Document Detail


Striatal cell signaling in chronically food-restricted rats under basal conditions and in response to brief handling.
MedLine Citation:
PMID:  16239070     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic food restriction increases exploratory behavior, cognitive function, and the rewarding effects of abused drugs. Recently, striatal neuroadaptations that may be involved in these effects were observed. Specifically, D-1 dopamine (DA) receptor agonist challenge produced stronger activation of extracellular signal-regulated kinase (ERK), calcium-calmodulin-dependent kinase II (CaMKII), and the nuclear transcription factor cAMP response element binding protein (CREB) in nucleus accumbens (NAc) of food-restricted (FR) relative to ad libitum fed (AL) rats. Further, when FR rats were injected intracerebroventricularly (i.c.v.) with vehicle (saline) they displayed stronger activation of c-Jun N-terminal protein kinase (JNK), ERK and CaMKII than did AL rats. It is not known to what extent the latter effects represent the basal state of FR rats or an amplified response to the brief handling involved in the i.c.v. injection procedure. Using Western blotting it was found that basal phospho-JNK is higher in caudate-putamen (CPu) and NAc of FR relative to AL rats. Interestingly, brief handling decreased phospho-JNK levels in FR subjects. Basal phospho-ERK1/2 also tended to be elevated in CPu and NAc of FR rats but the elevation was not significant. However, phospho-MEK--the activated kinase upstream of ERK1/2--was significantly elevated in NAc of FR rats. Neither ERK1/2 nor MEK were activated by brief handling. CaMKII was selectively activated by handling in NAc of FR rats, suggesting a state-dependent response to a salient event. Given the established involvement of mitogen-activated protein kinase (MAPK) and CaMKII in synaptic plasticity, learning and memory, the increase in basal phospho-MEK and hyperresponsiveness of CaMKII in NAc may represent adaptive cellular responses to persistent negative energy balance that facilitate associative learning in connection with food-seeking.
Authors:
Yan Pan; Ermanda Siregar; Kenneth D Carr
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2005-10-18
Journal Detail:
Title:  Neuroscience letters     Volume:  393     ISSN:  0304-3940     ISO Abbreviation:  Neurosci. Lett.     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2005-12-26     Completed Date:  2006-03-14     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7600130     Medline TA:  Neurosci Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  243-8     Citation Subset:  IM    
Affiliation:
Department of Psychiatry, Millhauser Laboratories, room HN607, New York University School of Medicine, 550 First Avenue, NY 10016, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western / methods
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases / metabolism
Corpus Striatum / metabolism*
Extracellular Signal-Regulated MAP Kinases / metabolism
Food Deprivation / physiology*
Handling (Psychology)*
MAP Kinase Kinase 4 / metabolism
MAP Kinase Kinase Kinases / metabolism
Male
Phosphorylation
Rats
Rats, Sprague-Dawley
Signal Transduction / physiology*
Grant Support
ID/Acronym/Agency:
K02 DA00292/DA/NIDA NIH HHS; R01 DA03956/DA/NIDA NIH HHS; T32 DA07254/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25/MAP Kinase Kinase Kinases; EC 2.7.12.2/MAP Kinase Kinase 4

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Functional characterization of Na+-independent choline transport in primary cultures of neurons from...
Next Document:  Differences in neuritogenic response to nitric oxide in PC12 and PC12h cells.