TY - JOUR
T1 - A New Component in Synaptic Plasticity
T2 - Upregulation of Kinesin in the Neurons of the Gill-Withdrawal Reflex
AU - Puthanveettil, Sathyanarayanan V.
AU - Monje, Francisco J.
AU - Miniaci, Maria Concetta
AU - Choi, Yun Beom
AU - Karl, Kevin A.
AU - Khandros, Eugene
AU - Gawinowicz, Mary Ann
AU - Sheetz, Michael P.
AU - Kandel, Eric R.
N1 - Funding Information:
We thank Thomas Jessell, Steven Siegelbaum, Kausik Si, and Kandel lab members Joseph Rayman and Ilias Pavlopoulos for their critical comments on an earlier version of this manuscript. We are grateful to Peter Schieffele for the gift of anti-neurexin antibody. We thank Joun-Hun Kim for help with Piccolo antisense microinjection experiments, Aviva Olsavsky for help with the RTPCR experiments, and John Edwards of Columbia's Genome Center for help with kinesin ESTs. Special thanks to Vivian Zhu for help with cell cultures, Hannah Cho for technical help, and Charles Lam for help with graphics. This work is supported by HHMI, and NIH grants P50 HG002806 and R01 MH075026.
PY - 2008/11/28
Y1 - 2008/11/28
N2 - To explore how gene products, required for the initiation of synaptic growth, move from the cell body of the sensory neuron to its presynaptic terminals, and from the cell body of the motor neuron to its postsynaptic dendritic spines, we have investigated the anterograde transport machinery in both the sensory and motor neurons of the gill-withdrawal reflex of Aplysia. We found that the induction of long-term facilitation (LTF) by repeated applications of serotonin, a modulatory transmitter released during learning in Aplysia, requires upregulation of kinesin heavy chain (KHC) in both pre- and postsynaptic neurons. Indeed, upregulation of KHC in the presynaptic neurons alone is sufficient for the induction of LTF. However, KHC is not required for the persistence of LTF. Thus, in addition to transcriptional activation in the nucleus and local protein synthesis at the synapse, our studies have identified a third component critical for long-term learning-related plasticity: the coordinated upregulation of kinesin-mediated transport.
AB - To explore how gene products, required for the initiation of synaptic growth, move from the cell body of the sensory neuron to its presynaptic terminals, and from the cell body of the motor neuron to its postsynaptic dendritic spines, we have investigated the anterograde transport machinery in both the sensory and motor neurons of the gill-withdrawal reflex of Aplysia. We found that the induction of long-term facilitation (LTF) by repeated applications of serotonin, a modulatory transmitter released during learning in Aplysia, requires upregulation of kinesin heavy chain (KHC) in both pre- and postsynaptic neurons. Indeed, upregulation of KHC in the presynaptic neurons alone is sufficient for the induction of LTF. However, KHC is not required for the persistence of LTF. Thus, in addition to transcriptional activation in the nucleus and local protein synthesis at the synapse, our studies have identified a third component critical for long-term learning-related plasticity: the coordinated upregulation of kinesin-mediated transport.
KW - CELLBIO
KW - MOLNEURO
KW - PROTEINS
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U2 - 10.1016/j.cell.2008.11.003
DO - 10.1016/j.cell.2008.11.003
M3 - Article
C2 - 19041756
AN - SCOPUS:56349150148
SN - 0092-8674
VL - 135
SP - 960
EP - 973
JO - Cell
JF - Cell
IS - 5
ER -