PMID- 18312583
OWN - NLM
STAT- MEDLINE
DCOM- 20080603
LR  - 20191210
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Linking)
VI  - 27
IP  - 5
DP  - 2008 Mar
TI  - Long-term increase in GAD67 mRNA expression in the central amygdala of rats 
      sensitized by drugs and stress.
PG  - 1220-30
LID - 10.1111/j.1460-9568.2008.06095.x [doi]
AB  - Repeated administration of addictive drugs and prolonged exposure to stressful 
      stimuli induce sensitization to their behavioural stimulant properties. In this 
      study, male Sprague-Dawley rats were repeatedly exposed to morphine [twice a day 
      for 3 days at increasing doses, 10, 20, 40 mg/kg subcutaneously (s.c)], 
      amphetamine (1 mg/kg s.c., once a day for 10 days), nicotine (0.4 mg/kg s.c., 
      once a day for 5 days) and stress (food restriction for 7 days). After an 
      interval of 3-30 days, depending on the pretreatment, rats were challenged with 
      vehicle, with the same drug received as pretreatment (5 mg/kg of morphine, 0.5 
      mg/kg of amphetamine or 0.4 mg/kg of nicotine, respectively) or, in the case of 
      food-restricted rats, with 0.5 mg/kg of amphetamine. Thereafter, changes in the 
      expression of glutamic acid decarboxylase (GAD)67 mRNA were estimated by in situ 
      hybridization in the central nucleus of the amygdala (CeA), basolateral amygdala 
      (BLA), dorsolateral striatum (dLStr), nucleus accumbens shell (AcS) and core 
      (AcC). All sensitizing pretreatments increased GAD67 mRNA in the CeA. Drug 
      challenge did not further affect GAD67 mRNA in the CeA of saline, drug and stress 
      pre-exposed rats. As to the other areas, no differences were observed in drug 
      pre-exposed compared with saline pre-exposed and fed ad libitum rats, except for 
      amphetamine. Amphetamine pre-exposure decreased GAD67 mRNA levels in the dLStr 
      and the AcC and AcS, and this effect was reversed by amphetamine challenge. The 
      results show that different drugs and stress models of behavioural sensitization 
      have in common an increase of GA67 in the CeA but not in the BLA, and suggest the 
      changes of GAD67 in the CeA are a substrate of the sensitized response to drug 
      challenge.
FAU - Carta, Anna R
AU  - Carta AR
AD  - Department of Toxicology, University of Cagliari, Cagliari, Italy. 
      acarta@unica.it
FAU - Moreno, Carmen Casal
AU  - Moreno CC
FAU - Cadoni, Cristina
AU  - Cadoni C
FAU - Tronci, Elisabetta
AU  - Tronci E
FAU - Di Chiara, Gaetano
AU  - Di Chiara G
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20080229
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Illicit Drugs)
RN  - 0 (RNA, Messenger)
RN  - EC 4.1.1.15 (Glutamate Decarboxylase)
RN  - EC 4.1.1.15 (glutamate decarboxylase 1)
SB  - IM
MH  - Amygdala/drug effects/*enzymology
MH  - Animals
MH  - Food Deprivation/physiology
MH  - Gene Expression Regulation, Enzymologic/drug effects/*physiology
MH  - Glutamate Decarboxylase/*biosynthesis/genetics
MH  - Illicit Drugs/*pharmacology
MH  - Male
MH  - RNA, Messenger/*biosynthesis/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Stress, Physiological/*enzymology/genetics/psychology
MH  - Time
EDAT- 2008/03/04 09:00
MHDA- 2008/06/05 09:00
CRDT- 2008/03/04 09:00
PHST- 2008/03/04 09:00 [pubmed]
PHST- 2008/06/05 09:00 [medline]
PHST- 2008/03/04 09:00 [entrez]
AID - EJN6095 [pii]
AID - 10.1111/j.1460-9568.2008.06095.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2008 Mar;27(5):1220-30. doi: 10.1111/j.1460-9568.2008.06095.x. 
      Epub 2008 Feb 29.