The Journal of Neuroscience, June 14, 2006, ():
Opposing Crosstalk between Leptin and Glucocorticoids Rapidly Modulates Synaptic Excitation via Endocannabinoid Release
J. Neurosci. Malcher-Lopes et al.
26: 6643
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplementary figure 1. Signature responses for Magnocellular and parvocellular neuroendocrine cells. A, Magnocellular neuroendocrine cells respond to positive pulses (top) delivered at a hyperpolarized holding potential with a characteristic dampening of the membrane depolarization (arrow) and a delayed onset of action potentials (botton). B. Parvocellular neuroendocrine cells respond to a similar protocol (top) with a monotonic depolarization and action potential generation (botton) without the delay seen in magnocellular neurons. Responses to incrementally larger current pulses are superimposed in both A and B.
- supplemental material
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Supplementary figure 2. Proposed model of non-genomic signaling crosstalk between leptin and glucocorticoids to control endocannabinoid synthesis and retrograde release in the PVN. Rapid glucocorticoid-induced endocannabinoid release depends on the activation of a putative Gαs-coupled membrane glucocorticoid receptor and a cAMP-PKA signaling pathway. Endocannabinoids suppress presynaptic glutamate release via retrograde activation of CB1 receptors. Leptin binding to Ob-Rb receptors blocks glucocorticoid-induced, cAMP/PKA-dependent endocannabinoid synthesis by converting cAMP to the inactive 5’-AMP via JAK2-PI3 kinase-protein kinase B (PKB) activation of PDE-3B, as previously described (reviewed in Sahu, 2004).
