GAP 43-like immunoreactivity in normal adult rat sciatic nerve, spinal cord, and motoneurons: Axonal transport and effect of spinal cord transection

Li, Jiayi; Kling-Petersen, Anne; Dahlström, Annica

doi:10.1016/0306-4522(93)90022-8

Cited by 32 publications

(21 citation statements)

References 48 publications

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“…Immunofluorescence microscopy revealed that B-50/GAP-43 had accumulated, both, at the proximal and distal side of the iigation (results not shown). The accumulation is in agreement with previous findings of Tetzlaff et al 54 and Li et al 35 We have restricted our ultrastructural study of the sciatic nerve, consisting of motor and sensory axons, to the anterograde axonal transport, interrupted at the proximal side of the ligature. For detailed analysis, electron micrographs of longitudinally sectioned myelinated and unmyelinated axons were taken from the proximal side of the ligature.…”

Section: Accumulation Of Anterogradely Transported Materialssupporting

confidence: 92%

“…Recently Li et al 35 used immunofluorescence light and confocal Transport vesicles of B-50 laser microscopy to study the distribution of B-50/GAP-43 with markers of vesicles during axonal transport in the sciatic nerve of adult rat. To observe the accumulation of the transported proteins they placed two crushes within 1-2 mm distance.…”

Section: Various Types Of Transport Vesicles Move Rapidly Anterogradementioning

confidence: 99%

“…Double immunolabelling of the sciatic nerve axons for both antigens showed that B-50/GAP-43 and synaptophysin were partially co-localized and transported in the same axon, but these proteins appeared not to be stored in the same intra-axonal organelles. Li et al 35 concluded that B-50/GAP-43 is bidirectional transported through the normal sciatic nerve.…”

Section: Various Types Of Transport Vesicles Move Rapidly Anterogradementioning

confidence: 99%

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Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

et al. 1996

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Abstract--The growth-associated protein-43/B-50 (B-50/GAP-43) is conveyed from the neuronal soma into the axon by fast axonal transport and moved to the nerve terminal. To visualize and determine the type of vesicles by which B-50/GAP-43 is anterogradely transported in the regenerating rat sciatic nerve, we have investigated Lowicryl HM20 embedded nerve pieces dissected from the proximal side of a collection ligature. Ultrastructurally, numerous vesicular profiles of various sizes, tubules and mitochondria were seen to accumulate proximal to the collection ligature. Both, in unmyelinated and myelinated axons, B-50/GAP-43 immunoreactivity was associated with vesicular profiles which had a diameter of 50 nm. A fraction of the B-50/GAP-43 label co-localized with the small vesicle marker synaptophysin. Co-localization of B-50/GAP-43 was not detected with the large dense-core vesicle marker calcitonin gene-related peptide.These results indicate that, in rat sciatic nerve axons, B-50/GAP-43 is anterogradely transported in small 50 nm vesicles of the constitutive pathway. These transport vesicles were distinguished in two types. We suggest that one type carrying, both, B-50 GAP-43 and synaptophysin has as destination the nerve terminal, whereas the second type, which only contains B-50/GAP-43 and no synaptophysin, may be primarily targeted to the axolemma for local membrane fusion.

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Section: Accumulation Of Anterogradely Transported Materialssupporting

confidence: 92%

Section: Various Types Of Transport Vesicles Move Rapidly Anterogradementioning

confidence: 99%

Section: Various Types Of Transport Vesicles Move Rapidly Anterogradementioning

confidence: 99%

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Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

et al. 1996

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“…19 These nerve growth factors can be transported to remaining GP or stellate ganglia through axonal retrograde transport. 20 Increased nerve-sprouting activity within the remaining GP and stellate ganglion can cause extensive cardiac nerve sprouting. 21 Fourth, it is possible that intensive and repetitive HFS of the GP may have induced the observed hyper-innervation, even at distant sites.…”

Section: Systematic Gp Ablation and Afmentioning

confidence: 99%

Ablation of Epicardial Ganglionated Plexi Increases Atrial Vulnerability to Arrhythmias in Dogs

Mao

Yin

Zhang

et al. 2014

Circ: Arrhythmia and Electrophysiology

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Background-Previous studies have suggested that systematic ablation of ganglionated plexi (GP) could increase the shortterm success rate of radiofrequency ablation for atrial fibrillation, but the long-term efficacy of this approach is not fully established. Methods and Results-Twenty-four mongrel dogs were divided into 3 groups: epicardial GP ablation group 1 (n=8), epicardial GP ablation group 2 (n=8), and a sham operation group (n=8). In the 2 epicardial GP ablation groups, the 4 major GP and the ligament of Marshall were systematically ablated. The effective refractory period and inducibility of tachyarrhythmias were measured before and immediately after GP ablation in epicardial GP ablation group 1 and 8 weeks later in the other 2 groups. Tyrosine hydroxylase and choline acetyltransferase expressions were also determined immunohistochemically 8 weeks later in the latter groups. Compared with epicardial GP ablation group 1 and the sham operation group, epicardial GP ablation group 2 had the shortest atrial and ventricular effective refractory period and the highest inducibility of atrial tachyarrhythmias. The inducibility of ventricular tachyarrhythmias among the 3 groups was comparable. The density of tyrosine hydroxylase-and choline acetyltransferase-positive nerves in the atrium was the highest in epicardial GP group 2, whereas there were no significant intergroup differences in the densities of these 2 types of nerves in the ventricle. Conclusions-After 8 weeks of healing, epicardial GP ablation without additional atrial ablation was potentially proarrhythmic, which may be attributable to decreased atrial effective refractory period and hyper-reinnervation involving both sympathetic and parasympathetic nerves. Methods Animal PreparationAll animal studies were reviewed and approved by the Institutional Animal Care and Use Committee at our institution. Twenty-four adult mongrel dogs (18-25 kg) were divided into 3 groups: epicardial GP ablation group 1 (n=8), epicardial GP ablation group 2 (n=8), and a sham operation group (n=8). All dogs were anesthetized with 5% sodium pentobarbital (2-3 mL/kg) given intravenously, followed by an additional dose of 1 mL/kg at the end of each hour. A tracheal cannula was inserted, and intermittent positive pressure ventilation with room air was delivered by a respirator. A 6-lead frontal ECG was recorded continuously during the procedure (filter, 0.05-30 Hz). After left thoracotomy at the fourth intercostal space, the heart was exposed in a pericardial cradle. GP AblationIn the 2 epicardial GP ablation groups, the LOM and the fat pads that contain the superior left GP and inferior left GP were exposed by left thoracotomy. After the superior left GP, inferior left GP, and LOM were ablated, the fat pads that contain the anterior right GP and inferior right GP were exposed by lifting up the pericardium, and the anterior right GP and inferior right GP were ablated sequentially through the left incision. The GP was localized by applying high-frequency stimulation (HFS; 20 Hz; ...

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“…This implies that the higher levels of GAP43 in the sympathetic ganglia result from retrograde axonal transport rather than local synthesis, consistent with previous finding that GAP43 is bidirectionally transported in neurons of normal sciatic nerves. 22 GAP43 is a major protein kinase C substrate of growth cones and developing nerve terminals. In the growth cone, it accumulates near the plasma membrane, where it associates with the cortical cytoskeleton and membranes.…”

Section: Gap43 and Mechanisms Of Cardiac Nerve Sprouting After MImentioning

confidence: 99%

Mechanisms of Cardiac Nerve Sprouting After Myocardial Infarction in Dogs

Zhou

Chen

Miyauchi

et al. 2004

Circulation Research

306

291

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Abstract-Cardiac nerve sprouting and sympathetic hyperinnervation after myocardial infarction (MI) both contribute to arrhythmogenesis and sudden death. However, the mechanisms responsible for nerve sprouting after MI are unclear. The expression of nerve growth factor (NGF), growth associated protein 43 (GAP43), and other nerve markers were studied at the infarcted site, the noninfarcted left ventricle free wall (LVFW), and the left stellate ganglion (LSG) at several time points (30 minutes to 1 month) after MI. Transcardiac (difference between coronary sinus and aorta) NGF levels were also assayed. Acute MI resulted in the immediate elevation of the transcardiac NGF concentration within 3.5 hours after MI, followed by the upregulation of cardiac NGF and GAP43 expression, which was earlier and more pronounced at the infarcted site than the noninfarcted LVFW. However, cardiac nerve sprouting and sympathetic hyperinnervation were more pronounced in the noninfarcted than the infarcted LVFW site and peaked at 1 week after MI. The NGF and GAP43 protein levels significantly increased in the LSG from 3 days (PϽ0.01 for all) after MI, without a concomitant increase in mRNA. There was persistent elevation of NGF levels in aorta and coronary sinus within 1 month after MI. We conclude MI results in immediate local NGF release, followed by upregulation of NGF and GAP43 expression at the infarcted site. NGF and GAP43 are transported retrogradely to LSG, which triggers nerve sprouting at the noninfarcted LVFW. A rapid and persistent upregulation of NGF and GAP43 expression at the infarcted site underlies the mechanisms of cardiac nerve sprouting after MI. Key Words: nerve growth factor Ⅲ nerve sprouting Ⅲ sympathetic nerve Ⅲ ventricular arrhythmia W e previously demonstrated that heterogeneous cardiac nerve sprouting and sympathetic hyperinnervation play important roles in arrhythmogenesis and sudden cardiac death in both human patients and animal models of myocardial infarction (MI). 1-6 However, the mechanisms and time course of nerve sprouting after MI are unclear. Nerve growth factor (NGF) is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. 7,8 NGF also regulates the synthesis of neurofilament and tubulin proteins, promotes Schwann cell migration, 9 modulates synaptic transmission between sympathetic neurons and cardiac myocytes, 10 and increases the half-life of growth associated protein-43 (GAP43). 11 Overexpression of NGF within the heart of transgenic mice causes hyperinnervation. 12 Peripheral nerve injury results in increased local NGF expression, which facilitates nerve regeneration. 13 It is possible that increased NGF expression also underlies the mechanisms of cardiac nerve sprouting after ischemic injury and MI. In the present study, we sampled blood and harvested tissues from the left ventricle and from the left stellate ganglion at different time points after experimental canine MI. NGF expression and the magnitude of cardiac nerve sprouting...

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GAP 43-like immunoreactivity in normal adult rat sciatic nerve, spinal cord, and motoneurons: Axonal transport and effect of spinal cord transection

Cited by 32 publications

References 48 publications

Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

Ablation of Epicardial Ganglionated Plexi Increases Atrial Vulnerability to Arrhythmias in Dogs

Mechanisms of Cardiac Nerve Sprouting After Myocardial Infarction in Dogs

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