Opposing crosstalk between leptin and glucocorticoids rapidly modulates synaptic excitation via endocannabinoid release

J Neurosci. 2006 Jun 14;26(24):6643-50. doi: 10.1523/JNEUROSCI.5126-05.2006.

Abstract

The hypothalamic paraventricular nucleus (PVN) integrates preautonomic and neuroendocrine control of energy homeostasis, fluid balance, and the stress response. We recently demonstrated that glucocorticoids act via a membrane receptor to rapidly cause endocannabinoid-mediated suppression of synaptic excitation in PVN neurosecretory neurons. Leptin, a major signal of nutritional state, suppresses CB(1) cannabinoid receptor-dependent hyperphagia (increased appetite) in fasting animals by reducing hypothalamic levels of endocannabinoids. Here we show that glucocorticoids stimulate endocannabinoid biosynthesis and release via a Galpha(s)-cAMP-protein kinase A-dependent mechanism and that leptin blocks glucocorticoid-induced endocannabinoid biosynthesis and suppression of excitation in the PVN via a phosphodiesterase-3B-mediated reduction in intracellular cAMP levels. We demonstrate this rapid hormonal interaction in both PVN magnocellular and parvocellular neurosecretory cells. Leptin blockade of the glucocorticoid-induced, endocannabinoid-mediated suppression of excitation was absent in leptin receptor-deficient obese Zucker rats. Our findings reveal a novel hormonal crosstalk that rapidly modulates synaptic excitation via endocannabinoid release in the hypothalamus and that provides a nutritional state-sensitive mechanism to integrate the neuroendocrine regulation of energy homeostasis, fluid balance, and the stress response.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Arachidonic Acids / metabolism
  • Cannabinoid Receptor Modulators / metabolism*
  • Cannabinoid Receptor Modulators / pharmacology
  • Cyclic AMP / metabolism
  • Dexamethasone / pharmacology
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Endocannabinoids*
  • Enzyme Inhibitors / pharmacology
  • Excitatory Postsynaptic Potentials / drug effects
  • Excitatory Postsynaptic Potentials / physiology
  • Excitatory Postsynaptic Potentials / radiation effects
  • Glucocorticoids / pharmacology
  • Glucocorticoids / physiology*
  • Glycerides / metabolism
  • In Vitro Techniques
  • Leptin / physiology*
  • Male
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / physiology*
  • Obesity / genetics
  • Obesity / metabolism
  • Paraventricular Hypothalamic Nucleus / cytology*
  • Patch-Clamp Techniques / methods
  • Rats
  • Rats, Sprague-Dawley
  • Rats, Zucker
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Synapses / drug effects
  • Synapses / physiology*

Substances

  • Arachidonic Acids
  • Cannabinoid Receptor Modulators
  • Endocannabinoids
  • Enzyme Inhibitors
  • Glucocorticoids
  • Glycerides
  • Leptin
  • Dexamethasone
  • glyceryl 2-arachidonate
  • Cyclic AMP