Role of N- and L-type calcium channels in depolarization-induced activation of tyrosine hydroxylase and release of norepinephrine by sympathetic cell bodies and nerve terminals
✍ Scribed by Rittenhouse, Ann R. ;Zigmond, Richard E.
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 154 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0022-3034
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✦ Synopsis
Multiple types of voltage-activated calcium (Ca 2؉ ) channels are present in all nerve cells examined so far; however, the underlying functional consequences of their presence is often unclear. We have examined the contribution of Ca 2؉ influx through Nand L-type voltage-activated Ca 2؉ channels in sympathetic neurons to the depolarization-induced activation of tyrosine hydroxylase (TH), the rate-limiting enzyme in norepinephrine (NE) synthesis, and the depolarization-induced release of NE. Superior cervical ganglia (SCG) were decentralized 4 days prior to their use to eliminate the possibility of indirect effects of depolarization via preganglionic nerve terminals. The presence of both -conotoxin GVIA (1 M), a specific blocker of N-type channels, and nimodipine (1 M), a specific blocker of L-type Ca 2؉ channels, was necessary to inhibit completely the stimulation of TH activity by 55 mM K ؉ , indicating that Ca 2؉ influx through both types of channels contributes to enzyme activation. In contrast, K ؉ stimulation of TH activity in nerve fibers and terminals in the iris could be inhibited completely by -conotoxin GVIA alone and was unaffected by nimodipine as previously shown. K ؉ stimulation of NE release from both ganglia and irises was also blocked completely when -conotoxin GVIA was included in the medium, while nimodipine had no significant effect in either tissue. These results indicate that particular cellular processes in specific areas of a neuron are differentially dependent on Ca 2؉ influx through N-and Ltype Ca 2؉ channels.