PMID- 16901517
OWN - NLM
STAT- MEDLINE
DCOM- 20070112
LR  - 20161124
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 51
IP  - 5
DP  - 2006 Oct
TI  - Blockade of group II metabotropic glutamate receptors in the nucleus accumbens 
      produces hyperlocomotion in rats previously exposed to amphetamine.
PG  - 986-92
AB  - The neurotransmitter glutamate is known to participate in both the induction and 
      expression of locomotor sensitization by psychostimulant drugs like amphetamine. 
      Previously, it was reported that subtype nonselective blockade of metabotropic 
      glutamate receptors (mGluRs) in the nucleus accumbens (NAcc) produces 
      hyperlocomotion in rats previously exposed to amphetamine. The present 
      experiments examined whether group II mGluRs may contribute to this effect. Rats 
      in different groups were administered five injections of either saline or 
      amphetamine (1.0 mg/kg, i.p.), one injection given every third day. Two weeks 
      later, they were tested for 2 h following an injection of either saline or the 
      group II mGluR antagonist LY341495. In one experiment, test injections were 
      administered systemically (saline or LY341495, 1.0 mg/kg, i.p.). Rats previously 
      exposed to amphetamine showed a greater locomotor response to LY341495 on the 
      test compared to controls previously exposed to saline. This hyperlocomotor 
      response was absent in rats tested with a combination of LY341495 and the group 
      II mGluR agonist LY379268 (1.0 mg/kg, i.p.). In a second experiment, different 
      rats were tested following microinjections into the NAcc (saline or LY341495, 
      0.1, 10 or 100 microg/0.5 microl/side). Again, rats previously exposed to 
      amphetamine showed a greater dose-dependent locomotor response to LY341495 on the 
      test relative to saline-exposed controls. Locomotor activity in saline-exposed 
      rats challenged with LY341495 did not differ from that observed in rats 
      previously exposed and tested with saline in either experiment. These results 
      indicate that group II mGluRs, particularly those found in the NAcc, are well 
      positioned to modulate the expression of locomotor sensitization by amphetamine.
FAU - Chi, Henry
AU  - Chi H
AD  - Department of Psychiatry, University of Chicago, 5841 South Maryland Avenue, 
      MC3077, Chicago, IL 60637, USA.
FAU - Jang, Ju Kyong
AU  - Jang JK
FAU - Kim, Jeong-Hoon
AU  - Kim JH
FAU - Vezina, Paul
AU  - Vezina P
LA  - eng
GR  - DA09860/DA/NIDA NIH HHS/United States
GR  - T32-DA07255/DA/NIDA NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20060808
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Amino Acids)
RN  - 0 (Bridged Bicyclo Compounds, Heterocyclic)
RN  - 0 (Central Nervous System Stimulants)
RN  - 0 (LY 341495)
RN  - 0 (LY 379268)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 0 (Xanthenes)
RN  - 0 (metabotropic glutamate receptor 2)
RN  - CK833KGX7E (Amphetamine)
SB  - IM
MH  - Amino Acids/pharmacology
MH  - Amphetamine/*pharmacology
MH  - Analysis of Variance
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Bridged Bicyclo Compounds, Heterocyclic/pharmacology
MH  - Central Nervous System Stimulants/*pharmacology
MH  - Drug Interactions
MH  - Hyperkinesis/*etiology
MH  - Male
MH  - Motor Activity/drug effects
MH  - Nucleus Accumbens/*drug effects/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Metabotropic Glutamate/agonists/antagonists & inhibitors/*physiology
MH  - Xanthenes/pharmacology
EDAT- 2006/08/12 09:00
MHDA- 2007/01/16 09:00
CRDT- 2006/08/12 09:00
PHST- 2006/04/09 00:00 [received]
PHST- 2006/06/03 00:00 [revised]
PHST- 2006/06/13 00:00 [accepted]
PHST- 2006/08/12 09:00 [pubmed]
PHST- 2007/01/16 09:00 [medline]
PHST- 2006/08/12 09:00 [entrez]
AID - S0028-3908(06)00192-4 [pii]
AID - 10.1016/j.neuropharm.2006.06.008 [doi]
PST - ppublish
SO  - Neuropharmacology. 2006 Oct;51(5):986-92. doi: 10.1016/j.neuropharm.2006.06.008. 
      Epub 2006 Aug 8.