 children submitted to a ventricular shunting procedure aimed at analysing factors influencing this type of complication. The causes for the hydrocephalus were congenital (n=172), post-myelomeningocele (n=123), posthemorrhagic (n=103), tumoral (n=64), postmeningitis (n=40) and posttraumatic (n=10). Eighty-eight children (17.8%) evolved with a complication related to the excessive function of the valve. The authors investigated the relationship between hydrocephalus' etiology and type of overdrainage syndromes. The most frequent complication was ventricular catheter block (n=50), followed by symptomatic slit ventricle syndrome (SVS) (n=19), subdural hematoma (n=10) and trapped fourth ventricle (n=9). There were no statistical differences regarding complications for each etiologic subset of hydrocephalus. SVS occurred in 19 children (3.71%), a low rate according to the current literature. Posthemorrhagic and postinfectious hydrocephalus grouped together showed a higher rate of SVS (p=0.005), a feature that we attributed to the cerebral destruction caused by these two conditions. Treatment of SVS was complex and required diverse procedures, applied in an escalated way, which included five decompressive craniectomies. The authors suggest avoiding, as much as possible, the use of ventricular shunts, and recommend the alternative use of new technology valves and neuroendoscopic procedures.

Cerebrospinal Fluid Shunts↗

PubMed2005

The "interfascial" veins of the lower limbs.

The veins of the lower limb are commonly divided in deep and superficial ones according to their position with respect to the Muscular Fascia (MF). Anatomical textbooks affirm that all superficial veins are thin walled vessels that run in a yielding layer of fat. Accordingly, no differences between saphenous Veins (SVs) and their tributaries (TVs) are reported by physiologists and pathophysiologists. On the contrary, the SVs do not correspond to the classic anatomic, physiologic and clinical descriptions of the "superficial" veins. In fact, the SVs: 1) are not superficial because they course between the SF and the MF; 2) they are not thin vessels, being their wall thick and rich in muscular cells; 3) they actively contribute to the complex mechanisms of venous return from the lower limbs; and finally, 4) they are quite resistant to hypertension and usually afflicted with limited varicose changes. As a consequence, the SVs should not be longer considered "real" superficial veins and the venous bed of the lower limb would be better represented by a three-layered model.

Adipose Tissue↗

PubMed1987

Scintigraphic evaluation of brain death: significance of sagittal sinus visualization.

Radiotracer scintigraphy has been commonly used in this country to confirm and document the clinical diagnosis of brain death. Whether the presence of radiotracer activity in the region of sagittal venous sinus (SVS) represents actual blood flow to the brain in the absence of demonstrable cerebral arterial flow remains a controversial issue. Our retrospective study was performed to review the significance of such sagittal tracer activity. Of the 53 patients showing no cerebral arterial flow, 26 showed tracer activity in the region of SVS. The clinical status, EEG findings, and outcome of all 53 patients were the same irrespective of the presence or absence of SVS tracer activity. We conclude that the mere presence of SVS in the absence of demonstrable cerebral arterial flow activity is not clinically significant and does not contradict the diagnosis of brain death.

Brain Death↗

PubMed1993

Synaptotagmin: a membrane constituent of neuropeptide-containing large dense-core vesicles.

Synaptotagmin is known to be a major membrane protein of synaptic vesicles (SVs) in neurons. We have now used an immunoisolation procedure to demonstrate that synaptotagmin is also present in the membranes of peptide containing large dense-core vesicles (LDCVs) of rat hypothalamus and bovine posterior pituitary. Synaptotagmin bead-immunoisolated organelles from these tissues primarily consisted of SVs but contained occasionally larger structures reminiscent of LDCVs that were absent from vesicle populations immunoisolated with a synaptophysin antibody. Furthermore, the vesicles immunoisolated with synaptotagmin beads contained significant amounts of neuropeptide Y (NPY). In contrast, vesicles immunoisolated with synaptophysin beads did not contain detectable levels of NPY. Sucrose density gradient fractionation of postnuclear supernatants obtained from the bovine posterior pituitary resulted in a bimodal distribution of synaptotagmin, corresponding to the positions of both SVs and neurosecretory granules. A similar distribution was found for cytochrome b561 and the 116 kDa subunit of the vacuolar proton pump. In contrast, the SV proteins synaptophysin, SV2, and p29 were restricted to the SV-containing fractions. Immunoisolation of small and large vesicles from the sucrose gradient confirmed the differential distribution of synaptotagmin and synaptophysin in the two types of secretory vesicles in nerve endings of the posterior pituitary. We conclude that synaptotagmin is a constituent of both SVs and peptide-containing secretory vesicles in the nervous system. Since both types of organelles undergo Ca(2+)-dependent exocytosis, these findings support a general role of synaptotagmin as an exocytotic Ca2+ receptor.

Animals↗

PubMed1997

Post-transcriptional regulation of synaptic vesicle protein expression and the developmental control of synaptic vesicle formation.

The regulated expression of synaptic vesicle (SV) proteins during development and the assembly of these proteins into functional SVs are critical aspects of nervous system maturation. We have examined the expression patterns of four SV proteins in embryonic hippocampal neurons developing in culture and have found that increases in the levels of these proteins result primarily from post-transcriptional regulation. Synaptotagmin I, vamp 2, and synapsin I proteins are synthesized at nearly constant rates as the neurons develop. However, these proteins are relatively unstable at early times in culture and undergo a progressive increase in half-life with time, possibly as a result of an increase in the efficiency with which they are incorporated into SVs. In contrast, synaptophysin is synthesized at a very low rate at early times in culture, and its rate of synthesis increases dramatically with time. The increase in synaptophysin synthesis is not simply the result of an increase in mRNA level, but is largely attributable to an increase in the rate of translational initiation. Despite the nearly constant rates of synthesis of synaptotagmin I, vamp 2, and synapsin I, we show that the number of SVs in these developing neurons increases, and that SV proteins are more efficiently targeted to SVs at later times in culture. Our results suggest that SV production during development is not limited by the rates of transcription of genes encoding the component proteins, thus allowing control of this process by cytoplasmic mechanisms, without signaling to the nucleus.

Animals↗

PubMed1983

Morphological changes in neuromuscular junctions during exercise.

Long lasting exercise produces several morphological changes in teleostean neuromuscular junctions (NJs), consisting of progressive synaptic vesicles (SVs) depletion and lamellar branching of the nerve endings. Exercised fishes kept swimming during 1 hr against a 3.5 1/min flow of oxygenated water in spite of the fact that the number of SVs was reduced in about 70% after 10 min of exercise. This observation indicates that the SVs formation fails to restore their original number and consequently, under such circumstances, the transmitter release may occur by a different mechanism.

Animals↗

PubMed1988

Ultrastructural reversible changes in fish neuromuscular junctions after chronic exercise.

Neuromuscular junctions (NJs) of fin muscles of teleostean fishes, Lebistes reticulatus, were ultrastructurally analyzed during 60 min of chronic exercise and a subsequent period of 90 min of induced recovery. NJs from 30-min-exercised fishes showed an almost complete depletion of synaptic vesicles (SVs), corresponding to 83% of SV consumption; 76% of axon terminals were branched at the end of this period. During the recovery period, it was possible to observe the reversibility of the changes induced by the exercise and the transitory events that lead to the reacquirement of the normal NJ morphology. After 15 min of rest, SV population increased to a value of 54.6 SVs/micron2 and the percentage of branched axons was 66.5%. At 60 min of recovery the number of SVs reached a value of 84.6 SVs/micron2. The SV population was fully reestablished at 80 min of rest, while the percentage of branched axons was found within normal ranges after 90 min of recovery. These results demonstrate that chronic exercise induced physiological depletion of NJ SVs and other axon terminal morphological changes, as well as that postexercise rest induces the reestablishment of the normal NJ morphology.

Animals↗

PubMed1987

Ultrastructure and immunohistochemistry of the lateral prostate in aged rats.

Ultrastructural, histological, and immunohistochemical studies were performed on lateral prostates of 1) aged rats from different strains, 2) rats permitted different levels of sexual activity, and 3) castrated rats. Antibodies against the following proteins were used as immunohistochemical markers: SVS II from seminal vesicle, LP 28 from lateral prostate, acid phosphatase isoenzymes from ventral prostate, transglutaminase from coagulating gland, and a commercial monoclonal antibody against cytokeratin. SVS II is a marker of lateral prostatic secretion, while immunoreactions to LP 28 and acid phosphatase (pI 7.1) were cytoplasmic. In aged animals the amount of intracellular secretion is decreased, and focally metaplastic transformation can be visualized by using immunohistochemical markers. Epithelial ultrastructure varied considerably with experimental conditions. Intensive sexual activity resulted in increased polymorphism and increased number of secretory granules within the glandular cells, while castration was followed by a rapid loss of secretory material. Also, in rats older than 10 months, a reduction in the number of secretion granules was common. The epithelium developed a positive immunoreaction to transglutaminase antibodies that were not observed in juvenile glands. Cells, presumably macrophages, which had an intense immunoreactivity for transglutaminase, were increased in number both within and outside the prostatic acini of aged rats. The possible interaction between secretory SVS II, a substrate of transglutaminase, the release of this enzyme from macrophages or its reflux from coagulating glands, the spontaneous cellular exfoliation that is due to decreased androgen levels, and dietary noxae may be of importance in the development of lateral prostatic nonbacterial inflammation in aged rats.

Acid Phosphatase↗

PubMed1996

Induction of seminal vesicle morphogenesis from dog epididymal epithelium.

A number of carnivores, including the dog, do not have seminal vesicles (SVs). They have been induced experimentally by heterotypic recombination of adult dog epididymal epithelium with mesenchyme of neonatal rat SV and allowed to grow for 4 weeks under the renal capsule of male athymic nude mice. The induced SVs bore a striking similarity to rat SV both histologically and ultrastructurally. However, they secreted proteins which were different from those in the rat SV and reacted negatively to antibodies specific to rat SV secretory proteins and dog prostate secretory proteins. The results strongly suggested that the glands induced from dog epididymal epithelium were likely to be "dog" SVs.

Animals↗