Development of cholinergic terminals around rat spinal motor neurons and their potential relationship to developmental cell death
| Autor: | James E. Vaughn, Richard Wetts |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Male
Programmed cell death Vesicular Acetylcholine Transport Proteins Immunocytochemistry Vesicular Transport Proteins In Vitro Techniques Biology Cholinergic Antagonists Rats Sprague-Dawley Embryonic and Fetal Development Postsynaptic potential Vesicular acetylcholine transporter medicine Animals Motor Neurons Nerve Endings Cell Death General Neuroscience Membrane Transport Proteins Embryo Mammalian Spinal cord Immunohistochemistry Embryonic stem cell Rats medicine.anatomical_structure Cholinergic Fibers Spinal Cord Cholinergic Female Carrier Proteins Neuron death Neuroscience |
| Zdroj: | The Journal of Comparative Neurology. 435:171-183 |
| ISSN: | 1096-9861 0021-9967 |
| DOI: | 10.1002/cne.1200 |
| Popis: | Neuron death seems to be regulated mainly by postsynaptic target cells. In chicks, nicotinic antagonists such as alpha-bungarotoxin (αBT) can prevent normal cell death of somatic motor neurons (SMNs). For this effect, however, αBT could be acting at peripheral neuromuscular junctions and/or central cholinergic synapses. To investigate this issue, we first studied the development of cholinergic terminals in the rat spinal cord by using vesicular acetylcholine transporter immunocytochemistry. Labeled terminals were seen in the ventral horn as early as embryonic day 15 (E15), the beginning of the cell death period. Thus, central cholinergic synapses form at the correct time and place to be able to influence SMN death. We next added αBT to organotypic, spinal slice cultures made at E15. After 5 days in vitro, the number of SMNs in treated cultures was substantially greater than in control cultures, indicating that αBT can reduce SMN cell death in rats as it does in chicks. Moreover, peripheral target removal led to extensive loss of SMNs, and such a loss occurred even in the presence of αBT, indicating the necessity of peripheral target for the αBT effect. Finally, to determine whether central cholinergic terminals also may be involved in SMN death, we delayed the αBT treatment until after central cholinergic terminals had disappeared from the slice cultures. The increased number of surviving SMNs, even in the absence of central terminals, argued that αBT acts at peripheral, not central, cholinergic synapses to rescue SMNs from developmental cell death. J. Comp. Neurol. 435:171–183, 2001. © 2001 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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