The Regeneration of Peripheral Noradrenergic Nerves after Chemical Sympathectomy in Diabetic Rats: Effects of Nerve Growth Factor

Vo, Phuong A.; Tomlinson, David R.

doi:10.1006/exnr.1999.7018

Cited by 19 publications

(8 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In OVX rats, substantial numbers of sympathetic axons were present by 12 days after lesion, whereas the rate of reinnervation appeared to slow thereafter and no further increase was observed through 25 days. These findings compare favorably with reports from other peripheral targets with regard to time course for reinnervation and their failure to attain their pre-lesion innervation densities 23,24. Thus, only partial reinnervation of the proximal urethra is achieved in OVX rats.…”

Section: Discussionsupporting

confidence: 82%

Estrogen Promotes Sympathetic Nerve Regeneration in Rat Proximal Urethra

Smith

George

Bradshaw

2009

Urology

View full text Add to dashboard Cite

Objectives: Sympathetic innervation mediates tonic contraction of proximal urethral smooth muscle, thus contributing to urinary continence. Urethral innervation is particularly susceptible to damage during vaginal delivery, a time characterized by decreasing estrogen levels. Because regeneration of other nerves types can be influenced by estrogen, the present study was conducted to assess whether sympathetic reinnervation of the rat proximal urethra is affected by differences in estrogen levels. Methods: Adult female rats were ovariectomized and implanted with pellets containing vehicle or estrogen to achieve serum levels similar to rodent pregnancy. Rats were injected intravenously with vehicle or the selective sympathetic neurotoxin 6-hydroxydopamine, which produces uniform and complete destruction of terminal sympathetic axons. At 1, 4, 12 and 25 days, tyrosine hydroxylase-immunoreactive sympathetic innervation of the proximal urethral smooth muscle was assessed quantitatively. Results: In rats with intact innervation, the proximal urethra is densely innervated, and nerve density is comparable irrespective of estrogen status. 6-Hydroxydopamine induced marked sympathetic axon disruption by 1 day and complete denervation by 4 days post-injection in ovariectomized rats receiving vehicle or estrogen. In vehicle-treated rats, few nerves were present at 12 days post-sympathectomy, and innervation remained substantially below normal levels at 25 days. In estrogen-treated rats, sympathetic reinnervation was 2-fold greater at 12 days, and by 25 days was comparable to controls. Conclusion: Estrogen improves sympathetic reinnervation of the proximal urethra. Estrogen titers in individuals with urethral sympathetic nerve damage may therefore influence the rate and extent of urethral smooth muscle reinnervation.

show abstract

Section: Discussionsupporting

confidence: 82%

Estrogen Promotes Sympathetic Nerve Regeneration in Rat Proximal Urethra

Smith

George

Bradshaw

2009

Urology

View full text Add to dashboard Cite

show abstract

“…In addition to regeneration following injury, sympathetic nerves innervating the uterus undergo degeneration and regeneration during each estrous cycle (Zoubina and Smith, 2000). The presence of nerve growth factor (NGF) in the target tissue is important for promoting innervation of during development (Glebova and Ginty, 2004) and reinnervation of a tissue after denervation (Aloe et al, 1985; Gloster and Diamond, 1995; Vo and Tomlinson, 1999). …”

Section: Introductionmentioning

confidence: 99%

Infarct-Derived Chondroitin Sulfate Proteoglycans Prevent Sympathetic Reinnervation after Cardiac Ischemia-Reperfusion Injury

Gardner

Habecker

2013

J. Neurosci.

View full text Add to dashboard Cite

Sympathetic nerve can regenerate after injury to re-innervate target tissues. Sympathetic regeneration is well documented after chronic cardiac ischemia, so we were surprised that the cardiac infarct remained denervated following ischemia-reperfusion (I-R). We used mice to ask if the lack of sympathetic regeneration into the scar was due to blockade by inhibitory extracellular matrix within the infarct. We found that chondroitin sulfate proteoglycans (CSPGs) were present in the infarct after I-R, but not after chronic ischemia, and that CSPGs caused inhibition of sympathetic axon outgrowth in vitro. Ventricle explants after I-R and chronic ischemia stimulated sympathetic axon outgrowth that was blocked by NGF antibodies. However, growth in I-R co-cultures was asymmetrical, with axons growing toward the heart tissue consistently shorter than axons growing in other directions. Growth toward I-R explants was rescued by adding chondroitinase ABC (ChABC) to the co-cultures, suggesting that I-R infarct-derived CSPGs prevented axon extension. Sympathetic ganglia lacking Protein Tyrosine Phosphatase Sigma (PTPRS) were not inhibited by CSPGs or I-R explants in vitro, suggesting PTPRS is the major CSPG receptor in sympathetic neurons. To test directly if infarct-derived CSPGs prevented cardiac reinnervation, we carried out ischemia-reperfusion in ptprs-/- and ptprs+/- mice. Cardiac infarcts in ptprs-/- mice were hyperinnervated, while infarcts in ptprs+/- littermates were denervated, confirming that CSPGs prevent sympathetic reinnervation of the cardiac scar after I-R. This is the first example of CSPGs preventing sympathetic reinnervation of an autonomic target following injury, and may have important consequences for cardiac function and arrhythmia susceptibility after myocardial infarction.

show abstract

“…Treating rats with 6-hydroxydopamine (6-OHDA) effectively models cardiac sympathetic denervation and decreases heart tyrosine hydroxylase activity, which causes a concomitant decrease in heart norepinephrine and dopamine levels (24). Sympathetic denervation of rat heart with 6-OHDA (100 mg/kg ip) may also increase the number of ␤-adrenergic receptors in heart (50), although others have demonstrated no effect of denervation on ␤-adrenergic receptor number (51). A similar level of denervation is accomplished by injecting rats with 6-OHDA (50 mg/kg ip) on two consecutive days, 10 days before studies (20).…”

mentioning

confidence: 99%

Arachidonic acid incorporation and turnover is decreased in sympathetically denervated rat heart

Patrick¹,

McHowat²,

Rosenberger³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

. Arachidonic acid incorporation and turnover is decreased in sympathetically denervated rat heart. Am J Physiol Heart Circ Physiol 288: H2611-H2619, 2005 C]20:4 n-6), and kinetic parameters were assessed using a steady-state radiotracer model. Heart norepinephrine and epinephrine levels were decreased 82 and 85%, respectively, in denervated rats, and this correlated with a 34% reduction in weight gain in treated rats. Fatty acid tracer uptake was not significantly different between groups for either tracer, although the dilution coefficient was increased in [1-14 C]20:4 n-6-infused rats, which indicates that less 20:4 n-6 was recycled in denervated rats. In [1-14 C]16:0-infused rats, incorporation rate and turnover values of 16:0 in stable lipid compartments were unchanged, which is indicative of preservation of ␤-oxidation. In [1-14 C]20:4 n-6-infused rats, there were dramatic reductions in incorporation rate (60 -84%) and turnover value (56 -85%) in denervated rats that were dependent upon the lipid compartment. In addition, phospholipase A2 activity was reduced 40% in treated rats, which is consistent with the reduction observed in 20:4 n-6 turnover. These results demonstrate marked reductions in 20:4 n-6 incorporation rate and turnover in sympathetic denervated rats and thereby suggest an effect on lipid-mediated signal transduction mediated by a reduction in phospholipase A2 activity. palmitic acid; signal transduction; phospholipase A 2; catecholamines; phospholipids UNDER NORMAL PHYSIOLOGICAL conditions, the mammalian heart uses palmitic acid (16:0) as a primary source of metabolic energy via ␤-oxidation (11

show abstract

The Regeneration of Peripheral Noradrenergic Nerves after Chemical Sympathectomy in Diabetic Rats: Effects of Nerve Growth Factor

Cited by 19 publications

References 41 publications

Estrogen Promotes Sympathetic Nerve Regeneration in Rat Proximal Urethra

Estrogen Promotes Sympathetic Nerve Regeneration in Rat Proximal Urethra

Infarct-Derived Chondroitin Sulfate Proteoglycans Prevent Sympathetic Reinnervation after Cardiac Ischemia-Reperfusion Injury

Arachidonic acid incorporation and turnover is decreased in sympathetically denervated rat heart

Contact Info

Product

Resources

About