Distinct muscle targets do not vary in the developmental regulation of brain‐derived neurotrophic factor

Vernon, Elizabeth; Oppenheim, Ronald W.; Johnson, James E.

doi:10.1002/cne.20018

Cited by 6 publications

(3 citation statements)

References 75 publications

(65 reference statements)

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“…Therefore, increased activity would decrease branching/synaptogenesis and promote MN PCD, whereas decreased activity would increase branching/synaptogenesis and promote MN survival. Although these two hypotheses are not mutually exclusive, the evidence is more consistent with the access hypothesis (Tanaka, 1987;Houenou et al, 1990;D'Costa et al, 1998;Vernon et al, 2004).…”

Section: Introductionsupporting

confidence: 48%

The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle‐specific nicotinic acetylcholine receptor

Oppenheim

Calderó

Cuitat

et al. 2008

Developmental Neurobiology

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In an attempt to determine whether the rescue of developing motoneurons (MNS) from programmed cell death (PCD) in the chick embryo following reductions in neuromuscular function involves muscle or neuronal nicotinic acetylcholine receptors (nAChRs), we have employed a novel cone snail toxin alphaA-OIVA that acts selectively to antagonize the embryonic/fetal form of muscle nAChRs. The results demonstrate that alphaA-OIVA is nearly as effective as curare or alpha-bungarotoxin (alpha-BTX) in reducing neuromuscular function and is equally effective in increasing MN survival and intramuscular axon branching. Together with previous reports, we also provide evidence consistent with a transition between the embryonic/fetal form to the adult form of muscle nAChRs in chicken that involves the loss of the gamma subunit in the adult receptor. We conclude that selective inhibition of the embryonic/fetal form of the chicken muscle nAChR is sufficient to rescue MNs from PCD without any involvement of neuronal nAChRs.

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Section: Introductionsupporting

confidence: 48%

The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle‐specific nicotinic acetylcholine receptor

Oppenheim

Calderó

Cuitat

et al. 2008

Developmental Neurobiology

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“…Similarly, BDNF protein levels, measured by a highly sensitive electrochemiluminescent immunosorbent assay, fail to differ between chick thigh muscles during the period of MN PCD (Vernon et al, 2004). These results, together with the fact that every neuron within a pool expresses specific NTF-Rs, suggest that differential target expression of these molecules does not likely account for the normal reduction of MNs by PCD.…”

Section: Ntf-rs Are Expressed Heterogeneously In the Spinal Cord And mentioning

confidence: 95%

The Function of Neurotrophic Factor Receptors Expressed by the Developing Adductor Motor PoolIn Vivo

Gould¹,

Oppenheim²

2004

J. Neurosci.

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We examined the spatio-temporal relationship between neurotrophic factor receptor (NTF-R) expression and motoneuron (MN) survival in the developing avian spinal cord and observed heterogeneity in the expression of NTF-Rs between, but not within, pools of MNs projecting to individual muscles. We then focused on the role of NTFs in regulating the survival of one motor pool of MNs, all of which innervate a pair of adductor muscles in the thigh and hence compete for survival during the period of programmed cell death (PCD). The complete NTF-R complement of these MNs was analyzed and found to include many, but not all, NTF-Rs. Treatment with exogenous individual NTFs rescued some, but not all, adductor MNs expressing appropriate NTF-Rs. In contrast, administration of multiple NTFs completely rescued adductor MNs from PCD. Additionally, adductor MNs were partially rescued from PCD by NTFs for which they failed to express receptors. NTF-Rs expressed by the nerve but not in the muscle target were capable of mediating survival signals to MNs in trans. Finally, the expression of some NTF-Rs by adductor MNs was not required for MN survival. These studies demonstrate the complexity in NTF regulation of a defined subset of competing MNs and suggest that properties other than NTF-R expression itself can play a role in mediating trophic responses to NTFs.

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“…In fact, BDNF and NT-3 immunoreactivity is present in large neurons (possibly phrenic motor neurons) in the cervical ventral spinal cord (Johnson et al, 2000). The neurotrophins BDNF, NT-3 and NT-4 are also expressed in skeletal muscle (Henderson et al, 1993; Griesbeck et al, 1995), but it is unclear whether there are differences in neurotrophin expression across motor unit types (Funakoshi et al, 1995; Sakuma et al, 2001; Vernon et al, 2004). …”

Section: Trophic Factors and Their Receptorsmentioning

confidence: 99%

Trophic factor expression in phrenic motor neurons

Mantilla

Sieck

2008

Respiratory Physiology & Neurobiology

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The function of a motor neuron and the muscle fibers it innervates (i.e., a motor unit) determines neuromotor output. Unlike other skeletal muscles, respiratory muscles (e.g., the diaphragm, DIAm) must function from birth onwards in sustaining ventilation. DIAm motor units are capable of both ventilatory and non-ventilatory behaviors, including expulsive behaviors important for airway clearance. There is significant diversity in motor unit properties across different types of motor units in the DIAm. The mechanisms underlying the development and maintenance of motor unit diversity in respiratory muscles (including the DIAm) are not well understood. Recent studies suggest that trophic factor influences contribute to this diversity. Remarkably little is known about the expression of trophic factors and their receptors in phrenic motor neurons. This review will focus on the contribution of trophic factors to the establishment and maintenance of motor unit diversity in the DIAm, during development and in response to injury or disease.

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Distinct muscle targets do not vary in the developmental regulation of brain‐derived neurotrophic factor

Cited by 6 publications

References 75 publications

The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle‐specific nicotinic acetylcholine receptor

The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle‐specific nicotinic acetylcholine receptor

The Function of Neurotrophic Factor Receptors Expressed by the Developing Adductor Motor PoolIn Vivo

Trophic factor expression in phrenic motor neurons

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