PMID- 18848604
OWN - NLM
STAT- MEDLINE
DCOM- 20090409
LR  - 20191220
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 157
IP  - 2
DP  - 2008 Nov 19
TI  - Signal transduction and gene expression in cultured accessory olfactory bulb 
      neurons.
PG  - 340-8
LID - 10.1016/j.neuroscience.2008.09.016 [doi]
AB  - Glutamate and norepinephrine (NE) are believed to mediate the long-lasting 
      synaptic plasticity in the accessory olfactory bulb (AOB) that underlies 
      pheromone recognition memory. The mechanisms by which these neurotransmitters 
      bring about the synaptic changes are not clearly understood. In order to study 
      signals that mediate synaptic plasticity in the AOB, we used AOB neurons in 
      primary culture as a model system. Because induction of pheromone memory requires 
      coincident glutamatergic and noradrenergic input to the AOB, and requires new 
      protein synthesis, we reasoned that glutamate and NE must induce gene expression 
      in the AOB. We used a combination of agonists that stimulate alpha1 and alpha2 
      adrenergic receptors in combination with N-methyl-d-aspartic acid and tested 
      expression of the immediate-early gene (IEG) c-Fos. We found that the 
      glutamatergic and noradrenergic stimulation caused significant induction of c-Fos 
      mRNA and protein. Induction of c-Fos was significantly reduced in the presence of 
      inhibitors of protein kinase C, mitogen-activated protein kinase (MAPK) and 
      phospholipase C. These results suggest that glutamate and NE induce gene 
      expression in the AOB through a signaling pathway mediated by protein kinase C 
      and MAPK.
FAU - Skinner, C B
AU  - Skinner CB
AD  - Department of Neurobiology and Anatomy, Wake Forest University Health Sciences, 
      Medical Center Boulevard, Winston-Salem, NC 27157, USA.
FAU - Upadhya, S C
AU  - Upadhya SC
FAU - Smith, T K
AU  - Smith TK
FAU - Turner, C P
AU  - Turner CP
FAU - Hegde, A N
AU  - Hegde AN
LA  - eng
GR  - T32 DC000057/DC/NIDCD NIH HHS/United States
GR  - T32 DC000057-09/DC/NIDCD NIH HHS/United States
GR  - T32 DC000057-10/DC/NIDCD NIH HHS/United States
GR  - Z01 DC000057/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080916
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - QK318GVY3Y (cirazoline)
SB  - IM
MH  - Adrenergic alpha-Agonists/pharmacology
MH  - Age Factors
MH  - Animals
MH  - Animals, Newborn
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Gene Expression/drug effects/*physiology
MH  - Gene Expression Regulation, Developmental/drug effects/physiology
MH  - Imidazoles/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - N-Methylaspartate/pharmacology
MH  - Nerve Tissue Proteins/genetics/metabolism
MH  - Olfactory Bulb/*cytology
MH  - Proto-Oncogene Proteins c-fos/genetics/metabolism
MH  - Sensory Receptor Cells/*physiology
MH  - Signal Transduction/genetics/*physiology
MH  - Type C Phospholipases/pharmacology
PMC - PMC2615302
MID - NIHMS81157
EDAT- 2008/10/14 09:00
MHDA- 2009/04/10 09:00
PMCR- 2009/11/19
CRDT- 2008/10/14 09:00
PHST- 2008/03/24 00:00 [received]
PHST- 2008/08/07 00:00 [revised]
PHST- 2008/09/09 00:00 [accepted]
PHST- 2008/10/14 09:00 [pubmed]
PHST- 2009/04/10 09:00 [medline]
PHST- 2008/10/14 09:00 [entrez]
PHST- 2009/11/19 00:00 [pmc-release]
AID - S0306-4522(08)01347-X [pii]
AID - 10.1016/j.neuroscience.2008.09.016 [doi]
PST - ppublish
SO  - Neuroscience. 2008 Nov 19;157(2):340-8. doi: 10.1016/j.neuroscience.2008.09.016. 
      Epub 2008 Sep 16.