PMID- 15328036
OWN - NLM
STAT- MEDLINE
DCOM- 20041108
LR  - 20141120
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1021
IP  - 1
DP  - 2004 Sep 17
TI  - Dopamine D1/D5 receptor activation fails to initiate an activity-independent 
      late-phase LTP in rat hippocampus.
PG  - 92-100
AB  - The role of dopamine in the hippocampus remains poorly defined. Numerous studies 
      have suggested that it acts as a neuromodulator of late-phase long-term 
      potentiation (L-LTP) in CA1, while other reports controversially indicate that 
      D1/D5 receptor (D1/D5R) activation may directly initiate activity-independent 
      LTP. We have further investigated this putative role of dopamine in area CA1 in 
      rat hippocampal slices using field potential recording techniques. Application of 
      the dopamine D1/D5 receptor agonists SKF 38393 and 6-bromo-APB at 100 microM for 
      20 min did not induce an activity-independent L-LTP. Varying the incubation 
      conditions still did not permit either SKF 38393 or an alternative D1/D5R 
      agonist, 6-chloro-PB, to induce L-LTP. To further determine if intracellular 
      mechanisms, which may act to limit the expression of LTP, were preventing 
      D1/D5R-induced L-LTP expression, we inhibited protein phosphatase 1 activity by 
      reducing cyclin-dependent kinase 5 (cdk5) inhibition of inhibitor 1. Inhibition 
      of cdk5 by roscovitine (10 microM, 40 min) did not facilitate the ability of SKF 
      38393 to induce L-LTP in CA1. Biochemical experiments confirmed that the 
      concentration of agonist used significantly elevated intracellular cAMP levels, 
      suggesting that effective D1/D5R activation was achieved. Furthermore, 
      coactivation with NMDA receptors (NMDAR) resulted in a synergistic increase in 
      cAMP. These findings demonstrate that D1/D5R activation in CA1 initiates 
      intracellular second messenger accumulation, but that this is insufficient to 
      induce an activity-independent L-LTP.
FAU - Mockett, Bruce G
AU  - Mockett BG
AD  - Department of Psychology, University of Otago, P.O. Box 56, Dunedin 9001, New 
      Zealand. mockettb@psy.otago.ac.nz
FAU - Brooks, Wendy M
AU  - Brooks WM
FAU - Tate, Warren P
AU  - Tate WP
FAU - Abraham, Wickliffe C
AU  - Abraham WC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Dopamine Agents)
RN  - 0 (Drd5 protein, rat)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 137750-35-7 (Receptors, Dopamine D5)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - 67287-49-4 (2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine)
RN  - E0399OZS9N (Cyclic AMP)
SB  - IM
MH  - 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology
MH  - Animals
MH  - Cyclic AMP/metabolism
MH  - Dopamine Agents/pharmacology
MH  - Drug Synergism
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Hippocampus/*physiology
MH  - In Vitro Techniques
MH  - Long-Term Potentiation/*physiology
MH  - Male
MH  - N-Methylaspartate/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine D1/*physiology
MH  - Receptors, Dopamine D5
MH  - Receptors, N-Methyl-D-Aspartate/physiology
MH  - Synaptic Transmission/drug effects/physiology
EDAT- 2004/08/26 05:00
MHDA- 2004/11/09 09:00
CRDT- 2004/08/26 05:00
PHST- 2004/06/27 00:00 [accepted]
PHST- 2004/08/26 05:00 [pubmed]
PHST- 2004/11/09 09:00 [medline]
PHST- 2004/08/26 05:00 [entrez]
AID - S0006-8993(04)01034-0 [pii]
AID - 10.1016/j.brainres.2004.06.039 [doi]
PST - ppublish
SO  - Brain Res. 2004 Sep 17;1021(1):92-100. doi: 10.1016/j.brainres.2004.06.039.