PMID- 16476997
OWN - NLM
STAT- MEDLINE
DCOM- 20060613
LR  - 20181113
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 103
IP  - 8
DP  - 2006 Feb 21
TI  - Role for calcium/calmodulin-dependent protein kinase II in the p75-mediated 
      regulation of sympathetic cholinergic transmission.
PG  - 2915-9
AB  - Neurotrophins regulate sympathetic neuron cotransmission by modulating the 
      activity-dependent release of norepinephrine and acetylcholine. Nerve growth 
      factor promotes excitatory noradrenergic transmission, whereas brain-derived 
      neurotrophic factor (BDNF), acting through the p75 receptor, increases inhibitory 
      cholinergic transmission. This regulation of corelease by target-derived factors 
      leads to the functional modulation of myocyte beat rate in neuron-myocyte 
      cocultures. Calcium/calmodulin-dependent protein kinase II (CaMKII) has been 
      implicated in the control of both pre- and postsynaptic mechanisms of synaptic 
      plasticity. We demonstrate that CaMKII acts in conjunction with p75 signaling to 
      regulate cholinergic transmission between sympathetic neurons and heart cells. 
      Inhibition of presynaptic CaMKII prevents the BDNF-dependent shift to inhibitory 
      neurotransmission, whereas presynaptic expression of a constitutively active 
      CaMKII results in inhibitory neurotransmission in the absence of added BDNF, 
      suggesting that activation of presynaptic CaMKII is both necessary and sufficient 
      for a shift from excitatory to inhibitory transmission. Several isozymes of 
      CaMKII are expressed in sympathetic neurons, with the delta-CaMKII being 
      activated by BDNF and nerve growth factor. Activated CaMKII is less effective at 
      promoting cholinergic transmission in the absence of p75 signaling, demonstrating 
      that p75 and CaMKII act to coordinate neurotransmitter selection in sympathetic 
      neurons.
FAU - Slonimsky, John D
AU  - Slonimsky JD
AD  - Department of Biology, National Center for Behavior Genomics, Brandeis 
      University, M/S 008, 415 South Street, Waltham, MA 02454, USA.
FAU - Mattaliano, Mark D
AU  - Mattaliano MD
FAU - Moon, Jung-Il
AU  - Moon JI
FAU - Griffith, Leslie C
AU  - Griffith LC
FAU - Birren, Susan J
AU  - Birren SJ
LA  - eng
GR  - R01 NS040168/NS/NINDS NIH HHS/United States
GR  - GM54408/GM/NIGMS NIH HHS/United States
GR  - R01 GM054408-10/GM/NIGMS NIH HHS/United States
GR  - R01 GM054408/GM/NIGMS NIH HHS/United States
GR  - NS40168/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20060213
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2
MH  - Calcium-Calmodulin-Dependent Protein Kinases/genetics/metabolism/*physiology
MH  - Cells, Cultured
MH  - Enzyme Activation
MH  - Mice
MH  - Nerve Growth Factors/pharmacology
MH  - Neurons/physiology
MH  - Rats
MH  - Receptor, Nerve Growth Factor/agonists/*physiology
MH  - Sympathetic Nervous System/metabolism/*physiology
MH  - *Synaptic Transmission
PMC - PMC1413855
COIS- Conflict of interest statement: No conflicts declared.
EDAT- 2006/02/16 09:00
MHDA- 2006/06/14 09:00
PMCR- 2006/08/21
CRDT- 2006/02/16 09:00
PHST- 2006/02/16 09:00 [pubmed]
PHST- 2006/06/14 09:00 [medline]
PHST- 2006/02/16 09:00 [entrez]
PHST- 2006/08/21 00:00 [pmc-release]
AID - 0511276103 [pii]
AID - 1295 [pii]
AID - 10.1073/pnas.0511276103 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2915-9. doi: 
      10.1073/pnas.0511276103. Epub 2006 Feb 13.