ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Lack of neurotrophin-4 causes selective structural and chemical deficits in sympathetic ganglia and their preganglionic innervation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 37 citations in OpenAlex.
- To celebrate the 80th birthday of Klaus Unsicker: discovery of a new growth factor and studies on the effects of growth factors on adrenal chromaffin cells and neurons.Cell and tissue research · 2022Article
- Retrograde influences of SCG axotomy on uninjured preganglionic neurons.Brain research · 2018Article
- Cell loss and autophagy in the extra-adrenal chromaffin organ of Zuckerkandl are regulated by glucocorticoid signalling.Journal of neuroendocrinology · 2013Article
- Development of the vagal innervation of the gut: steering the wandering nerve.Neurogastroenterology and motility · 2011Review
- Impaired activation of celiac ganglion neurons in vivo after damage to their sympathetic nerve terminals.Journal of neuroscience research · 2008Article
- Neurotrophic factors in autonomic nervous system plasticity and dysfunction.Neuromolecular medicine · 2008Review
- Pathophysiological mechanisms for actions of the neurotrophins.Brain pathology (Zurich, Switzerland) · 2006Review
- Neurotrophin-regulated signalling pathways.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2006Review
- Loss of leukemia inhibitory factor receptor beta or cardiotrophin-1 causes similar deficits in preganglionic sympathetic neurons and adrenal medulla.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Heterogeneous requirement of NGF for sympathetic target innervation in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Neurotrophin-4 deficient mice have a loss of vagal intraganglionic mechanoreceptors from the small intestine and a disruption of short-term satiety.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotrophin-4 (NT-4) is perhaps the still most enigmatic member of the neurotrophin family. We show here that NT-4 is expressed in neurons of paravertebral and prevertebral sympathetic ganglia, i.e., the superior cervical (SCG), stellate (SG), and celiac (CG) ganglion. Mice deficient for NT-4 showed a significant reduction (20-30%) of preganglionic sympathetic neurons in the intermediolateral column (IML) of the thoracic spinal cord. In contrast, neuron numbers in the SCG, SG, and CG were unchanged. Numbers of axons in the thoracic sympathetic trunk (TST) connecting the SG with lower paravertebral ganglia were also reduced, whereas axon numbers in the cervical sympathetic trunk (CST) were unaltered. Axon losses in the TST were paralleled by losses of synaptic terminals on SG neurons visualized by electron microscopy. Furthermore, immunoreactivity for the synaptic vesicle antigen SV2 was clearly reduced in the SG and CG. Levels of catecholamines and tyrosine hydroxylase immunoreactivity were dramatically reduced in the SG and the CG but not in the SCG. Despite this severe phenotype in the sympathetic system, blood pressure levels were not reduced and displayed a pattern more typical of deficits in baroreceptor afferents. Numbers of IML neurons were unaltered at postnatal day 4, suggesting a postnatal requirement for their maintenance. In light of these and previous data, we hypothesize that NT-4 provided by postganglionic sympathetic neurons is required for establishing and/or maintaining synapses of IML neurons on postganglionic cells. Impairment of synaptic connectivity may consequently reduce impulse flow, causing a reduction in transmitter synthesis in postganglionic neurons.
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Identifiers
11312292PMC6762558W2153700867What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.