PMID- 15226384
OWN - NLM
STAT- MEDLINE
DCOM- 20050125
LR  - 20220331
IS  - 0022-3565 (Print)
IS  - 0022-3565 (Linking)
VI  - 311
IP  - 2
DP  - 2004 Nov
TI  - Serotonin1B receptors in the ventral tegmental area modulate cocaine-induced 
      increases in nucleus accumbens dopamine levels.
PG  - 711-9
AB  - Previous work has demonstrated that peripheral serotonin(1B) (5-HT(1B)) receptor 
      agonist administration facilitates the behavioral and neurochemical effects of 
      cocaine. This study used dual probe microdialysis to investigate whether 
      activation of serotonin(1B) (5-HT(1B)) receptors in the ventral tegmental area 
      (VTA) alters the ability of peripherally administered cocaine to elevate dopamine 
      (DA) levels in the ipsilateral nucleus accumbens (NAcc) of drug-naive Wistar 
      rats. Intra-VTA administration of the selective 5-HT(1B) agonist 
      1,4-dihydro-3-(1,2,3,6-tetrahydro-4-pyridinyl)-5H-pyrrolo [3,2-b]pyridin-5-one 
      dihydrochloride (CP 93,129) by reverse dialysis produced a dose-dependent (30 and 
      100 microM) potentiation of cocaine-induced (10 mg/kg i.p.) increases in NAcc DA 
      efflux and concurrent cocaine-induced decreases in VTA GABA efflux. There was no 
      effect of either local CP 93,129 or peripheral cocaine on VTA glutamate efflux. 
      Intra-VTA administration of the 5-HT(1A/7) receptor agonist 
      8-hydroxy-2-dipropylaminotetralin (8-OH-DPAT; 100 microM) did not alter 
      cocaine-induced alterations in NAcc DA or VTA GABA, suggesting that the effects 
      of CP 93,129 were not mediated through 5-HT(1A) receptors. Moreover, the effects 
      of intra-VTA CP 93,129 (100 microM) on both cocaine-induced increases in NAcc DA 
      levels and cocaine-induced decreases in VTA GABA levels were reversed by 
      coadministration of the selective 5-HT(1B) receptor antagonist 
      3-[3-(dimethylamine)propyl]-4-hydroxy-N-[4-(4-pyridinyl] phenyl] benzamide 
      dihydrochloride (GR 55562; 300 microM). In the absence of cocaine, intra-VTA CP 
      93,139 produced an increase in NAcc DA and decrease in VTA GABA levels. However, 
      intra-VTA GR 55562 alone had no effect on any of our neurochemical measures. 
      These findings indicate that activation of VTA 5-HT(1B) receptors potentiates 
      cocaine-induced increases in NAcc DA levels by enhancing the ability of cocaine 
      to decrease VTA GABA efflux.
FAU - O'Dell, L E
AU  - O'Dell LE
AD  - Department of Neuropharmacology, The Scripps Research Institute, CVN-7, 10550 N. 
      Torrey Pines Road, La Jolla, CA 92037, USA.
FAU - Parsons, L H
AU  - Parsons LH
LA  - eng
GR  - DA 11004/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20040628
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Receptor, Serotonin, 5-HT1B)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - I5Y540LHVR (Cocaine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Cocaine/*pharmacology
MH  - Dopamine/*metabolism
MH  - Glutamic Acid/metabolism
MH  - Male
MH  - Nucleus Accumbens/*drug effects/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Serotonin, 5-HT1B/*metabolism
MH  - Ventral Tegmental Area/*metabolism
EDAT- 2004/07/01 05:00
MHDA- 2005/01/26 09:00
CRDT- 2004/07/01 05:00
PHST- 2004/07/01 05:00 [pubmed]
PHST- 2005/01/26 09:00 [medline]
PHST- 2004/07/01 05:00 [entrez]
AID - jpet.104.069278 [pii]
AID - 10.1124/jpet.104.069278 [doi]
PST - ppublish
SO  - J Pharmacol Exp Ther. 2004 Nov;311(2):711-9. doi: 10.1124/jpet.104.069278. Epub 
      2004 Jun 28.