PMID- 10479714
OWN - NLM
STAT- MEDLINE
DCOM- 19991004
LR  - 20240720
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 18
DP  - 1999 Sep 15
TI  - The effects of acute nicotine on the metabolism of dopamine and the expression of 
      Fos protein in striatal and limbic brain areas of rats during chronic nicotine 
      infusion and its withdrawal.
PG  - 8145-51
AB  - The effects of acute nicotine (0.5 mg/kg, s.c.) on dopamine (DA) metabolism and 
      Fos protein expression in striatal and limbic areas of rats on the seventh day of 
      chronic nicotine infusion (4 mg. kg(-1). d(-1)) and after 24 or 72 hr withdrawal 
      were investigated. In saline-infused rats, acute nicotine elevated striatal and 
      limbic 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) 
      concentrations significantly. During the nicotine infusion, no such increases 
      were seen in the striatum, but limbic HVA was somewhat elevated. After 24 hr 
      withdrawal when no nicotine was found in the plasma, acute nicotine elevated 
      striatal DOPAC and HVA and limbic HVA. However, the limbic DOPAC was unaffected. 
      Acute nicotine increased Fos immunostaining (IS) in the caudate-putamen (CPU), 
      the core of nucleus accumbens (NAcc), the cingulate cortex (Cg), and the central 
      nucleus of amygdala (ACe) significantly. During nicotine infusion the 
      nicotine-induced responses were attenuated in CPU and NAcc, whereas in ACe and Cg 
      Fos immunostaining was increased as in saline-infused rats. After 24 hr 
      withdrawal, acute nicotine did not increase Fos immunostaining in CPU, NAcc, and 
      Cg, but increased it clearly in ACe. After 72 hr withdrawal, nicotine's effects 
      were restored. Our findings suggest that the nicotinic receptors in the striatal 
      areas are desensitized more easily than those in the limbic areas. Furthermore, 
      the effects of nicotine on various DA metabolites differ. We also found evidence 
      for long-lasting inactivation of nicotinic receptors in vivo regulating limbic 
      dopamine metabolism and Fos expression in striatal and limbic areas. These 
      findings might be important for the protective effects of nicotine in Parkinson's 
      disease and in its dependence-producing properties.
FAU - Salminen, O
AU  - Salminen O
AD  - Division of Pharmacology and Toxicology, Department of Pharmacy, University of 
      Helsinki, FIN-00014 Helsinki, Finland.
FAU - Seppa, T
AU  - Seppa T
FAU - Gaddnas, H
AU  - Gaddnas H
FAU - Ahtee, L
AU  - Ahtee L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)
RN  - 2679MF687A (Niacin)
RN  - K5161X06LL (Cotinine)
RN  - VTD58H1Z2X (Dopamine)
RN  - X77S6GMS36 (Homovanillic Acid)
SB  - IM
MH  - 3,4-Dihydroxyphenylacetic Acid/metabolism
MH  - Amygdala/metabolism
MH  - Animals
MH  - Caudate Nucleus/metabolism
MH  - Corpus Striatum/drug effects/*metabolism
MH  - Cotinine/blood
MH  - Dopamine/*metabolism
MH  - Drug Administration Schedule
MH  - Gyrus Cinguli/metabolism
MH  - Homovanillic Acid/metabolism
MH  - Immunohistochemistry
MH  - Infusions, Parenteral
MH  - Injections, Subcutaneous
MH  - Limbic System/drug effects/*metabolism
MH  - Male
MH  - Niacin/administration & dosage/blood/*pharmacology
MH  - Nucleus Accumbens/metabolism
MH  - Proto-Oncogene Proteins c-fos/*genetics
MH  - Putamen/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Substance Withdrawal Syndrome
PMC - PMC6782454
EDAT- 1999/09/10 00:00
MHDA- 1999/09/10 00:01
PMCR- 2000/03/15
CRDT- 1999/09/10 00:00
PHST- 1999/09/10 00:00 [pubmed]
PHST- 1999/09/10 00:01 [medline]
PHST- 1999/09/10 00:00 [entrez]
PHST- 2000/03/15 00:00 [pmc-release]
AID - 3427 [pii]
AID - 10.1523/JNEUROSCI.19-18-08145.1999 [doi]
PST - ppublish
SO  - J Neurosci. 1999 Sep 15;19(18):8145-51. doi: 10.1523/JNEUROSCI.19-18-08145.1999.