Protease Activated Receptor 2 (PAR2) Induces Long-Term Depression in the
Hippocampus through Transient Receptor Potential Vanilloid 4 (TRPV4)
#MMPMID28303089
Shavit-Stein E
; Artan-Furman A
; Feingold E
; Ben Shimon M
; Itzekson-Hayosh Z
; Chapman J
; Vlachos A
; Maggio N
Front Mol Neurosci
2017[]; 10
(?): 42
PMID28303089
show ga
Protease activated receptors (PARs) are involved in regulating synaptic
transmission and plasticity in the brain. While it is well-accepted that PAR1
mediates long-term potentiation (LTP) of excitatory synaptic strength, the role
of PAR2 in synaptic plasticity remains not well-understood. In this study, we
assessed the role of PAR2-signaling in plasticity at hippocampal Schaffer
collateral-CA1 synapses. Using field potential recordings, we report that
PAR2-activation leads to long-term depression (LTD) of synaptic transmission
through a protein kinase A -dependent, Transient Receptor Potential Vanilloid 4
-mediated mechanism, which requires the activation of N-methyl-D-aspartate
receptors. These results demonstrate that the effects of PAR2 on synaptic
plasticity are distinct from what is observed upon PAR1-activation. Thus, we
propose that the activation of different classes of PARs, i.e., PAR1 and PAR2,
may set the threshold of synaptic plasticity in the hippocampal network by
balancing LTP and LTD.