scholarly journals Long‐term, induced expression of Hand2 in peripheral sympathetic neurons ameliorates sarcopenia in geriatric mice

2021 ◽  
Author(s):  
Anna Carolina Zaia Rodrigues ◽  
María Laura Messi ◽  
Zhong‐Min Wang ◽  
Henry Jacob Bonilla ◽  
Willard M. Freeman ◽  
...  
Keyword(s):  
Sympathetic Neurons ◽  
Induced Expression

Unusual Intranuclear Structures in Chick Sympathetic Neurons

1967 ◽  
Vol 25 ◽  
pp. 188-189
Author(s):  
E. B. Masurovsky ◽  
H. H. Benitez ◽  
M. R. Murray
Keyword(s):  
Electron Microscope ◽  
Sympathetic Neurons ◽  
Uranyl Acetate ◽  
Sympathetic Ganglia ◽  
Lead Citrate ◽  
Thin Sections ◽  
Cns Neurons ◽  
Mammalian Cns

Recent light- and electron microscope studies concerned with the effects of D2O on the development of chick sympathetic ganglia in long-term, organized culture revealed the presence of rod-like fibrillar formations, and associated granulofibrillar bodies, in the nuclei of control and deuterated neurons. Similar fibrillar formations have been reported in the nuclei of certain mammalian CNS neurons; however, related granulofibrillar bodies have not been previously described. Both kinds of intranuclear structures are observed in cultures fixed either in veronal acetate-buffered 2%OsO4 (pH 7. 4), or in 3.5% glutaraldehyde followed by post-osmication. Thin sections from such Epon-embedded cultures were stained with ethanolic uranyl acetate and basic lead citrate for viewing in the electron microscope.

scholarly journals Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity.

1991 ◽  
Vol 115 (2) ◽  
pp. 461-471 ◽  
Author(s):  
A Batistatou ◽  
L A Greene
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Endonuclease Activity ◽  
Term Survival ◽  
Serum Free

Past studies have shown that serum-free cultures of PC12 cells are a useful model system for studying the neuronal cell death which occurs after neurotrophic factor deprivation. In this experimental paradigm, nerve growth factor (NGF) rescues the cells from death. It is reported here that serum-deprived PC12 cells manifest an endonuclease activity that leads to internucleosomal cleavage of their cellular DNA. This activity is detected within 3 h of serum withdrawal and several hours before any morphological sign of cell degeneration or death. NGF and serum, which promote survival of the cells, inhibit the DNA fragmentation. Aurintricarboxylic acid (ATA), a general inhibitor of nucleases in vitro, suppresses the endonuclease activity and promotes long-term survival of PC12 cells in serum-free cultures. This effect appears to be independent of macromolecular synthesis. In addition, ATA promotes long-term survival of cultured sympathetic neurons after NGF withdrawal. ATA neither promotes nor maintains neurite outgrowth. It is hypothesized that the activation of an endogenous endonuclease could be responsible for neuronal cell death after neurotrophic factor deprivation and that growth factors could promote survival by leading to inhibition of constitutively present endonucleases.

scholarly journals Ca2+ transients are not required as signals for long-term neurite outgrowth from cultured sympathetic neurons.

1990 ◽  
Vol 110 (4) ◽  
pp. 1295-1306 ◽  
Author(s):  
A M Tolkovsky ◽  
A E Walker ◽  
R D Murrell ◽  
H S Suidan
Keyword(s):  
Nerve Growth Factor ◽  
Neurite Outgrowth ◽  
Sympathetic Neurons ◽  
Optimal Growth ◽  
Normal Medium ◽  
Growth And Survival ◽  
Neurite Elongation ◽  
Cultured Sympathetic Neurons ◽  
Ca2 Channels

A method for clamping cytosolic free Ca2+ ([Ca2+]i) in cultures of rat sympathetic neurons at or below resting levels for several days was devised to determine whether Ca2+ signals are required for neurite outgrowth from neurons that depend on Nerve Growth Factor (NGF) for their growth and survival. To control [Ca2+]i, normal Ca2+ influx was eliminated by titration of extracellular Ca2+ with EGTA and reinstated through voltage-sensitive Ca2+ channels. The rate of neurite outgrowth and the number of neurites thus became dependent on the extent of depolarization by KCl, and withdrawal of KCl caused an immediate cessation of growth. Neurite outgrowth was completely blocked by the L type Ca2+ channel antagonists nifedipine, nitrendipine, D600, or diltiazem at sub- or micromolar concentrations. Measurement of [Ca2+]i in cell bodies using the fluorescent Ca2+ indicator fura-2 established that optimal growth, similar to that seen in normal medium, was obtained when [Ca2+]i was clamped at resting levels. These levels of [Ca2+]i were set by serum, which elevated [Ca2+]i by integral of 30 nM, whereas the addition of NGF had no effect on [Ca2+]i. The reduction of [Ca2+]o prevented neurite fasciculation but this had no effect on the rate of neurite elongation or on the number of extending neurites. These results show that neurite outgrowth from NGF-dependent neurons occurs over long periods in the complete absence of Ca2+ signals, suggesting that Ca2+ signals are not necessary for operating the basic machinery of neurite outgrowth.

scholarly journals Ciliary neurotrophic factor induces cholinergic differentiation of rat sympathetic neurons in culture.

1989 ◽  
Vol 108 (5) ◽  
pp. 1807-1816 ◽  
Author(s):  
S Saadat ◽  
M Sendtner ◽  
H Rohrer
Keyword(s):  
Neurotrophic Factor ◽  
Specific Activity ◽  
Sympathetic Neurons ◽  
Ciliary Neurotrophic Factor ◽  
Activity Levels ◽  
Term Survival ◽  
Selective Survival ◽  
Enzyme Molecules

Ciliary neurotrophic factor (CNTF) influences the levels of choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) in cultures of dissociated sympathetic neurons from newborn rats. In the presence of CNTF both the total and specific activity of ChAT was increased 7 d after culture by 15- and 18-fold, respectively, as compared to cultures kept in the absence of CNTF. Between 3 and 21 d in culture in the presence of CNTF the total ChAT activity increased by a factor of greater than 100. Immunotitration demonstrated that the elevated ChAT levels were due to an increased number of enzyme molecules. In contrast to the increase in ChAT levels, the total and specific activity levels of TH were decreased by 42 and 36%, respectively, after 7 d in culture. Half-maximal effects for both ChAT increase and TH decrease were obtained at CNTF concentrations of approximately 0.6 ng and maximal levels were reached at 1 ng of CNTF per milliliter of medium. The effect of CNTF on TH and ChAT levels were seen in serum-containing medium as well as in serum-free medium. CNTF was shown to have only a small effect on the long-term survival of rat sympathetic neurons. We therefore concluded that the effects of CNTF on ChAT and TH are not due to selective survival of cells that acquire cholinergic traits in vitro, but are rather due to the induction of cholinergic differentiation of noradrenergic sympathetic neurons.

Synaptic plasticity in sympathetic ganglia from acquired and inherited forms of ouabain-dependent hypertension

2001 ◽  
Vol 281 (2) ◽  
pp. R635-R644 ◽  
Author(s):  
Azeez A. Aileru ◽  
Aline De Albuquerque ◽  
John M. Hamlyn ◽  
Paolo Manunta ◽  
Jui R. Shah ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Neurons ◽  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Term Potentiation ◽  
Compound Action Potentials ◽  
Cervical Ganglia

Altered sympathetic nervous system activity has been implicated often in hypertension. We examined short-term potentiation [posttetanic potentiation (PTP)] and long-term potentiation (LTP) in the isolated superior cervical ganglia (SCG) from Sprague-Dawley (SD) rats given vehicle, digoxin, or ouabain by subcutaneous implants as well as in animals with ouabain-induced hypertension (OHR), and inbred Baltimore ouabain-resistant (BOR) and Baltimore ouabain-sensitive (BOS) strains of rats. Postganglionic compound action potentials (CAP) were used to determine PTP and LTP following a tetanic stimulus (20 Hz, 20 s). Baseline CAP magnitude was greater in ganglia from OHR than in vehicle-treated SD rats before tetanus, but the decay time constant of PTP was significantly decreased in OHR and in rats infused with digoxin that were normotensive. In hypertensive BOS and OHR, the time constants for the decay of both PTP and LTP ( t L) were increased and correlated with blood pressure (slope = 0.15 min/mmHg, r = 0.52, P < 0.047 and 6.7 min/mmHg, r = 0.906, P < 0.0001, respectively). In BOS and OHR, t L (minutes) was 492 ± 40 ( n = 7) and 539 ± 41 ( n = 5), respectively, and differed ( P < 0.05) from BOR (257 ± 48, n = 4), SD vehicle rats (240 ± 18, n = 4), and captopril-treated OHR (370 ± 52, n = 5). After the tetanus, the CAP at 90 min in BOS and OHR SCG declined less rapidly vs. SD vehicle rats or BOR. Captopril normalized blood pressure and t L in OHR. We conclude that the duration of ganglionic LTP and blood pressure are tightly linked in ouabain-dependent hypertension. Our results favor the possibility that enhanced duration of LTP in sympathetic neurons contributes to the increase in sympathetic nerve activity in ouabain-dependent hypertension and suggest that a captopril-sensitive step mediates the link of ouabain with LTP.

scholarly journals NGF and Neurotrophin-3 Both Activate TrkA on Sympathetic Neurons but Differentially Regulate Survival and Neuritogenesis

1997 ◽  
Vol 136 (2) ◽  
pp. 375-388 ◽  
Author(s):  
Daniel J. Belliveau ◽  
Irena Krivko ◽  
Judi Kohn ◽  
Christian Lachance ◽  
Christine Pozniak ◽  
...  
Keyword(s):  
Time Course ◽  
Sympathetic Neurons ◽  
Sympathetic Neuron ◽  
Activation Time ◽  
Short Term ◽  
Trka Receptor ◽  
Trk Receptor ◽  
Neurotrophin 3 ◽  
Differential Responsiveness

In this report we examine the biological and molecular basis of the control of sympathetic neuron differentiation and survival by NGF and neurotrophin-3 (NT-3). NT-3 is as efficient as NGF in mediating neuritogenesis and expression of growth-associated genes in NGF-dependent sympathetic neurons, but it is 20–40fold less efficient in supporting their survival. Both NT-3 and NGF induce similar sustained, long-term activation of TrkA, while NGF is 10-fold more efficient than NT-3 in mediating acute, short-term TrkA activity. At similar acute levels of TrkA activation, NT-3 still mediates neuronal survival two- to threefold less well than NGF. However, a mutant NT-3 that activates TrkC, but not TrkA, is unable to support sympathetic neuron survival or neuritogenesis, indicating that NT3–mediated TrkA activation is necessary for both of these responses. On the basis of these data, we suggest that NGF and NT-3 differentially regulate the TrkA receptor both with regard to activation time course and downstream targets, leading to selective regulation of neuritogenesis and survival. Such differential responsiveness to two ligands acting through the same Trk receptor has important implications for neurotrophin function throughout the nervous system.

A proteasome inhibitor reduces concurrent, sequential, and long-term IL-1β- and TNF-α-induced ECAM expression and adhesion

2003 ◽  
Vol 285 (4) ◽  
pp. C813-C822 ◽  
Author(s):  
Nilesh M. Dagia ◽  
Douglas J. Goetz
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Proteasome Inhibitor ◽  
Umbilical Vein ◽  
Hl60 Cell ◽  
Induced Expression ◽  
Tnf Α ◽  
Short Period

A promising approach for reducing aberrant leukocyte-endothelial adhesion during pathological inflammation is to inhibit endothelial cell adhesion molecule (ECAM) expression at the transcription level. Several compounds have been shown to decrease cytokine-induced upregulation of ECAMs primarily by modulating the activity of transcription factors [e.g., nuclear factor-κB (NF-κB)]. The majority of the in vitro studies have focused on the effect of transcription inhibitors on endothelial cells exposed to a single cytokine [primarily tumor necrosis factor-α (TNF-α)] for a relatively short period of time (primarily 4-6 h). However, in the in vivo setting, multiple cytokines [e.g., interleukin-1β (IL-1β) and TNF-α] may be present for extended periods of time. Thus we studied the effects of a transcription inhibitor, the proteasome inhibitor lactacystin, on ECAM expression and myeloid (HL60) cell adhesion to human umbilical vein endothelial cells (HUVEC) activated by concurrent, sequential, and long-term (24 h) treatment with IL-1β and TNF-α. We show, for the first time, that lactacystin inhibits 1) 4-h concurrent IL-1β- and TNF-α-induced expression of E-selectin, VCAM-1, ICAM-1, and HL60 cell adhesion to HUVEC; 2) 4-h TNF-α-induced expression of E-selectin, VCAM-1, and HL60 cell adhesion to HUVEC that have become desensitized to IL-1β activation; 3) 24-h TNF-α-induced expression of E-selectin and VCAM-1 but not ICAM-1; and 4) 24-h TNF-α-induced HL60 cell adhesion to HUVEC. Combined, our results demonstrate that a proteasome inhibitor can reduce concurrent, sequential, and long-term IL-1β- and TNF-α-induced ECAM expression and myeloid cell adhesion.

scholarly journals CREB as a Memory Modulator: induced expression of a dCREB2 activator isoform enhances long-term memory in drosophila

Cell ◽  
1995 ◽  
Vol 81 (1) ◽  
pp. 107-115 ◽  
Author(s):  
J.C.P Yin ◽  
M Del Vecchio ◽  
H Zhou ◽  
T Tully
Keyword(s):  
Long Term Memory ◽  
Induced Expression ◽  
Term Memory

scholarly journals PRIMARY CULTURES OF DISSOCIATED SYMPATHETIC NEURONS

1973 ◽  
Vol 59 (2) ◽  
pp. 329-345 ◽  
Author(s):  
Richard E. Mains ◽  
Paul H. Patterson
Keyword(s):  
Sympathetic Neurons ◽  
Primary Cultures ◽  
Sympathetic Ganglia ◽  
Aminobutyric Acid ◽  
Fluorescence Histochemistry ◽  
Neural Cells ◽  
Primary Neurons ◽  
Isolated Neurons ◽  
Mechanical Agitation

Rat sympathetic ganglia were disrupted by mechanical agitation to yield dissociated primary neurons, and the conditions for long-term growth in culture of the isolated neurons were examined. The neurons were grown with or without non-neural cells, simply by the addition or deletion of bicarbonate during growth in culture. Fluorescence histochemistry indicated that the isolated neurons contained catecholamines; incubations with radioactive precursors were used to verify the synthesis and accumulation of both dopamine and norepinephrine. The neurons also produced octopamine using tyramine as precursor, but not with tyrosine as the precursor. In the presence of eserine, older cultures synthesized and stored small amounts of acetylcholine. The cultures did not synthesize and accumulate detectable levels of radioactive γ-aminobutyric acid, 5-hydroxytryptamine, or histamine.

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