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Purinergic Signalling (1)
The Journal of Cell Biology (1)
Palygin, Oleg (2)
Anderson, Mark E. (1)
Bhasin, Naina (1)
Boyden, Penelope A. (1)
Grebenyuk, Sergei (1)
Hund, Thomas J. (1)
Ievglevskyi, Olexandr (1)
Kondratskaya, Elena (1)
Krishtal, Oleg (1)
Lowe, John S. (1)
Mohler, Peter J. (1)
Shibata, Erwin (1)
Year of Publication
Modulation of ATP-induced LTP by cannabinoid receptors in rat hippocampus
Cannabinoids exert powerful action on various forms of synaptic plasticity. These retrograde messengers modulate GABA and glutamate release from presynaptic terminals by acting on presynaptic CB1 receptors. In particular, they inhibit long-term potentiation (LTP) elicited by electrical stimulation of excitatory pathways in rat hippocampus. Recently, LTP of the field excitatory postsynaptic potential (fEPSP) induced by exogenous ATP has been thoroughly explored. The present study demonstrates that cannabinoids inhibit ATP-induced LTP in hippocampal slices of rat. Administration of 10 μM of ATP led to strong inhibition of fEPSPs in CA1/CA3 hippocampal synapses. Within 40 min after ATP removal from bath solution, robust LTP was observed (fEPSP amplitude comprised 130.1 ± 3.8% of control, n = 10). This LTP never appeared when ATP was applied in addition to cannabinoid receptor agonist WIN55,212-2 (100 nM). Selective CB1 receptor antagonist, AM251 (500 nM), completely abolished this effect of WIN55,212-2. Our data indicate that like canonical LTP elicited by electrical stimulation, ATP-induced LTP is under control of CB1 receptors.
Electronic supplementary material
The online version of this article (doi:10.1007/s11302-012-9296-5) contains supplementary material, which is available to authorized users.
LTP; ATP; Cannabinoids; WIN; Adenosine
Voltage-gated Nav channel targeting in the heart requires an ankyrin-G–dependent cellular pathway
Lowe, John S.
Hund, Thomas J.
Boyden, Penelope A.
Anderson, Mark E.
Mohler, Peter J.
The Journal of Cell Biology
Voltage-gated Nav channels are required for normal electrical activity in neurons, skeletal muscle, and cardiomyocytes. In the heart, Nav1.5 is the predominant Nav channel, and Nav1.5-dependent activity regulates rapid upstroke of the cardiac action potential. Nav1.5 activity requires precise localization at specialized cardiomyocyte membrane domains. However, the molecular mechanisms underlying Nav channel trafficking in the heart are unknown. In this paper, we demonstrate that ankyrin-G is required for Nav1.5 targeting in the heart. Cardiomyocytes with reduced ankyrin-G display reduced Nav1.5 expression, abnormal Nav1.5 membrane targeting, and reduced Na+ channel current density. We define the structural requirements on ankyrin-G for Nav1.5 interactions and demonstrate that loss of Nav1.5 targeting is caused by the loss of direct Nav1.5–ankyrin-G interaction. These data are the first report of a cellular pathway required for Nav channel trafficking in the heart and suggest that ankyrin-G is critical for cardiac depolarization and Nav channel organization in multiple excitable tissues.
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