PMID- 20800659
OWN - NLM
STAT- MEDLINE
DCOM- 20110202
LR  - 20220309
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 171
IP  - 1
DP  - 2010 Nov 24
TI  - Peripheral nerve injury differentially regulates dopaminergic pathways in the 
      nucleus accumbens of rats with either 'pain alone' or 'pain and disability'.
PG  - 329-43
LID - 10.1016/j.neuroscience.2010.08.040 [doi]
AB  - Following unilateral chronic constriction injury (CCI) of the sciatic nerve, 
      histochemical and gene expression changes were examined in the rat nucleus 
      accumbens (NAcc), a region critical to affective-motivational regulation. Rats 
      were categorised as having Pain alone (45%) or Pain and Disability (30%), on the 
      basis of either unaltered or decreased dominance behaviour in the 
      resident-intruder paradigm, respectively. Tyrosine hydroxylase (TH) expression 
      was significantly increased bilaterally, throughout the rostrocaudal extent of 
      the NAcc in Pain alone animals. Increased TH likely reflects increased dopamine 
      levels in the Pain alone group, which may modulate dopamine receptor subtype 2 
      (D2) receptor expression. Stereological analyses of D2 receptor immunoreactive 
      (D2-IR) cells revealed lateralised changes which correlated significantly with 
      dominance behaviour. In the contralateral NAcc, D2-IR negatively correlated with 
      post-CCI dominance behaviour (i.e. Pain alone animals have decreased D2-IR), 
      whereas ipsilaterally there was a positive correlation between D2-IR and post-CCI 
      dominance behaviour (i.e. Pain and Disability animals have decreased D2-IR). 
      Western blots for D2 protein expression confirmed these correlations. 
      Additionally, D2 mRNA expression within the NAcc showed lateralised and group 
      specific changes. In the ipsilateral NAcc D2 mRNA was increased in Pain alone 
      animals. It is hypothesised that increased D2 mRNA in the ipsilateral NAcc of 
      Pain alone animals may be a protective mechanism, maintaining D2-IR despite 
      increased dopamine, which may otherwise induce receptor desensitisation. D2 mRNA 
      is not altered in the ipsilateral NAcc of Pain and Disability animals, therefore 
      loss of D2-IR is likely, albeit by an alternate mechanism. In summary, unilateral 
      CCI in rats induces specific and lateralised adaptations in the dopaminergic 
      circuitry of the NAcc. These distinct neural adaptations correlate with changes 
      in social behaviour, and likely underlie some of the affective-motivational state 
      changes associated with neuropathic pain in a subset of rats (i.e. Pain and 
      Disability group).
CI  - Copyright (c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Austin, P J
AU  - Austin PJ
AD  - School of Medical Sciences (Anatomy and Histology), The University of Sydney, NSW 
      2006, Australia. paustin@unsw.edu.au
FAU - Beyer, K
AU  - Beyer K
FAU - Bembrick, A L
AU  - Bembrick AL
FAU - Keay, K A
AU  - Keay KA
LA  - eng
PT  - Journal Article
DEP - 20100826
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Calbindins)
RN  - 0 (Receptors, Dopamine D2)
RN  - 0 (Receptors, Dopamine D3)
RN  - 0 (S100 Calcium Binding Protein G)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Calbindins
MH  - Disability Evaluation
MH  - Disease Models, Animal
MH  - Dopamine/genetics/*metabolism
MH  - Functional Laterality
MH  - Gene Expression Regulation/*physiology
MH  - Hyperalgesia/etiology
MH  - Linear Models
MH  - Male
MH  - Nucleus Accumbens/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine D2/genetics/*metabolism
MH  - Receptors, Dopamine D3/genetics/*metabolism
MH  - S100 Calcium Binding Protein G/metabolism
MH  - Sciatic Neuropathy/complications/*pathology
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 2010/08/31 06:00
MHDA- 2011/02/03 06:00
CRDT- 2010/08/31 06:00
PHST- 2010/07/22 00:00 [received]
PHST- 2010/08/18 00:00 [revised]
PHST- 2010/08/19 00:00 [accepted]
PHST- 2010/08/31 06:00 [entrez]
PHST- 2010/08/31 06:00 [pubmed]
PHST- 2011/02/03 06:00 [medline]
AID - S0306-4522(10)01168-1 [pii]
AID - 10.1016/j.neuroscience.2010.08.040 [doi]
PST - ppublish
SO  - Neuroscience. 2010 Nov 24;171(1):329-43. doi: 10.1016/j.neuroscience.2010.08.040. 
      Epub 2010 Aug 26.