PMID- 16159377
OWN - NLM
STAT- MEDLINE
DCOM- 20060203
LR  - 20181201
IS  - 0953-8194 (Print)
IS  - 0953-8194 (Linking)
VI  - 17
IP  - 10
DP  - 2005 Oct
TI  - Regulation of prolactin gene expression by vasoactive intestinal peptide and 
      dopamine in the turkey: role of Ca signalling.
PG  - 649-55
AB  - Our recent work has demonstrated that dopamine, acting through D2 dopamine 
      receptors on pituitary cells, inhibits the stimulatory effects of vasoactive 
      intestinal peptide (VIP) on prolactin release and prolactin gene transcription. 
      It is hypothesised that the stimulatory and inhibitory roles of VIP and dopamine, 
      respectively, on prolactin synthesis and release are mediated by their opposite 
      effects on intracellular Ca2+ concentration ([Ca2+]i) in lactotrophs. The present 
      study aimed: (i) to investigate the effect of VIP and dopamine on [Ca2+]i of 
      cultured turkey anterior pituitary cells and (ii) to examine the role of Ca2+ 
      signalling in mediating the regulatory effects of VIP and dopamine on prolactin 
      mRNA levels and prolactin release. Changes in [Ca2+]i were measured 
      spectrofluorometrically using Fura-2/AM as a fluorescent Ca2+ indicator. 
      Semi-quantitative reverse transcription-polymerase chain reaction and 
      radioimmunoassay were used to determine prolactin mRNA levels and prolactin 
      release, respectively. VIP or the L-type Ca2+ channel activator, Bay K8644 (Bay) 
      increased [Ca2+]i in a concentration- and time-dependent fashion, an effect 
      abolished by preincubating the cells with R(-)-propylnorapomorphine HCl, a D2 
      dopamine receptor agonist (D2AG) or Verapamil (VR), a specific L-type Ca2+ 
      channel blocker. Similarly, either VR or D2Ag diminished the VIP/Bay stimulatory 
      effect on prolactin expression and release. On the other hand, pretreatment of 
      pituitary cells with thapsigargin (TG) or neomycin (NEO), to deplete the 
      intracellular Ca2+ stores, showed no effect on basal or VIP-stimulated prolactin 
      mRNA levels; although VIP-induced prolactin release was partially inhibited by 
      NEO but not TG. These results suggest that intracellular Ca2+ represents a common 
      signal transduction pathway through which VIP and dopamine can exert antagonistic 
      control on prolactin synthesis and release in avian lactotrophs.
FAU - Al Kahtane, A
AU  - Al Kahtane A
AD  - Department of Animal Science, University of Minnesota, St Paul, MN, USA.
FAU - Kannan, M
AU  - Kannan M
FAU - Kang, S W
AU  - Kang SW
FAU - El Halawani, M E
AU  - El Halawani ME
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
RN  - 0 (RNA, Messenger)
RN  - 37221-79-7 (Vasoactive Intestinal Peptide)
RN  - 9002-62-4 (Prolactin)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Calcium Signaling/*physiology
MH  - Cells, Cultured
MH  - Dopamine/*physiology
MH  - Female
MH  - Gene Expression Regulation/*physiology
MH  - Intracellular Fluid/metabolism
MH  - Pituitary Gland, Anterior/cytology/metabolism
MH  - Prolactin/genetics/*metabolism
MH  - RNA, Messenger/analysis
MH  - Signal Transduction/physiology
MH  - Turkeys/genetics/*metabolism
MH  - Vasoactive Intestinal Peptide/*physiology
EDAT- 2005/09/15 09:00
MHDA- 2006/02/04 09:00
CRDT- 2005/09/15 09:00
PHST- 2005/09/15 09:00 [pubmed]
PHST- 2006/02/04 09:00 [medline]
PHST- 2005/09/15 09:00 [entrez]
AID - JNE1352 [pii]
AID - 10.1111/j.1365-2826.2005.01352.x [doi]
PST - ppublish
SO  - J Neuroendocrinol. 2005 Oct;17(10):649-55. doi: 10.1111/j.1365-2826.2005.01352.x.