PMID- 19580852
OWN - NLM
STAT- MEDLINE
DCOM- 20100114
LR  - 20211020
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 163
IP  - 3
DP  - 2009 Oct 20
TI  - Protein kinase Calpha mediates a novel form of plasticity in the accessory 
      olfactory bulb.
PG  - 811-24
LID - 10.1016/j.neuroscience.2009.06.069 [doi]
AB  - Modification of synapses in the accessory olfactory bulb (AOB) is believed to 
      underlie pheromonal memory that enables mate recognition in mice. The memory, 
      which is acquired with single-trial learning, forms only with coincident 
      noradrenergic and glutamatergic inputs to the AOB. The mechanisms by which 
      glutamate and norepinephrine (NE) alter the AOB synapses are not well understood. 
      Here we present results that not only reconcile the earlier, seemingly 
      contradictory, observations on the role of glutamate and NE in changing the AOB 
      synapses, but also reveal novel mechanisms of plasticity. Our studies suggest 
      that initially, glutamate acting at Group II metabotropic receptors and NE acting 
      at alpha(2)-adrenergic receptors inhibit N-type and R-type Ca(2+) channels in 
      mitral cells via a G-protein. The N-type and R-type Ca(2+) channel inhibition is 
      reversed by activation of alpha(1)-adrenergic receptors and protein kinase Calpha 
      (PKCalpha). Based on these results, we propose a hypothetical model for a new 
      kind of synaptic plasticity in the AOB that accounts for the previous behavioral 
      data on pheromonal memory. According to this model, initial inhibition of the 
      Ca(2+) channels suppresses the GABAergic inhibitory feedback to mitral cells, 
      causing disinhibition and Ca(2+) influx. NE also activates phospholipase C (PLC) 
      through alpha(1)-adrenergic receptors generating inositol 1,4,5-trisphosphate and 
      diacylglycerol (DAG). Calcium and DAG together activate PKCalpha which switches 
      the disinhibition to increased inhibition of mitral cells. Thus, PKCalpha is 
      likely to be a coincidence detector integrating glutamate and NE input in the AOB 
      and bridging the short-term signaling to long-term structural changes resulting 
      in enhanced inhibition of mitral cells that is thought to underlie memory 
      formation.
FAU - Dong, C
AU  - Dong C
AD  - Department of Neurobiology and Anatomy, Wake Forest University Health Sciences, 
      Medical Center Boulevard, Winston-Salem, NC 27157-0001, USA.
FAU - Godwin, D W
AU  - Godwin DW
FAU - Brennan, P A
AU  - Brennan PA
FAU - Hegde, A N
AU  - Hegde AN
LA  - eng
GR  - R21 DC006856/DC/NIDCD NIH HHS/United States
GR  - R21 DC006856-01/DC/NIDCD NIH HHS/United States
GR  - R21DC006856/DC/NIDCD NIH HHS/United States
GR  - R21 EY018159/EY/NEI NIH HHS/United States
GR  - R21EY0018159/EY/NEI NIH HHS/United States
GR  - R21 DC006856-02/DC/NIDCD NIH HHS/United States
GR  - R01AA016852/AA/NIAAA NIH HHS/United States
GR  - R01 AA016852/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20090704
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Calcium Channels, N-Type)
RN  - 0 (Calcium Channels, R-Type)
RN  - 0 (Isoenzymes)
RN  - 0 (Receptors, Adrenergic, alpha-1)
RN  - 0 (Receptors, Adrenergic, alpha-2)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 0 (Sex Attractants)
RN  - 0 (metabotropic glutamate receptor 2)
RN  - 0 (metabotropic glutamate receptor 3)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.11.13 (Protein Kinase C-alpha)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - SY7Q814VUP (Calcium)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Animals
MH  - Calcium/physiology
MH  - Calcium Channels, N-Type/physiology
MH  - Calcium Channels, R-Type/physiology
MH  - Female
MH  - GTP-Binding Proteins/physiology
MH  - Glutamic Acid/pharmacology/physiology
MH  - In Vitro Techniques
MH  - Inhibitory Postsynaptic Potentials/drug effects
MH  - Isoenzymes/physiology
MH  - Mice
MH  - Neuronal Plasticity/*physiology
MH  - Norepinephrine/pharmacology/physiology
MH  - Olfactory Bulb/*physiology
MH  - Patch-Clamp Techniques
MH  - Protein Kinase C-alpha/*physiology
MH  - Receptors, Adrenergic, alpha-1/physiology
MH  - Receptors, Adrenergic, alpha-2/physiology
MH  - Receptors, Metabotropic Glutamate/agonists/physiology
MH  - Sex Attractants/physiology
MH  - Synapses/physiology
MH  - Type C Phospholipases/physiology
PMC - PMC2748972
MID - NIHMS137985
EDAT- 2009/07/08 09:00
MHDA- 2010/01/15 06:00
PMCR- 2010/10/20
CRDT- 2009/07/08 09:00
PHST- 2009/05/12 00:00 [received]
PHST- 2009/06/29 00:00 [revised]
PHST- 2009/06/30 00:00 [accepted]
PHST- 2009/07/08 09:00 [entrez]
PHST- 2009/07/08 09:00 [pubmed]
PHST- 2010/01/15 06:00 [medline]
PHST- 2010/10/20 00:00 [pmc-release]
AID - S0306-4522(09)01119-1 [pii]
AID - 10.1016/j.neuroscience.2009.06.069 [doi]
PST - ppublish
SO  - Neuroscience. 2009 Oct 20;163(3):811-24. doi: 10.1016/j.neuroscience.2009.06.069. 
      Epub 2009 Jul 4.