PMID- 6738811
OWN - NLM
STAT- MEDLINE
DCOM- 19840807
LR  - 20180214
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 38
IP  - 6
DP  - 1984 Jun
TI  - Prolactin-induced activation of tuberoinfundibular dopaminergic neurons: evidence 
      for both a rapid 'tonic' and a delayed 'induction' component.
PG  - 467-75
AB  - Results of previous studies have revealed that prolactin causes a delayed (12-16 
      h) increase in the rate of synthesis and turnover of dopamine (DA) in terminals 
      of tuberoinfundibular (TI) neurons in the median eminence. Attempts to 
      demonstrate a rapid in vivo action of prolactin on these neurons has been 
      frustrated because pharmacological manipulations needed to make the biochemical 
      measurements of TIDA neuronal activity (i.e., administration of 
      alpha-methyltyrosine or NSD 1015) inhibit DA synthesis and thereby remove the 
      tonic inhibitory control of DA on prolactin secretion. Thus, 'control' rates of 
      synthesis and turnover of DA in terminals of TIDA neurons are actually values 
      obtained in the presence of high circulating concentrations of prolactin. Results 
      of the present in vivo studies demonstrate that there are two components to the 
      activation of TIDA neurons by prolactin: a rapid 'tonic' component, which is 
      responsive to acute changes in prolactin concentrations, and a delayed 
      'induction' component, which is activated by long-term changes in prolactin 
      concentrations. Experimental observations which support this proposal are 
      described below. Hypophysectomy or treatment with bromocriptine (a DA agonist) 
      reduce circulating levels of prolactin and reduce the rate of DA synthesis in the 
      median eminence. Intracerebroventricular (i.c.v.) administration of prolactin to 
      these animals increases the rate of DA synthesis in the median eminence within 4 
      h (rapid 'tonic' component) and then causes a further increase after 12 h 
      (delayed 'induction' component); only the latter component is blocked by 
      treatment with cycloheximide, indicating the involvement in protein 
      synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Demarest, K T
AU  - Demarest KT
FAU - Riegle, G D
AU  - Riegle GD
FAU - Moore, K E
AU  - Moore KE
LA  - eng
GR  - AG02644/AG/NIA NIH HHS/United States
GR  - NS09174/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 3A64E3G5ZO (Bromocriptine)
RN  - 9002-62-4 (Prolactin)
RN  - 98600C0908 (Cycloheximide)
RN  - J6292F8L3D (Haloperidol)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Bromocriptine/pharmacology
MH  - Cycloheximide/pharmacology
MH  - Dopamine/metabolism/*physiology
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Haloperidol/pharmacology
MH  - Median Eminence/cytology/metabolism/*physiology
MH  - Neurons/physiology
MH  - Prolactin/*pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Reaction Time
EDAT- 1984/06/01 00:00
MHDA- 1984/06/01 00:01
CRDT- 1984/06/01 00:00
PHST- 1984/06/01 00:00 [pubmed]
PHST- 1984/06/01 00:01 [medline]
PHST- 1984/06/01 00:00 [entrez]
AID - 10.1159/000123935 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1984 Jun;38(6):467-75. doi: 10.1159/000123935.