 |
||||
|
||||
|
||||
|
||||
The Journal of Neuroscience, April 28, 2004, 24(17):4205-4212; doi:10.1523/JNEUROSCI.0111-04.2004
Previous Article | Next Article
Cellular/Molecular
Roles of Ca2+, Hyperpolarization and Cyclic Nucleotide-Activated Channel Activation, and Actin in Temporal Synaptic Tagging
Ning Zhong andRobert S. Zucker Department of Molecular and Cell Biology and Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720
At crayfish neuromuscular junctions, cAMP increases transmitter released by action potentials by activating two effectors, hyperpolarization and cyclic nucleotide-activated channels (HCNCs) and a separate target that has been tentatively identified as exchange protein activated by cAMP (Epac). Intense electrical activity in the motor neuron induces a long-term facilitation (LTF) of transmitter release in which hyperpolarization from an electrogenic Na+-K+ exchanger activates HCNCs. The coupling of HCNCs to transmission involves actin. After LTF induction, cAMP further increases transmission in an HCNC-independent manner, activating the second target. This relaxation of the requirement for HCNC activation to enhance release is called temporal synaptic tagging. Tagging lasts at least 1 d but develops only in the 10 min period after electrical activity. The HCNCs are activated by the post-tetanic hyperpolarization occurring during this time. Both synaptic tagging and LTF induction depend on presynaptic Ca2+ accumulation during activity; both are blocked by EGTA-AM, and LTF is also prevented by stimulation in a low-[Ca2+] medium. Actin depolymerizers prevent induction of LTF and tagging, with little effect on HCNCs, whose sensitivity to cAMP and HCNC blockers is unaffected by tagging. Enhancement of actin polymerization can rescue tagging from HCNC block, suggesting that actin acts at a step after HCNC activation. These and other recent results suggest a model in which HCNC activation, followed by a process involving actin polymerization, acts cooperatively with [Ca2+] to induce tagging, after which only Epac activation is required for cAMP to further enhance transmission.
Key words: synaptic transmission; synaptic tagging; calcium; HCN channels; actin; neuromuscular junction; crayfish
Received Jan 12, 2004; revised March 1, 2004; accepted March 11, 2004.
This article has been cited by other articles:
Y.-F. Wang and G. I. Hatton
Interaction of Extracellular Signal-Regulated Protein Kinase 1/2 with Actin Cytoskeleton in Supraoptic Oxytocin Neurons and Astrocytes: Role in Burst Firing
J. Neurosci., December 12, 2007; 27(50): 13822 - 13834.
[Abstract] [Full Text] [PDF]
A. Minami, Y.-f. Xia, and R. S. Zucker
Increased Ca2+ influx through Na+/Ca2+ exchanger during long-term facilitation at crayfish neuromuscular junctions
J. Physiol., December 1, 2007; 585(2): 413 - 427.
[Abstract] [Full Text] [PDF]
S. Jablonka, M. Beck, B. D. Lechner, C. Mayer, and M. Sendtner
Defective Ca2+ channel clustering in axon terminals disturbs excitability in motoneurons in spinal muscular atrophy
J. Cell Biol., October 8, 2007; 179(1): 139 - 149.
[Abstract] [Full Text] [PDF]
O. Zamir and M. P. Charlton
Cholesterol and synaptic transmitter release at crayfish neuromuscular junctions
J. Physiol., February 15, 2006; 571(1): 83 - 99.
[Abstract] [Full Text] [PDF]
S. Seino and T. Shibasaki
PKA-Dependent and PKA-Independent Pathways for cAMP-Regulated Exocytosis
Physiol Rev, October 1, 2005; 85(4): 1303 - 1342.
[Abstract] [Full Text] [PDF]
F. Saitow, H. Suzuki, and S. Konishi
{beta}-Adrenoceptor-mediated long-term up-regulation of the release machinery at rat cerebellar GABAergic synapses
J. Physiol., June 1, 2005; 565(2): 487 - 502.
[Abstract] [Full Text] [PDF]
N. Zhong and R. S. Zucker
cAMP Acts on Exchange Protein Activated by cAMP/cAMP-Regulated Guanine Nucleotide Exchange Protein to Regulate Transmitter Release at the Crayfish Neuromuscular Junction
J. Neurosci., January 5, 2005; 25(1): 208 - 214.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|