PMID- 15863226 OWN - NLM STAT- MEDLINE DCOM- 20050715 LR - 20131121 IS - 0166-4328 (Print) IS - 0166-4328 (Linking) VI - 160 IP - 2 DP - 2005 May 28 TI - Ibotenic acid lesions of the medial prefrontal cortex block the development and expression of 3,4-methylenedioxymethamphetamine-induced behavioral sensitization in rats. PG - 304-11 AB - There is ample evidence that plastic changes in the nervous system require the excitatory amino acid transmission. This appears to be also the case for psychostimulant-induced behavioral sensitization. More specifically the glutamatergic input from the medial prefrontal cortex (mPFC) to the VTA and the NAc appears to be involved in behavioral sensitization processes. However, dissociations regarding the role of the mPFC with respect to the development and expression of sensitization, as well as with respect to the psychostimulant being studied (amphetamine versus cocaine) appear to exist. The present study examined the role of the dorsal mPFC in the development and expression of 3,4-methylenedioxymethamphetamine (MDMA)-induced sensitization. Bilateral ibotenic acid or sham lesions of the dorsal mPFC were performed 7 days prior to or 4 days after a context-dependent sensitization-inducing regimen of MDMA (15 mg/kg i.p.) or saline. Rats were then challenged with MDMA (5 mg/kg i.p.) after 12 days of withdrawal. Ibotenic acid lesions did not affect the activating effects of MDMA, but prevented the development and expression of MDMA sensitization. Thus, the distance traveled during the development phase of sensitization increased in sham-lesioned rats but not in ibotenic-lesioned animals. Similarly, sham-lesioned rats showed a sensitized response when challenged with MDMA after the withdrawal period, an effect not observed in ibotenic-lesioned animals. These data reinforce the view that the dorsal mPFC is involved in psychostimulant sensitization and more specifically they indicate that the dorsal mPFC plays a key role in the development and expression of MDMA-induced behavioral sensitization. FAU - Ramos, Maria AU - Ramos M AD - Department of Pharmacology, School of Medicine, University of Navarra, Spain. FAU - Goni-Allo, Beatriz AU - Goni-Allo B FAU - Aguirre, Norberto AU - Aguirre N LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Netherlands TA - Behav Brain Res JT - Behavioural brain research JID - 8004872 RN - 0 (Adrenergic Uptake Inhibitors) RN - 0 (Excitatory Amino Acid Agonists) RN - 2552-55-8 (Ibotenic Acid) RN - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine) SB - IM MH - Adrenergic Uptake Inhibitors/*pharmacology MH - Analysis of Variance MH - Animals MH - Behavior, Animal/*drug effects MH - Brain Diseases/physiopathology MH - Drug Interactions MH - Excitatory Amino Acid Agonists/*toxicity MH - Ibotenic Acid/*toxicity MH - Male MH - Motor Activity/drug effects MH - N-Methyl-3,4-methylenedioxyamphetamine/*pharmacology MH - Neural Inhibition/drug effects MH - Prefrontal Cortex/injuries/pathology/*physiology MH - Rats MH - Time Factors EDAT- 2005/05/03 09:00 MHDA- 2005/07/16 09:00 CRDT- 2005/05/03 09:00 PHST- 2004/09/10 00:00 [received] PHST- 2004/12/13 00:00 [revised] PHST- 2004/12/16 00:00 [accepted] PHST- 2005/05/03 09:00 [pubmed] PHST- 2005/07/16 09:00 [medline] PHST- 2005/05/03 09:00 [entrez] AID - S0166-4328(04)00478-4 [pii] AID - 10.1016/j.bbr.2004.12.010 [doi] PST - ppublish SO - Behav Brain Res. 2005 May 28;160(2):304-11. doi: 10.1016/j.bbr.2004.12.010.