scholarly journals Cutaneous overexpression of NT-3 increases sensory and sympathetic neuron number and enhances touch dome and hair follicle innervation.

1996 ◽  
Vol 134 (2) ◽  
pp. 487-497 ◽  
Author(s):  
K M Albers ◽  
T N Perrone ◽  
T P Goodness ◽  
M E Jones ◽  
M A Green ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Sympathetic Neurons ◽  
Sympathetic Neuron ◽  
Nerve Fibers ◽  
Target Tissue ◽  
Cross Sectional ◽  
Touch Dome ◽  
Sensory Endings

Target-derived influences of nerve growth factor on neuronal survival and differentiation are well documented, though effects of other neurotrophins are less clear. To examine the influence of NT-3 neurotrophin overexpression in a target tissue of sensory and sympathetic neurons, transgenic mice were isolated that overexpress NT-3 in the epidermis. Overexpression of NT-3 led to a 42% increase in the number of dorsal root ganglia sensory neurons, a 70% increase in the number of trigeminal sensory neurons, and a 32% increase in sympathetic neurons. Elevated NT-3 also caused enlargement of touch dome mechanoreceptor units, sensory end organs innervated by slowly adapting type 1 (SA1) neurons. The enlarged touch dome units of the transgenics had an increased number of associated Merkel cells, cells at which SA1s terminate. An additional alteration of skin innervation in NT-3 transgenics was an increased density of myelinated circular endings associated with the piloneural complex. The enhancement of innervation to the skin was accompanied by a doubling in the number of sensory neurons expressing trkC. In addition, measures of nerve fibers in cross-sectional profiles of cutaneous saphenous nerves of transgenics showed a 60% increase in myelinated fibers. These results indicate that in vivo overexpression of NT-3 by the epidermis enhances the number of sensory and sympathetic neurons and the development of selected sensory endings of the skin.

scholarly journals Susceptibility of sensory neurons to apoptosis following infection by bovine herpesvirus type 1

2002 ◽  
Vol 83 (9) ◽  
pp. 2257-2267 ◽  
Author(s):  
Gustavo A. Delhon ◽  
Marcelo J. González ◽  
Pablo R. Murcia
Keyword(s):  
Dna Replication ◽  
Dna Fragmentation ◽  
Sensory Neurons ◽  
Bovine Herpesvirus ◽  
Viral Dna ◽  
Viral Dna Replication ◽  
Herpesvirus Type ◽  
Bovine Herpesvirus Type 1

Like other members of the alpha subfamily of herpesviruses, bovine herpesvirus type 1 (BHV-1) establishes latent infections in sensory neurons. BHV-1 induces apoptosis in lymphoid cells in vivo and in epithelial cell lines, but the ability of BHV-1 to induce apoptosis in sensory neurons remains unknown. In this report, the susceptibility of rabbit ganglionic neurons to infection by BHV-1 was examined in vitro and in vivo. Following infection of cultured neurons with BHV-1, hallmarks of apoptosis such as chromatin condensation, DNA fragmentation and membrane blebbing were detected. The appearance of these changes was preceded by active viral DNA replication as determined by in situ hybridization. When viral DNA replication was blocked by treatment of cultures with an inhibitor of eukaryotic DNA polymerases, apoptosis but not virus attachment to neurons or bICP0 gene expression was completely prevented. Taken together, these results demonstrate that sensory neurons are not intrinsically resistant to BHV-1-induced apoptosis and that viral DNA replication plays a role in triggering the apoptotic programme. Infection of rabbits with BHV-1 resulted in pathological changes in the trigeminal ganglia (TG) which included mononuclear cell infiltration and neuronophagia. Morphological evidence of apoptosis was not detected in neurons, even in cells with advanced cytophatology. Furthermore, whereas DNA fragmentation was common in infiltrating cells, it was very rare and sporadic in neurons. Therefore, mechanisms in the TG should exist to prevent neuronal apoptosis upon BHV-1 infection.

Cholinergic neuronal differentiation factors: evidence for the presence of both CNTF-like and non-CNTF-like factors in developing rat footpad

Development ◽  
1992 ◽  
Vol 114 (3) ◽  
pp. 689-698 ◽  
Author(s):  
H. Rohrer
Keyword(s):  
Sympathetic Neurons ◽  
Immunohistochemical Analysis ◽  
Sympathetic Neuron ◽  
Sweat Glands ◽  
Target Tissue ◽  
Differentiation Factors ◽  
Inducing Factors ◽  
Developing Rat ◽  
Transmitter Phenotype

Catecholaminergic sympathetic neurons are able to change their transmitter phenotype during development and to acquire cholinergic properties. Cholinergic sympathetic differentiation is only observed in fibers innervating specific targets like the sweat glands in the rat footpad. A function for ciliary neurotrophic factor (CNTF) in this process has been implied as it is able to induce cholinergic properties (ChAT, VIP) in cultured chick and rat neurons. We show here that a CNTF-like, VIP-inducing activity is present in rat footpads and that its increases 6-fold during the period of cholinergic sympathetic differentiation. Immunohistochemical analysis of P21 rat footpads demonstrated CNTF-like immunoreactivity in Schwann cells but not in sweat glands, the target tissue of cholinergic sympathetic neurons. The expression of this factor in footpads seems to be dependent on the presence of intact nerve axons, as nerve transection results in a loss of CNTF-like cholinergic activity and immunoreactivity. Immunoprecipitation experiments with rat footpad extracts provided evidence for the presence of ChAT-inducing factors other than CNTF, which may independently or together with CNTF be involved in the determination of sympathetic neuron phenotype.

scholarly journals Regulation of nerve growth factor receptor gene expression in sympathetic neurons during development.

1995 ◽  
Vol 130 (6) ◽  
pp. 1435-1446 ◽  
Author(s):  
S Wyatt ◽  
A M Davies
Keyword(s):  
Mrna Expression ◽  
Sensory Neurons ◽  
Sympathetic Neurons ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Early Developmental Stage ◽  
Mrna Levels ◽  
Fos Expression

We used quantitative reverse transcription (RT)/PCR to study the regulation of p75 mRNA and trkA mRNA expression in the developing sympathetic neurons of the mouse superior cervical sympathetic ganglion (SCG) in vivo and in vitro. At E13, the SCG contains proliferating cells that express many features of differentiated neurons. These immature neurons survived in culture without NGF, and NGF did not induce c-fos expression. Low levels of p75 and trkA mRNAs were expressed at this stage in vivo. There was no significant increase in the level of either trkA mRNA or p75 mRNA in E13 control cultures up to 72 h in vitro, and neither NGF nor depolarizing levels of K+ ions (40 mM KC1) affected the expression of trkA mRNA. In E14 cultures, NGF induced c-fos expression in 10-15% of the neurons and enhanced the survival of a similar percentage of neurons. The proportion of neurons responding to NGF increased with age, reaching 90% in E18 cultures. The in vivo level of trkA mRNA increased markedly from E14 onward, but in contrast to sensory neurons (in which p75 and trkA mRNA levels increase in parallel), the level of trkA mRNA initially increased far more rapidly than that of p75 mRNA. After E17, the level of p75 mRNA increased rapidly and approached that of trkA mRNA postnatally, but at no stage did this exceed the level of trkA mRNA. In E14 cultures, the level of trkA mRNA increased in the absence of neurotrophins or 40 mM KC1. The level of p75 mRNA in E14 cultures was enhanced by NGF but was unaffected by 40 mM KC1. Our findings show that NGF receptor expression during the earliest stages of sympathetic neuron development is not affected by depolarization but indicate that by an early developmental stage (between E13 and E14 in vivo), sympathetic neurons become specified to upregulate trkA mRNA in culture independently of added factors. In addition, our findings reveal several distinctive features of p75 mRNA and trkA mRNA expression in sympathetic neurons compared with sensory neurons and provide a plausible explanation for previously observed differences in the effects of a p75 null mutation on the response of sensory and sympathetic neurons during embryonic and postnatal development.

The transcription factor dHAND is a downstream effector of BMPs in sympathetic neuron specification

Development ◽  
2000 ◽  
Vol 127 (18) ◽  
pp. 4073-4081 ◽  
Author(s):  
M.J. Howard ◽  
M. Stanke ◽  
C. Schneider ◽  
X. Wu ◽  
H. Rohrer
Keyword(s):  
Transcription Factor ◽  
Bone Morphogenetic Proteins ◽  
Sympathetic Neurons ◽  
Sympathetic Neuron ◽  
Sympathetic Ganglia ◽  
Catecholaminergic Neurons ◽  
Helix Loop Helix ◽  
Downstream Effector

The dHAND basic helix-loop-helix transcription factor is expressed in neurons of sympathetic ganglia and has previously been shown to induce the differentiation of catecholaminergic neurons in avian neural crest cultures. We now demonstrate that dHAND expression is sufficient to elicit the generation of ectopic sympathetic neurons in vivo. The expression of the dHAND gene is controlled by bone morphogenetic proteins (BMPs), as suggested by BMP4 overexpression in vivo and in vitro, and by noggin-mediated inhibition of BMP function in vivo. The timing of dHAND expression in sympathetic ganglion primordia, together with the induction of dHAND expression in response to Phox2b implicate a role for dHAND as transcriptional regulator downstream of Phox2b in BMP-induced sympathetic neuron differentiation.

scholarly journals TrkA mediates developmental sympathetic neuron survival in vivo by silencing an ongoing p75NTR-mediated death signal

2001 ◽  
Vol 155 (7) ◽  
pp. 1275-1286 ◽  
Author(s):  
Marta Majdan ◽  
Gregory S. Walsh ◽  
Raquel Aloyz ◽  
Freda D. Miller
Keyword(s):  
Sympathetic Neurons ◽  
Sympathetic Neuron ◽  
Neurotrophin Receptor ◽  
Primary Neurons ◽  
P75 Neurotrophin Receptor ◽  
Neuron Death ◽  
Ngf Receptor ◽  
Survival Signaling ◽  
Apoptotic Signal

Developmental sympathetic neuron death is determined by functional interactions between the TrkA/NGF receptor and the p75 neurotrophin receptor (p75NTR). A key question is whether p75NTR promotes apoptosis by directly inhibiting or modulating TrkA activity, or by stimulating cell death independently of TrkA. Here we provide evidence for the latter model. Specifically, experiments presented here demonstrate that the presence or absence of p75NTR does not alter Trk activity or NGF- and NT-3–mediated downstream survival signaling in primary neurons. Crosses of p75NTR−/− and TrkA−/− mice indicate that the coincident absence of p75NTR substantially rescues TrkA−/− sympathetic neurons from developmental death in vivo. Thus, p75NTR induces death regardless of the presence or absence of TrkA expression. These data therefore support a model where developing sympathetic neurons are “destined to die” by an ongoing p75NTR-mediated apoptotic signal, and one of the major ways that TrkA promotes neuronal survival is by silencing this ongoing death signal.

Hair cell changes after cationic stimulation of corti's organ

1989 ◽  
Vol 47 ◽  
pp. 798-799
Author(s):  
Cesar D. Fermin ◽  
Hans-Peter Zenner
Keyword(s):  
Organ Of Corti ◽  
Cross Sectional ◽  
Surface Areas ◽  
High K ◽  
Anatomical Arrangement ◽  
Cell Cytosol ◽  
High Concentrations ◽  
K Concentration ◽  
Cell Changes

Contraction of outer and inner hair cells (OHC&IHC) in the Organ of Corti (OC) of the inner ear is necessary for sound transduction. Getting at HC in vivo preparations is difficult. Thus, isolated HCs have been used to study OHC properties. Even though viability has been shown in isolated (iOHC) preparations by good responses to current and cationic stimulation, the contribution of adjoining cells can not be explained with iOHC preparations. This study was undertaken to examine changes in the OHC after expossure of the OHC to high concentrations of potassium (K) and sodium (Na), by carefully immersing the OC in either artifical endolymph or perilymph. After K and Na exposure, OCs were fixed with 3% glutaraldehyde, post-fixed in osmium, separated into base, middle and apex and embedded in Araldite™. One μm thick sections were prepared for analysis with the light and E.M. Cross sectional areas were measured with Bioquant™ software.Potassium and sodium both cause isolated guinea pig OHC to contract. In vivo high K concentration may cause uncontrolled and sustained contractions that could contribute to Meniere's disease. The behavior of OHC in the vivo setting might be very different from that of iOHC. We show here changes of the cell cytosol and cisterns caused by K and Na to OHC in situs. The table below shows results from cross sectional area measurements of OHC from OC that were exposed to either K or Na. As one would expect, from the anatomical arrangement of the OC, OHC#l that are supported by rigid tissue would probably be displaced (move) less than those OHC located away from the pillar. Surprisingly, cells in the middle turn of the cochlea changed their surface areas more than those at either end of the cochlea. Moreover, changes in surface area do not seem to differ between K and Na treated OCs.

Perception of Therapeutic Education in Diabetic Patients at Tit Melil Health Center

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Mory Sanoh
Keyword(s):  
Well Being ◽  
Cross Sectional Study ◽  
Basic Element ◽  
Therapeutic Education ◽  
Diabetic Patients ◽  
Oral Antidiabetics ◽  
Educational Training ◽  
Cross Sectional ◽  
Type 2 Diabetics

Introduction : A chronic condition like diabetes interferes with an individual's well-being, and if some of their needs are not met because of the disease, their quality of life is reduced. In this context, therapeutic education constitutes a basic element in the management of diabetes.Materials and Methods : A cross-sectional study by self-administered questionnaire and interviews which were carried out with all type 1 and type 2 diabetics, consultants at the level of the Tit Mélil Primary Health Care establishment, in 2019 and who benefited from or not therapeutic education, with or without complications.Result : The study included 50 diabetic patients, surveys show us that type 1 diabetic patients were 13 (26%). And type 2.37 (74%). Regarding the organization of care, 74% of patients say they are under treatment with oral antidiabetics, 10% oral antidiabetics and insulins, 6% insulin therapy and others under diet. Speaking of Food, 76.5% of diabetics know the importance and know what foods to avoid.Conclusion : TVE is possible, it will result in a change in the structure of programs and new educational training for caregivers.

Sign in / Sign up

Export Citation Format

Share Document