Open AccessTransient Receptor Potential Vanilloid 4 Mediates Hypotonicity‐Induced Enhancement of Synaptic Transmission in Hippocampal Slices
Author(s) -
Li Lin,
Yin Jun,
Jie PingHui,
Lu ZiHong,
Zhou LiBin,
Chen Lei,
Chen Ling
Publication year - 2013
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12143
Subject(s) - hippocampal formation , transient receptor potential channel , neurotransmission , neuroscience , receptor potential , chemistry , biophysics , medicine , receptor , biology
Summary Aim and methods Changes in cerebrospinal fluid osmotic pressure modulate brain excitability. Transient receptor potential vanilloid 4 ( TRPV 4), which is sensitive to hypotonic stimulation, is expressed in hippocampus. The present study investigated the effect of hypotonic stimulation on hippocampal synaptic transmission and the role of TRPV 4 in hypotonicity‐action using electrophysiological recording and pharmacological technique. Results Accompanied with the decrease in paired pulse facilitation, field excitatory postsynaptic potential (f EPSP ) was enhanced by hypotonicity and TRPV 4 agonist 4α‐ PDD in hippocampal slices, which was sensitive to TRPV 4 antagonist HC ‐067047. Hypotonicity‐induced increase in f EPSP was blocked by α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid ( AMPA ) receptor antagonist, but not N ‐methyl‐ d ‐aspartate receptor or N‐ or P/Q‐type voltage‐gated calcium channel antagonist. High voltage‐gated calcium current ( I Ca ) in hippocampal CA 3 pyramidal neurons was not affected by hypotonicity. AMPA ‐activated current ( I AMPA ) in hippocampal CA 1 pyramidal neurons was increased by hypotonicity and 4α‐ PDD , which was attenuated by HC ‐067047. Inhibition of protein kinase C or protein kinase A markedly attenuated hypotonicity‐increased I AMPA , whereas antagonism of calcium/calmodulin‐dependent protein kinase II had no such effect. Conclusion TRPV 4 is involved in hypotonicity‐induced enhancement of hippocampal synaptic transmission, which may be mediated through promoting presynaptic glutamate release and increasing postsynaptic AMPA receptor function.