PMID- 11388699
OWN - NLM
STAT- MEDLINE
DCOM- 20010614
LR  - 20220318
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 68
IP  - 17
DP  - 2001 Mar 16
TI  - Involvement of central GABAergic neurons in basal and diurnal changes of 
      tuberoinfundibular dopaminergic neuronal activity and prolactin secretion.
PG  - 1965-75
AB  - Central administration of gamma-aminobutyric acid (GABA) has been shown to 
      stimulate the secretion of prolactin (PRL). Whether GABA acts via dopamine, the 
      major PRL-inhibiting hormone, and which GABA receptor type(s) is involved have 
      not been ascertained. Both GABA(A) and GABA(B) receptor agonists and/or 
      antagonists were administered centrally in this study and their effects on both 
      basal and diurnal changes of tuberoinfundibular dopaminergic (TIDA) neuronal 
      activity were determined by measuring the concentration of 
      3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence (ME). Serum PRL 
      level was determined by RIA. Ovariectomized, estrogen-primed Sprague-Dawley rats 
      implanted with intracerebroventricular (icv) cannulae were used. Muscimol (1 ng/3 
      microl/rat, icv), a GABA(A) receptor agonist, but not baclofen (1-100 ng/3 
      microl/rat, icv), a GABA(B) receptor agonist, injected in the morning 
      significantly lowered and elevated ME DOPAC and serum PRL levels, respectively at 
      15 and 30 min. Lower and higher doses of muscimol were not effective. The effects 
      of muscimol could also be prevented by co-administration of bicuculline (0.1-10 
      ng/3 microl, icv), a GABA(A) receptor antagonist. When bicuculline (10-500 ng/3 
      microl, icv) was given in the afternoon (at 1500 h), it significantly reversed 
      the lowered ME DOPAC level in the afternoon and prevented the concurrent PRL 
      surge. We conclude that endogenous GABA acting through GABA(A) receptors may play 
      a significant role in the control of basal and diurnal changes of TIDA neuronal 
      activity, and in turn, PRL secretion.
FAU - Lee, T Y
AU  - Lee TY
AD  - Department of Physiology, School of Life Science, National Yang-Ming University, 
      Taipei, Taiwan, ROC.
FAU - Pan, J T
AU  - Pan JT
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (GABA Agonists)
RN  - 0 (GABA Antagonists)
RN  - 0 (GABA-A Receptor Agonists)
RN  - 0 (GABA-A Receptor Antagonists)
RN  - 0 (GABA-B Receptor Agonists)
RN  - 0 (GABA-B Receptor Antagonists)
RN  - 0 (Receptors, GABA-A)
RN  - 0 (Receptors, GABA-B)
RN  - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)
RN  - 2763-96-4 (Muscimol)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
RN  - 9002-62-4 (Prolactin)
RN  - H789N3FKE8 (Baclofen)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - 3,4-Dihydroxyphenylacetic Acid/metabolism
MH  - Animals
MH  - Arcuate Nucleus of Hypothalamus/cytology/drug effects/*physiology
MH  - Baclofen/pharmacology
MH  - Circadian Rhythm/drug effects/*physiology
MH  - Dopamine/*physiology
MH  - Female
MH  - GABA Agonists/pharmacology
MH  - GABA Antagonists/pharmacology
MH  - GABA-A Receptor Agonists
MH  - GABA-A Receptor Antagonists
MH  - GABA-B Receptor Agonists
MH  - GABA-B Receptor Antagonists
MH  - Median Eminence/metabolism
MH  - Muscimol/pharmacology
MH  - Neurons/drug effects/*physiology
MH  - Prolactin/blood/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, GABA-A/physiology
MH  - Receptors, GABA-B/physiology
MH  - gamma-Aminobutyric Acid/*physiology
EDAT- 2001/06/05 10:00
MHDA- 2001/06/15 10:01
CRDT- 2001/06/05 10:00
PHST- 2001/06/05 10:00 [pubmed]
PHST- 2001/06/15 10:01 [medline]
PHST- 2001/06/05 10:00 [entrez]
AID - S0024320501009882 [pii]
AID - 10.1016/s0024-3205(01)00988-2 [doi]
PST - ppublish
SO  - Life Sci. 2001 Mar 16;68(17):1965-75. doi: 10.1016/s0024-3205(01)00988-2.