The novel gene glaikit, is expressed during neurogenesis in the Drosophila melanogaster embryo.
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A novel gene glaikit (gkt) has been identified which is expressed in the delaminating neuroblasts of the D. melanogaster embryonic central nervous system. At the earliest stages of embryonic development the expression of glaikit was ubiquitous, but by the time the neuroblasts are delaminating gkt expression became restricted to neuroblasts and a few ganglion mother cells. The gkt gene has no characterized homologues and encodes no previously described protein motifs. There are, however, evolutionary conserved predicted genes present in S. pombe, S. cerevisiae and C. elegans. Ectopic neuroblasts induced in either Notch or Delta mutant backgrounds also showed expression of glaikit. (+info)
Two orcokinins and the novel octapeptide orcomyotropin in the hindgut of the crayfish Orconectes limosus: identified myostimulatory neuropeptides originating together in neurones of the terminal abdominal ganglion.
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The tridecapeptides Asn(13)-orcokinin and Val(13)-orcokinin, two known members of the orcokinin neuropeptide family native to crustaceans, and a novel octapeptide, orcomyotropin, FDAFTTGFamide, have been identified from extracts of hindguts of the crayfish Orconectes limosus using an isolated hindgut contractility bioassay, high-performance liquid chromatography, microsequencing and mass spectrometry. All three peptides display strong inotropic actions on crayfish hindguts. Orcomyotropin showed higher potency than the two orcokinins. Threshold concentration was approximately 5 x 10(-12)mol l(-1)versus 10(-10)mol l(-1) for the two orcokinins. An approximately fivefold increase in contraction amplitude was observed with 10(-9)mol l(-1) orcomyotropin and 10(-7)mol l(-1) of the orcokinins. Asn(13)- and Val(13)-orcokinin did not differ significantly with regard to their biological effects. Semi-isolated crayfish hearts and locust oviducts did not respond to the three peptides. Immunocytochemistry using antisera against Asn(13)-orcokinin and orcomyotropin showed that these neuropeptides are co-localized in approximately 80-90 neurones of the terminal abdominal ganglion that have been shown to innervate the entire hindgut muscularis via the intestinal nerve. The neurones form elaborate terminal branches preferentially on longitudinal hindgut muscles. Orcomyotropin is a novel crustacean member of the GF-amide family of myotropic and/or allatotropic neuropeptides from annelids, molluscs and insects. (+info)
Sequence analysis of the leftward end of simian varicella virus (EcoRI-I fragment) reveals the presence of an 8-bp repeat flanking the unique long segment and an 881-bp open-reading frame that is absent in the varicella zoster virus genome.
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Simian varicella virus (SVV) causes varicella (chickenpox) in nonhuman primates, becomes latent in cranial and dorsal root ganglia, and reactivates to produce zoster (shingles). Because the clinical and molecular features of SVV closely resemble those of varicella zoster virus (VZV) infection of humans, SVV infection of primates has served as an experimental model of VZV pathogenesis and latency. The SVV genome has been completely mapped, but attempts to clone the 3600-bp EcoRI fragment located at the leftward end of the virus genome have hitherto been unsuccessful. Herein, we report the cloning and the complete nucleotide sequence of this region. Comparison of the SVV and VZV sequences in this region revealed an 8-bp inverted repeat sequence flanking the unique long segment of the SVV genome; an 879-bp open-reading frame (ORF) A in SVV that is absent in VZV but has 42% amino acid identity to SVV ORF 4 and 49% to VZV ORF 4; a 342-bp ORF B in SVV with 35% amino acid identity to a 387-bp ORF located to the left of ORF 1 on the VZV genome; and a 303-bp ORF in SVV with 27% amino acid identity to VZV ORF 1. No homologue of VZV ORF 2 was detected. Transcripts specific for ORFs A and B were present in SVV-infected cells in culture and in acutely infected monkey ganglia. Overall, there are more than 2000 bp of DNA in the SVV genome that are absent in the VZV genome. (+info)
The effects of minute direct electrical currents on cultured chick embryo trigeminal ganglia.
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The effects of low levels of electric current were determined on organ cultures of 6- to 19-day-old chick embryo trigeminal ganglia. Current levels ranged from 0.00115 to 11.5 nA/mm2; the time of electrical treatment varied from 2 h to 96 h. Low levels of electricity were found to have at least three major effects on this system of mixed cellular types: (1) Outgrowth of nerve fibers from the explant was enriched. This resulted in a greater number of fibers which were longer and more highly branched than those in control cultures. (2) Survival of neurons within the original explanted ganglion was enchanced by treatment with electricity. The presence of healthy neurons was found in 93.1% of the treated cultures and in 53.5% of untreated cultures. (3) Neurons, fibers and non-neural cells were stimulated to grow in the direction of the cathode. The rate of cathodal migration was calculated to be 0.1 mm/h (2.4 mm/day) in an explant from 12-day-old embryo. No differences were observed between surviving treated and control cultures in histochemical tests for acetycholinesterase. A similarity between the action of low levels of electrical current and nerve growth factor (NGF) is suggested. (+info)
The effects of antiviral therapy on the distribution of herpes simplex virus type 1 to ganglionic neurons and its consequences during, immediately following and several months after treatment.
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Both famciclovir (FCV) and valaciclovir (VACV) are potent inhibitors of herpes simplex virus type 1 (HSV-1) in a murine cutaneous infection model. The object of the present study was to determine whether either drug had an effect on the anatomical distribution of infected neurons in the peripheral nervous system and to assess the consequences for infected cells during, immediately following and several months after a 9 day period of continuous treatment. Mice were inoculated via the neck with a recombinant strain of HSV-1 expressing the lacZ reporter gene under the immediate-early gene promoter. Sensory ganglia were sampled daily up to day 11 post-inoculation (p.i.) and infected cells were detected by means of the reporter gene product. Ganglia were also removed at 1.5 and 10 months p.i. and latency was assessed by explant co-cultivation and by using in situ hybridization to detect LAT-expressing neurons. While both drugs reduced the severity of acute infection markedly, neither compound completely prevented the relentless distribution of infection among peripheral nervous tissue. Furthermore, there was a difference between the compounds regarding the expression of the reporter gene during and after termination of treatment and in the number of residual LAT-positive neurons. (+info)
Pax3 is required for enteric ganglia formation and functions with Sox10 to modulate expression of c-ret.
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Hirschsprung disease and Waardenburg syndrome are human genetic diseases characterized by distinct neural crest defects. Patients with Hirschsprung disease suffer from gastrointestinal motility disorders, whereas Waardenburg syndrome consists of defective melanocyte function, deafness, and craniofacial abnormalities. Mutations responsible for Hirschsprung disease and Waardenburg syndrome have been identified, and some patients have been described with characteristics of both disorders. Here, we demonstrate that PAX3, which is often mutated in Waardenburg syndrome, is required for normal enteric ganglia formation. Pax3 can bind to and activate expression of the c-RET gene, which is often mutated in Hirschsprung disease. Pax3 functions with Sox10 to activate transcription of c-RET, and SOX10 mutations result in Waardenburg-Hirschsprung syndrome. Thus, Pax3, Sox10, and c-Ret are components of a neural crest development pathway, and interruption of this pathway at various stages results in neural crest-related human genetic syndromes. (+info)
Functional interdependence of neurons in a single canine intrinsic cardiac ganglionated plexus.
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To determine the activity characteristics displayed by different subpopulations of neurons in a single intrinsic cardiac ganglionated plexus, the behaviour and co-ordination of activity generated by neurons in two loci of the right atrial ganglionated plexus (RAGP) were evaluated in 16 anaesthetized dogs during basal states as well as in response to increasing inputs from ventricular sensory neurites. These sub-populations of right atrial neurons received afferent inputs from sensory neurites in both ventricles that were responsive to local mechanical stimuli and the nitric oxide donor nitroprusside. Neurons in at least one RAGP locus were activated by epicardial application of veratridine, bradykinin, the beta1-adrenoceptor agonist prenaterol or glutamate. Epicardial application of angiotensin II, the selective beta2-adrenoceptor agonist terbutaline and selective alpha-adrenoceptor agonists elicited inconsistent neuronal responses. The activity generated by both populations of atrial neurons studied over 5 min periods during basal states displayed periodic coupled behaviour (cross-correlation coefficients of activities that reached, on average, 0.88 +/- 0.03; range 0.71-1) for 15-30 s periods of time. These periods of coupled activity occurred every 30-50 s during basal states, as well as when neuronal activity was enhanced by chemical activation of their ventricular sensory inputs. These results indicate that neurons throughout one intrinsic cardiac ganglionated plexus receive inputs from mechano- and chemosensory neurites located in both ventricles. That such neurons respond to multiple chemical stimuli, including those liberated from adjacent adrenergic efferent nerve terminals, indicates the complexity of the integrative processing of information that occurs within the intrinsic cardiac nervous system. It is proposed that the interdependent activity displayed by populations of neurons in different regions of one intrinsic cardiac ganglionated plexus, responding as they do to multiple cardiac sensory inputs, forms the basis for integrated regional cardiac control. (+info)
CALEB binds via its acidic stretch to the fibrinogen-like domain of tenascin-C or tenascin-R and its expression is dynamically regulated after optic nerve lesion.
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Recently, we described a novel chick neural transmembrane glycoprotein, which interacts with the extracellular matrix proteins tenascin-C and tenascin-R. This protein, termed CALEB, contains an epidermal growth factor-like domain and appears to be a novel member of the epidermal growth factor family of growth and differentiation factors. Here we analyze the interaction between CALEB and tenascin-C as well as tenascin-R in more detail, and we demonstrate that the central acidic peptide segment of CALEB is necessary to mediate this binding. The fibrinogen-like globe within tenascin-C or -R enables both proteins to bind to CALEB. We show that two isoforms of CALEB in chick and rodents exist that differed in their cytoplasmic segments. To begin to understand the in vivo function of CALEB and since in vitro antibody perturbation experiments indicated that CALEB might be important for neurite formation, we analyzed the expression pattern of the rat homolog of CALEB during development of retinal ganglion cells, after optic nerve lesion and during graft-assisted retinal ganglion cell axon regeneration by in situ hybridization. These investigations demonstrate that CALEB mRNA is dynamically regulated after optic nerve lesion and that this mRNA is expressed in most developing and in one-third of the few regenerating (GAP-43 expressing) retinal ganglion cells. (+info)