PMID- 16510485
OWN - NLM
STAT- MEDLINE
DCOM- 20060809
LR  - 20131121
IS  - 0269-8811 (Print)
IS  - 0269-8811 (Linking)
VI  - 20
IP  - 2
DP  - 2006 Mar
TI  - Pre-treatment with 3,4-methylenedioxymethamphetamine (MDMA) causes long-lasting 
      changes in 5-HT2A receptor-mediated glucose utilization in the rat brain.
PG  - 272-80
AB  - The current study examined the long-term effect of brief exposure to 
      3,4-methylenedioxymethamphetamine (MDMA) on local cerebral glucose utilization 
      (LCGU) in specific brain regions immediately following administration of the 
      5-HT2A/2C receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). 
      Wistar rats (post-natal day (PND) 28, n = 24) were administered MDMA (5 mg/kg, 
      i.p.) or saline (1 ml/kg, i.p.) four times daily for 2 consecutive days and core 
      body temperature was recorded. Fifty-five days later and 10 min following 
      injection of DOI (1 mg/kg, i.p.) or saline, LCGU was measured using the 
      [14C]2-deoxyglucose (2-DG) technique. In the 4 hours following the initial 
      injection (PND 28), MDMA-treated rats exhibited significant hyperthermia compared 
      with saline-treated controls (p < 0.05-0.01). Eight weeks later, immediately 
      following DOI challenge, LCGU was significantly elevated (an increase of 47%, p < 
      0.05) in the nucleus accumbens of MDMA/DOI pretreated rats, compared with that in 
      MDMA/saline pre-treated controls. A similar trend was observed in other areas 
      such as the lateral habenula, somatosensory cortex and hippocampal regions 
      (percentage changes of 27-41%), but these did not reach significance. Blood 
      glucose levels were significantly elevated in both groups of DOI-treated rats (p 
      < 0.05-0.01). Thus, brief exposure of young rats to an MDMA regimen previously 
      shown to cause anxiety-like behaviour and modest serotonergic neurotoxicity (Bull 
      et al., 2004) increased DOI-induced energy metabolism in the nucleus accumbens 
      and tended to increase metabolism in other brain regions, including the 
      hippocampus, consistent with the induction of long-term brain region specific 
      changes in synaptic plasticity.
FAU - Bull, Eleanor J
AU  - Bull EJ
AD  - Institute of Neuroscience, Queen's Medical Centre, University of Nottingham, UK.
FAU - Porkess, Veronica
AU  - Porkess V
FAU - Rigby, Michael
AU  - Rigby M
FAU - Hutson, Peter H
AU  - Hutson PH
FAU - Fone, Kevin C F
AU  - Fone KC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Psychopharmacol
JT  - Journal of psychopharmacology (Oxford, England)
JID - 8907828
RN  - 0 (Blood Glucose)
RN  - 0 (Hallucinogens)
RN  - 0 (Receptor, Serotonin, 5-HT2A)
RN  - 0 (Serotonin Agents)
RN  - 9G2MP84A8W (Deoxyglucose)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Animals
MH  - Autoradiography
MH  - Blood Glucose/*metabolism
MH  - Brain/*drug effects
MH  - Deoxyglucose/metabolism
MH  - Energy Metabolism/*drug effects
MH  - Hallucinogens/*toxicity
MH  - Injections, Intraperitoneal
MH  - Male
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*toxicity
MH  - Nucleus Accumbens/drug effects
MH  - Premedication
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Serotonin, 5-HT2A/*drug effects
MH  - Serotonin Agents/*toxicity
EDAT- 2006/03/03 09:00
MHDA- 2006/08/10 09:00
CRDT- 2006/03/03 09:00
PHST- 2006/03/03 09:00 [pubmed]
PHST- 2006/08/10 09:00 [medline]
PHST- 2006/03/03 09:00 [entrez]
AID - 20/2/272 [pii]
AID - 10.1177/0269881106059583 [doi]
PST - ppublish
SO  - J Psychopharmacol. 2006 Mar;20(2):272-80. doi: 10.1177/0269881106059583.