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Abstract

 
Abstract No.:113
Country:Canada
  
Title:RECRUITMENT AND PLASTICITY OF THE CENTRAL MU-OPIOID RECEPTOR SYSTEM IN RESPONSE TO A SUSTAINED NA+ CHALLENGE
  
Authors/Affiliations:1 Didier M. Mouginot*;
1 CHUL Research Centre, Québec, QC, Canada
  
Content:Salt appetite is a motivated behavior generated by sustained hypotonicity of the body fluid compartments. This ingestive behavior requires the detection of chemosensory signals such as plasma / CSF osmolality and Na+ level and their integration with modulatory signals involving neuropeptides. In this context, endogenous opioids may play a key role in the expression of salt appetite by increasing taste pleasantness and reward value of salt intake. Beside the modulation of reward and goal-directed behavior, little is known regarding the action of the opioid peptide and opioid receptor (OR) system within the network controlling Na+ detection and integration, i.e. the lamina terminalis.
Objective: (1) To identify the action and cellular mechanism of the OR on the excitability of the neuronal populations of the median preoptic nucleus, a structure of the lamina terminalis involved in detection and integration of chemosensory signals. (2) To investigate possible plasticity of the OR system in the MnPO induced by an episode of Na+ depletion/repletion.
Methods: The modulatory action of OR on neuronal excitability and putative plastic changes in opioid signaling was investigated with an electrophysiological approach (patch-clamp technique) applied to a rodent model of salt appetite (loop diuretic and Na+ depleted food).
Results: Activation of µ-, but not δ-OR triggered a membrane hyperpolarization by recruiting a GIRK conductance in 41% of the MnPO neurons tested. Interestingly, 24h Na+ depletion strengthened this opioid-mediated control of neuronal excitability. In Na+-depleted animals, the neuronal population displaying the µ-OR-induced hyperpolarization expanded to 60%, whereas Na+ repletion restored this population to the control level (39%). Among the neurons displaying µ-OR-induced hyperpolarization, Na+ depletion specifically increased the neuronal population responsive to variation in ambient Na+. In contrast, Na+ repletion dramatically reduced the population that was unresponsive to Na+. The observed change in the populations responding to μ-OR was not correlated with a change in either the basic properties of the neurons, or the characteristics of the µ-OR-induced response.
Conclusion: Our results indicate that an episode of Na+ depletion / Na+ repletion modifies the organization of the opioid-sensitive network of the MnPO. Such network plasticity might represent an essential aspect of both the homeostatic adaptation during Na+ depletion and the engagement of the salt ingestive behavior.
  
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