A monoclonal antibody to a parasympathetic neurotrophic factor causes immunoparasympathectomy in mice

Hendry, Ian A.; Hill, Caryl E.; Belford, David A.; Watters, Dianne Josephine

doi:10.1016/0006-8993(88)90211-9

Cited by 16 publications

(4 citation statements)

References 21 publications

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“…It is clear that presynaptic input, even in the ciliary ganglion, is not the only determinant of neuronal survival. It has been demonstrated that neurotrophic factors and postsynaptic target electrical activity both contribute to neuronal survival in the ganglion (Hendry et al, 1988;Meriney et al, 1987). These two factors are probably closely interrelated, because postsynaptic electrical activity has been implicated in regulating neuronal access to target-derived neurotrophic factors at the developing neuromuscular junction (Oppenheim, 1989).…”

Section: Discussionmentioning

confidence: 99%

Sustained increase in intracellular calcium promotes neuronal survival

Collins¹,

Schmidt²,

Guthrie³

et al. 1991

J. Neurosci.

199

109

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Ciliary ganglion neurons, half of which normally suffer developmental death in the embryo, will survive in culture in medium supplemented with depolarizing concentrations of potassium. It is not known how elevated potassium acts inside the cell to promote survival. We report here that depolarizing concentrations of extracellular potassium promote neuronal survival by causing a sustained increase in intracellular calcium. Raising extracellular potassium from 5 to 40 mM, an optimal concentration for survival, caused a sustained increase in intracellular calcium from 250 nM to greater than 600 nM. By 26 hr, at which time greater than 90% of neurons in 5 mM potassium had died, the calcium concentration of neurons in 40 mM potassium was still above 400 nM. Reduction of extracellular potassium from 40 to 5 nM, which prevents the increase in survival, also reduced intracellular calcium back to rest levels. PN200-110, a dihydropyridine calcium channel blocker that inhibits the survival-promoting effect of elevated potassium, also prevented and reversed the potassium,-mediated increase in intracellular calcium. In addition, there was a strong, quantitative correlation between the percentage of neuronal survival and the intracellular calcium concentration over a wide range of extracellular potassium concentrations. These results suggest that elevated potassium opens dihydropyridine-sensitive calcium channels, causing a sustained increase in intracellular calcium that quantitatively determines the number of surviving neurons.

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Section: Discussionmentioning

confidence: 99%

Sustained increase in intracellular calcium promotes neuronal survival

Collins¹,

Schmidt²,

Guthrie³

et al. 1991

J. Neurosci.

199

109

View full text Add to dashboard Cite

show abstract

“…The generally accepted notion of the importance of CNTF as a target-derived neurotrophic factor is still in question. On one hand, Hendry et al (1988) have observed immunoparasympathectomy in mice following treatment with a blocking monoclonal antibody to CNTF, but on the other hand, Oppenheim et al (199 1) were not able to show any increase in ciliary ganglion neuronal survival following mammalian CNTF application to the chicken embryo. This discrepancy could be due to the fact that chicken CNTF only has 57% homology with the mammalian CNTF (Lin et al, 1989;Eckenstein et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Endogenous opioids modulate neuronal survival in the developing avian ciliary ganglion

et al. 1991

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Most studies on the trophic regulation of the normal neuronal competition for survival have focused on interactions between neurons and their target environment. However, it is also likely that trophic modulators are released from premotor inputs onto motoneurons. We have examined the developmental distribution of endogenous enkephalin-like immunoreactivity and the role that these endogenous opioid peptides play in normal neuronal degeneration. During the early portion of the normal cell death period, enkephalin-like immunoreactivity is highest within preganglionic cell bodies in the midbrain and their nerve terminals in the ciliary ganglion. Exogenous daily morphine administration to the chick embryo has previously been shown to delay most of the normal neuronal death in the ciliary ganglion (see Meriney et al., 1985). We hypothesized that opiate receptor activation increases the probability that ciliary ganglion neurons will survive their developmental competition and, further, that the endogenous opioid peptides in the ciliary ganglion normally modulate this competition. However, in our previous report (Meriney et al., 1985), we noted that daily administration of the antagonist naloxone to the chorioallantoic membrane did not significantly alter neuronal survival, as would have been expected if endogenous opioids were involved in regulating cell death. In contrast, in this report we show that three times daily application of naltrexone (a long-lasting opiate antagonist) significantly decreased neuronal survival among the ciliary ganglion cells, and that the surviving cells were not ultrastructurally different than neurons from controls of the same developmental stage. To control for toxic effects of naltrexone, we performed cell counts following naltrexone, we performed cell counts following naltrexone treatment in another population of cholinergic motoneurons (lumbar spinal motoneurons). In this population of cells, the total number of motoneurons remains unchanged following naltrexone treatment. To test for a specific toxic effect on the neurons of the ciliary ganglion, we generated a dose-response curve for toxicity in vitro and determined that naltrexone was not toxic over concentration ranges that are likely to exist in vivo. It appears, therefore, that a multiple daily antagonist application protocol blocks opiate receptors sufficiently in the ciliary ganglion to decrease an endogenous opiate influence significantly. We tested the possibility that endogenous opioids exert their effect by modifying transmission at peripheral and ganglionic synapses. In the generally accepted hypothesis, paralysis at the peripheral nerve-striated muscle synapse would rescue cells, while paralysis of ganglionic synapses would decrease survival. Iris neuromuscular junctions onto striated muscle cells were not blocked by opioids, but neuromuscular transmission in the smooth muscle of the choroid coat was blocked.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…The leukaemia inhibitory factor (LIF) has been shown to promote the survival of sensory neurons and to result in the differentiation of sympathetic neurons from adrenergic to cholinergic phenotype, the signal for which is believed to be derived from the target cell. There is retrograde axonal transport of LIF in sensory neurons but no detectable transport in the sympathetic system (Hendry et al 1992).…”

Section: Leukaemic Inhibitory Factormentioning

confidence: 97%

“…1988). However, no convincing retrograde axonal transport of this molecule has been demonstrated (Hendry & Belford 1991).…”

Section: Fibroblast Growth Factormentioning

confidence: 99%

Developmental Signalling

Hendry

Johanson

Heydon

1995

Clin Exp Pharma Physio

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1. In investigating the communication paths between target tissue and neurons we have been led to propose two classes of neurotrophic factors. One comprises the factors which transport themselves, the other factors relying on the transport of a second messenger. The former may have labile second messenger systems necessitating the translocation of agonist and receptor from the nerve terminal to the cell body and the latter must possess a stable second messenger system that itself is sufficiently robust to survive the transport to the cell body. 2. One such class of stable messengers may be the GTP-binding protein family and it has been shown that the alpha subunits of both Gi alpha and Gz alpha can be retrogradely transported in the mouse sciatic nerve. 3. Examination of the cell bodies in the dorsal root ganglia revealed that Gz alpha accumulated in the nucleus of cells with intact axons but that 24 h after axonal ligation this immunoreactivity decreased. 4. It is suggested that Gz is activated at the nerve terminal and it, or at least its alpha subunit, undergoes retrograde transport to the cell body where it accumulates in the nucleus.

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A monoclonal antibody to a parasympathetic neurotrophic factor causes immunoparasympathectomy in mice

Cited by 16 publications

References 21 publications

Sustained increase in intracellular calcium promotes neuronal survival

Sustained increase in intracellular calcium promotes neuronal survival

Endogenous opioids modulate neuronal survival in the developing avian ciliary ganglion

Developmental Signalling

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