Related Experiment Videos
Lactotrope subtypes are differentially responsive to calcium channel blockers
1Department of Physiology, Biophysics, and Neurosciences, Centro de Investigacion y de Estudios Avanzados, Mexico City, DF.
Molecular and Cellular Endocrinology
|April 1, 1993
Summary
Omega-conotoxin and nifedipine inhibit prolactin (PRL) secretion by blocking calcium channels. These drugs reduce large-plaque lactotropes, suggesting calcium channel blockers preferentially suppress PRL release from these cells.
Area of Science:
- Endocrinology
- Cell Biology
- Neuropharmacology
Background:
- Pituitary cultures contain two prolactin (PRL) cell subtypes: small-plaque (SP) and large-plaque (LP) lactotropes.
- These subtypes exhibit distinct basal secretion rates, forming different-sized plaques in assays.
Purpose of the Study:
- To investigate the effects of omega-conotoxin (omega-CgTx) and nifedipine on basal PRL secretion.
- To determine how these calcium channel blockers influence PRL release from distinct lactotrope subtypes.
Main Methods:
- Utilized plaque assays to study single male rat lactotropes.
- Administered omega-conotoxin (omega-CgTx) and nifedipine to block high voltage-activated (HVA) calcium channels.
Main Results:
- Both omega-conotoxin and nifedipine potently inhibited PRL secretion.
- These drugs decreased the number of large-plaque (LP) PRL-secreting cells.
- A comparable increase in small-plaque (SP) PRL-secreting cells was observed.
Conclusions:
- Blocking HVA calcium channels preferentially suppresses PRL release from LP lactotropes.
- Inhibited LP lactotropes functionally resemble SP lactotropes.
- This suggests a critical role for HVA calcium channels in regulating PRL secretion from specific lactotrope populations.