Activating transcription factor 3 induction in sympathetic neurons after axotomy: Response to decreased neurotrophin availability

Sachs, H. Hyatt; Schreiber, R. C.; Shoemaker, S.E.; Sabe, Ashraf A.; Reed, E.; Zigmond, Richard E.

doi:10.1016/j.neuroscience.2007.10.008

Cited by 31 publications

(50 citation statements)

References 90 publications

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“…A similar induction of ATF-3 is known to occur in sympathetic post- ganglionic cells and dorsal root ganglion cells following injury or explant culture (Tsujino et al, 2000;Wang et al, 2003;Averill et al, 2004;Lindwall and Kanje, 2005;Hyatt-Sachs et al, 2007). An induction of ATF-3 following injury or nerve section has also been reported for neurons within the CNS (Takeda et al, 2000;Mason et al, 2003).…”

Section: Discussionmentioning

confidence: 63%

“…Activating transcription factor 3 (ATF-3), a member of the ATF/CREB family of transcription factors (Hai and Hartman, 2001), is induced in both peripheral and central neurons following injury or stress (Takeda et al, 2000;Tsujino et al, 2000;Mason et al, 2003;Wang et al, 2003;Averill et al, 2004;Boeshore et al, 2004;Hunt et al, 2004;Lindwall and Kanje, 2005;Hyatt-Sachs et al, 2007;Zigmond and Vaccariello, 2007). ATF-3 induction occurs so commonly in injured neurons that its expression is considered a marker for neuronal injury (Tsujino et al, 2000).…”

Section: Indexing Terms: Parasympathetic Ganglia; Injury Response; Trmentioning

confidence: 99%

“…P18847), the antibody epitope being amino acids 163-181 in the C-terminus (Santa Cruz Biotechnology). The antibody has been used extensively in prior studies in multiple species, including mice and rats (Hyatt-Sachs et al, 2007). Western blot analysis by Hyatt-Sachs et al (2007) demonstrated that ATF-3 immunoreactivity was detectable in extracts of axotomized superior cervical ganglia (SCG) but not in SCG extracts from sham animals.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…The antibody has been used extensively in prior studies in multiple species, including mice and rats (Hyatt-Sachs et al, 2007). Western blot analysis by Hyatt-Sachs et al (2007) demonstrated that ATF-3 immunoreactivity was detectable in extracts of axotomized superior cervical ganglia (SCG) but not in SCG extracts from sham animals. We confirmed by using extracts from 48-hour-cultured guinea pig cardiac ganglia that a single band with the appropriate molecular weight for ATF-3 was detected by Western blot analysis with the anti-ATF-3 antiserum.…”

Section: Immunohistochemistrymentioning

confidence: 99%

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Neurturin suppresses injury‐induced neuronal activating transcription factor 3 expression in cultured guinea pig cardiac ganglia

Young

Girard

Parsons

2008

J of Comparative Neurology

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Cultured guinea pig atrial whole mounts containing the intrinsic cardiac ganglia were used as an in vitro model to investigate the induction of the stress/injury marker activating transcription factor 3 (ATF-3). ATF-3 expression was quantified by using immunocytochemical labeling and real-time PCR. In freshly isolated ganglia, no neuronal or Schwann cell nuclei exhibited ATF-3 immunoreactivity. In 2-hour cultures, the induction of ATF-3 expression was evident in many Schwann cell nuclei, whereas no neuronal nuclei were ATF-3 immunoreactive. Beginning at 4 hours, the percentage of neurons with ATF-3-immunoreactive nuclei increased progressively, and, by 48 hours in culture, approximately 95% of the cardiac neurons had ATF-3-immunoreactive nuclei. Neurturin significantly suppressed ATF-3 expression in 48-hour-cultured neurons without effect on ATF-3 expression in Schwann cell nuclei. Neuturin also could reverse neuronal ATF-3 expression after its induction. The suppression of ATF-3 induction by neurturin was mediated by activation of the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways. Glial-derived neurotrophic factor (GDNF) also suppressed neuronal ATF-3 induction during culture. However, culture in serum-free media, presence of nerve growth factor, or addition of pituitary adenylate cyclase-activating polypeptide had no effect on ATF-3 induction in the 48-hour-cultured cardiac neurons. By 4 hours in culture, there was a significant increase in ATF-3 transcript levels, and neurturin partially suppressed ATF-3 transcript levels in 48-hour cultures. It is proposed that the loss of target-derived neurturin is a potential mechanism stimulating injury-induced expression of ATF-3 in cardiac neurons.

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Section: Discussionmentioning

confidence: 63%

Section: Indexing Terms: Parasympathetic Ganglia; Injury Response; Trmentioning

confidence: 99%

Section: Immunohistochemistrymentioning

confidence: 99%

Section: Immunohistochemistrymentioning

confidence: 99%

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Neurturin suppresses injury‐induced neuronal activating transcription factor 3 expression in cultured guinea pig cardiac ganglia

Young

Girard

Parsons

2008

J of Comparative Neurology

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“…In previous studies, we (3,4) used an explant cultured male mouse MPG whole mount as an in vitro model to study the neuronal response to injury. Our previous studies established that after 2-3 days in culture, MPG neurons in whole mount ganglia explant preparations increase expression, both transcript and protein levels, of three molecules (activating transcription factor 3, pituitary adenylate cyclaseactivating polypeptide, and galanin) that are known to be upregulated after axotomy in vivo in other autonomic ganglia (1,6,11,12,17,20,24). Consequently, we initially determined, as part of this study, whether transcript levels of the nAChR subunits ␣ 3 , ␤ 4 , and ␣ 7 were decreased when the MPG .…”

Section: Resultsmentioning

confidence: 99%

Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture

Girard

Merriam

Tompkins

et al. 2013

American Journal of Physiology-Renal Physiology

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Girard BM, Merriam LA, Tompkins JD, Vizzard MA, Parsons RL. Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture. Am J Physiol Renal Physiol 305: F1504 -F1512, 2013. First published September 18, 2013 doi:10.1152/ajprenal.00343.2013.-Quantitative real-time PCR was used to test whether cavernous nerve injury leads to a decrease in major pelvic ganglia (MPG) neuronal nicotinic ACh receptor (nAChR) subunit and postsynaptic density (PSD)-93 transcript levels. Subunits ␣3, ␤4, and ␣7, commonly expressed in the MPG, were selected for analysis. After 72 h in explant culture, MPG transcript levels for ␣3, ␤4, ␣7, and PSD-93 were significantly depressed. Three days after cavernous nerve axotomy or crush in vivo, transcript levels for ␣3, ␤4, and PSD-93, but not for ␣7, were significantly depressed. Three days after dissection of the cavernous nerve free of underlying tissue and application of a 5-mm lateral stretch (manipulation), transcript levels for ␣3 and PSD-93 were also significantly decreased. Seven days after all three surgical procedures, ␣ 3 transcript levels remained depressed, but PSD-93 transcript levels were still decreased only after axotomy or nerve crush. At 30 days postsurgery, transcript levels for the nAChR subunits and PSD-93 had recovered. AChinduced currents were significantly smaller in MPG neurons dissociated from 3-day explant cultured ganglia than from those recorded in neurons dissociated from acutely isolated ganglia; this observation provides direct evidence showing that a decrease in nAChR function was coincident with a decrease in nAChR subunit transcript levels. We conclude that a downregulation of nAChR subunit and PSD-93 expression after cavernous nerve injury, or even manipulation, could interrupt synaptic transmission within the MPG and thus contribute to the loss of neural control of urogenital organs after pelvic surgeries. major pelvic ganglia; neuronal nicotinic receptor subunits; axotomy of postganglionic neurons; neuronal response to injury IT IS WELL DOCUMENTED for the sympathetic superior cervical ganglia (SCG) that after axotomy or nerve crush, synaptic transmission is depressed for prolonged periods of time (8, 16). Matthews and Nelson (8) quantified the time course of loss of connectivity between pre-and postganglionic neurons in the rat SCG after axotomy, and Purves (16) showed that synaptic depression also followed nerve crush in the guinea pig SCG. A retraction of preganglionic fiber terminals from postganglionic neurons was first proposed to underlie the prolonged synaptic depression. Connectivity was reestablished upon reinnervation of the target tissues (16). In subsequent experiments, Zhou et al. (25) showed that a second mechanism likely contributing to the synaptic failure is a decreased expression of neuronal nicotinic ACh receptors (nAChRs) at synapses on the postganglionic neurons. This decrease in receptor subunit transcript expression occurred within ...

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Expression of the regeneration‐associated protein SPRR1A in primary sensory neurons and spinal cord of the adult mouse following peripheral and central injury

Starkey

Davies

Yip

et al. 2008

J of Comparative Neurology

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Small proline-rich repeat protein 1A (SPRR1A) is expressed in dorsal root ganglion (DRG) neurons following peripheral nerve injury but it is not known whether SPRR1A is differentially expressed following injury to peripheral versus central DRG projections and a detailed characterisation of expression in sensory neuron sub-populations and spinal cord has not been performed. Here we use immunocytochemical techniques to characterise SPRR1A expression following sciatic nerve, dorsal root and dorsal column injury in adult mice. SPRR1A was not detected in naïve spinal cord, DRG or peripheral nerves and there was minimal expression following injury to the centrally projecting branches of DRG neurons. However, following peripheral (sciatic) nerve injury, intense SPRR1A immunoreactivity was observed in the dorsal horn and motoneurons of the spinal cord, in L4/5 DRG neurons and in the injured nerve. A timecourse study comparing expression following sciatic nerve crush and transection revealed maximum SPRR1A levels at day 7 in both models. However, while SPRR1A was down-regulated to baseline by 30 days post-lesion following crush injury, it remained elevated 30 days after transection. Cell-size and double-labelling studies revealed that SPRR1A was expressed by DRG cells of all sizes and co-localized with classical markers of DRG subpopulations and their primary afferent terminals. High co-expression of SPRR1A with activating transcription factor-3 and growth-associated protein-43 was observed, indicating that it is expressed by injured and regenerating neurons. This study supports the hypothesis that SPRR1A is a regenerationassociated gene and that SPRR1A provides a valuable marker to assess the regenerative potential of injured neurons.

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Activating transcription factor 3 induction in sympathetic neurons after axotomy: Response to decreased neurotrophin availability

Cited by 31 publications

References 90 publications

Neurturin suppresses injury‐induced neuronal activating transcription factor 3 expression in cultured guinea pig cardiac ganglia

Neurturin suppresses injury‐induced neuronal activating transcription factor 3 expression in cultured guinea pig cardiac ganglia

Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture

Expression of the regeneration‐associated protein SPRR1A in primary sensory neurons and spinal cord of the adult mouse following peripheral and central injury

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