Abstract
Membrane capacitance measurements were used to study neuropeptide modulation of exocytosis by perforated patch clamped rat lactotrophs. We report that depolarizing voltage-clamp pulses evoke exocytosis that is steeply dependent on Ca2+ influx through voltage-gated Ca2+ channels. Furthermore, we find that the neuropeptide TRH (thyrotropin-releasing hormone) acts in three phases to promote exocytosis. First, TRH transiently (within ~0.5 min) triggers depolarization- and extracellular Ca2+- independent exocytosis. Second, within 3 min of application, TRH facilitates depolarization-evoked exocytosis while inhibiting voltage-gated Ca2+ current. Finally, after 8 min, TRH further enhances depolarization-evoked exocytosis by increasing high-voltage-activated (HVA) Ca2+ channel current. Activation of protein kinase C (PKC) with a phorbol ester also stimulates depolarization-evoked exocytosis by increasing Ca2+ current. Therefore, PKC can only account for the last effect of TRH. Thus, a single neuromodulator may employ several temporally distinct mechanisms to stimulate peptide secretion.
Original language | English (US) |
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Pages (from-to) | 4982-4991 |
Number of pages | 10 |
Journal | Journal of Neuroscience |
Volume | 15 |
Issue number | 7 I |
State | Published - Jul 1995 |
Externally published | Yes |
Keywords
- calcium channel
- exocytosis
- neuropeptide
- pituitary
- prolactin
- protein kinase C
ASJC Scopus subject areas
- Neuroscience(all)