Axotomy and nerve growth factor regulate levels of neuronal nicotinic acetylcholine receptor alpha 3 subunit protein in the rat superior cervical ganglion

Neuronal nicotinic acetylcholine receptors (nAChRs) play a significant role in sympathetic transmission in the superior cervical ganglia (SCG), with most of the signal carried by a nAChR containing an alpha 3 subunit. Work has shown that transection of the postganglionic nerves (axotomy) of the SCG...

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Veröffentlicht in:Journal of neurochemistry 2001-10, Vol.79 (2), p.258-265
Hauptverfasser: Yeh, J J, Ferreira, M, Ebert, S, Yasuda, R P, Kellar, K J, Wolfe, B B
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Sprache:eng
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Zusammenfassung:Neuronal nicotinic acetylcholine receptors (nAChRs) play a significant role in sympathetic transmission in the superior cervical ganglia (SCG), with most of the signal carried by a nAChR containing an alpha 3 subunit. Work has shown that transection of the postganglionic nerves (axotomy) of the SCG results in a decrease in mRNA transcripts for alpha 3, alpha 5, alpha 7 and beta 4 and in protein expression of alpha 7 and beta 4. To evaluate effects of axotomy on alpha 3 protein in the SCG, quantitative immunoblotting was used to demonstrate a dramatic decrease (> 80%) in the levels of this subunit 4 days after axotomy. Similarly, immunocytochemistry showed a marked decline in the number and the intensity of stained neurons for the alpha 3 subunit as well as tyrosine hydroxylase. Ganglia explanted into culture for 4 days also showed a substantial decrease in alpha 3 subunit protein. This decrease was partially prevented by the addition of nerve growth factor (NGF) to the culture medium at the time of explantation. Additionally, this decrease was reversed by the addition of NGF to the culture medium following 4 days in culture in the absence of NGF. These findings suggest that the loss of alpha 3 subunit contributes to the reported decrease in ganglionic synaptic transmission that follows axotomy, and that NGF plays an important role in regulating the expression of alpha 3-containing nAChRs in the SCG.
ISSN:0022-3042
DOI:10.1046/j.1471-4159.2001.00545.x